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  1. Psychology News Robot @[email protected] ·

    DATE: August 29, 2026 at 07:00AM
    SOURCE: PSYPOST.ORG

    ** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
    -------------------------------------------------

    TITLE: Brain scans reveal how artificial sweeteners affect our reward circuits differently than sugar

    URL: psypost.org/brain-scans-reveal

    An experimental study compared changes in brain activity after ingestion of water and different types of flavored waters. Results showed that cerebral blood flow in the hypothalamus (a brain region that controls homeostatic processes like hunger and thirst) was not differentially affected by any of the drinks. However, the ventral tegmental area (a midbrain region involved in reward and motivation) showed lower changes in cerebral blood flow after sucrose than after water, sucralose, or monk fruit drink ingestion. The paper was published in The American Journal of Clinical Nutrition.

    As obesity rates have risen worldwide, reducing excessive energy intake has become an important goal for both individuals and public health. One widely used strategy is to replace sugar with low- or no-calorie sweeteners, particularly in beverages, where added sugars can contribute substantially to daily calorie intake. Although concerns are often raised that exposure to sweetness might increase cravings for sweet foods, current evidence does not consistently support this idea.

    At the same time, low- and no-calorie sweeteners should not necessarily be viewed as a single, uniform group. Different sweeteners can vary in taste, metabolic effects, effects on the gut microbiome, and the physiological responses they produce after consumption. Sugars themselves also differ in how they are processed by the body and in their effects on blood glucose and other metabolic processes.

    Because the brain plays a central role in hunger, satiety, reward, and energy regulation, researchers are increasingly interested in how different sweeteners influence brain activity after consumption. Brain-imaging research suggests that caloric sugars and non-caloric sweeteners may sometimes produce different responses in regions involved in appetite regulation, including the hypothalamus, although findings remain inconsistent.

    Study author Paul AM Smeets and his colleagues conducted a study in which they examined changes in brain activity and physiological markers after the ingestion of flavored waters sweetened with the sugar sucrose or various low-no-calorie sweeteners. They hypothesized that sugar sucrose would elicit decreased cerebral blood flow (indicating decreased neural activity) in brain areas related to food intake regulation and reward 30 minutes after ingestion. They expected that low- or no-calorie sweeteners and water would not produce such effects due to their low or absent energy content.

    Study participants were 30 healthy individuals. Fifteen of them were men. Their average age was 23 years. They completed six treatment sessions between February 2023 and March 2024.

    The treatment consisted of ingestion of 500 milliliters of either water or one of five equally sweet, lemon-lime flavored waters sweetened with sucrose (25 grams, 97 kcal) or sucralose, stevia extract, monk fruit extract, or allulose + stevia extract.

    Sucralose is a high-intensity artificial sweetener made from modified sucrose that provides sweetness with virtually no calories. Stevia extract is a plant-derived sweetener obtained from Stevia rebaudiana and contains sweet compounds called steviol glycosides. Monk fruit extract is a natural high-intensity sweetener derived from Siraitia grosvenorii fruit. Allulose is a rare low-calorie sugar with properties similar to ordinary sugar. Stevia is mixed with allulose to increase sweetness while keeping calorie content low. These sweeteners add little or no calories to a drink.

    At the start of the treatment procedure, participants completed magnetic resonance imaging scans of their brains and of their stomachs. They also answered questions about appetite and well-being verbally. After this, they drank the drink assigned to them on the occasion. This was followed by two more scans of their brains and of their stomachs at different times up to 45 minutes after drinking.

    Participants gave blood samples at the start and five more times up to an hour after drinking their assigned beverage (except on the day they received water). After the first sip, participants rated the tastiness and sweetness of the drink they consumed. All participants consumed their drinks within five minutes. Sixty minutes after drinking, after all the procedures were completed, participants were offered a takeaway breakfast.

    Results showed that all sweet drinks were liked equally, except monk fruit, which was liked modestly less than the sucrose-sweetened drink. All sweetened drinks except the one with monk fruit were liked more than water. All sweetened drinks were perceived as sweeter than water. The monk fruit-sweetened drink and the drink sweetened with allulose+stevia were rated modestly less sweet than the sucrose-sweetened drink.

    Cerebral blood flow in the hypothalamus was similarly affected by all sweet drinks. Cerebral blood flow is an indirect indicator of activity in a particular region of the brain, with higher cerebral blood flow generally suggesting higher neural activity.

    In the ventral tegmental area, the change in the cerebral blood flow was lower after sucrose than after water, sucralose, and monk fruit drink 30 minutes after ingestion. This suggests that neural activity in that region of the brain was lower after ingesting the sucrose-sweetened drink than after water, and drinks sweetened with sucralose and monk fruit extract.

    Exploratory analyses showed increased cerebral blood flow (and thus increased neural activity) after consumption of the allulose+stevia-sweetened drink in the amygdala region of the brain and after the stevia-sweetened drink in the putamen region of the brain compared to the sucrose-sweetened drink. Despite its low energy content, the allulose+stevia-sweetened drink delayed gastric emptying (the speed at which food leaves the stomach) similar to the sucrose-sweetened drink, whereas only the sucrose-sweetened drink increased glucose and insulin concentrations.

    “Although flavored waters with LNCS [low or no calorie sweeteners] mostly elicit similar neural and gastrointestinal responses as water, they have some distinct effects on the brain compared with 25 g of sucrose, particularly in reward-related brain areas,” study authors concluded.

    The study contributes to the scientific knowledge about brain reactions to sweetened beverages. However, it should be noted that the study was conducted on a very small group of participants, which may have made some differences in brain reactions undetectable using usual statistical procedures. Also, participants were young people and results may not generalize to other age groups.

    The paper, “Brain and physiological responses to flavored waters with different sweeteners: a randomized crossover study in healthy young adults,” was authored by Paul AM Smeets, Ralf Veit, Els Oosterink, Saskia Meijboom, Davide Risso, Hubert Preissl, and Stephanie Kullmann.

    URL: psypost.org/brain-scans-reveal

    -------------------------------------------------

    Private, vetted email list for mental health professionals: clinicians-exchange.org

    Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot

    -------------------------------------------------

    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #BrainImaging #SweetenersVsSugar #VTA #Hypothalamus #Neuroscience #FlavorBevStudy #LowCalorieSweeteners #SucroseContrast #NeuralReward #FoodScience

    #psychology #counseling #socialwork #psychotherapy #mentalhealth #psychiatry
  2. Psychology News Robot @[email protected] ·

    DATE: August 29, 2026 at 07:00AM
    SOURCE: PSYPOST.ORG

    ** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
    -------------------------------------------------

    TITLE: Brain scans reveal how artificial sweeteners affect our reward circuits differently than sugar

    URL: psypost.org/brain-scans-reveal

    An experimental study compared changes in brain activity after ingestion of water and different types of flavored waters. Results showed that cerebral blood flow in the hypothalamus (a brain region that controls homeostatic processes like hunger and thirst) was not differentially affected by any of the drinks. However, the ventral tegmental area (a midbrain region involved in reward and motivation) showed lower changes in cerebral blood flow after sucrose than after water, sucralose, or monk fruit drink ingestion. The paper was published in The American Journal of Clinical Nutrition.

    As obesity rates have risen worldwide, reducing excessive energy intake has become an important goal for both individuals and public health. One widely used strategy is to replace sugar with low- or no-calorie sweeteners, particularly in beverages, where added sugars can contribute substantially to daily calorie intake. Although concerns are often raised that exposure to sweetness might increase cravings for sweet foods, current evidence does not consistently support this idea.

    At the same time, low- and no-calorie sweeteners should not necessarily be viewed as a single, uniform group. Different sweeteners can vary in taste, metabolic effects, effects on the gut microbiome, and the physiological responses they produce after consumption. Sugars themselves also differ in how they are processed by the body and in their effects on blood glucose and other metabolic processes.

    Because the brain plays a central role in hunger, satiety, reward, and energy regulation, researchers are increasingly interested in how different sweeteners influence brain activity after consumption. Brain-imaging research suggests that caloric sugars and non-caloric sweeteners may sometimes produce different responses in regions involved in appetite regulation, including the hypothalamus, although findings remain inconsistent.

    Study author Paul AM Smeets and his colleagues conducted a study in which they examined changes in brain activity and physiological markers after the ingestion of flavored waters sweetened with the sugar sucrose or various low-no-calorie sweeteners. They hypothesized that sugar sucrose would elicit decreased cerebral blood flow (indicating decreased neural activity) in brain areas related to food intake regulation and reward 30 minutes after ingestion. They expected that low- or no-calorie sweeteners and water would not produce such effects due to their low or absent energy content.

    Study participants were 30 healthy individuals. Fifteen of them were men. Their average age was 23 years. They completed six treatment sessions between February 2023 and March 2024.

    The treatment consisted of ingestion of 500 milliliters of either water or one of five equally sweet, lemon-lime flavored waters sweetened with sucrose (25 grams, 97 kcal) or sucralose, stevia extract, monk fruit extract, or allulose + stevia extract.

    Sucralose is a high-intensity artificial sweetener made from modified sucrose that provides sweetness with virtually no calories. Stevia extract is a plant-derived sweetener obtained from Stevia rebaudiana and contains sweet compounds called steviol glycosides. Monk fruit extract is a natural high-intensity sweetener derived from Siraitia grosvenorii fruit. Allulose is a rare low-calorie sugar with properties similar to ordinary sugar. Stevia is mixed with allulose to increase sweetness while keeping calorie content low. These sweeteners add little or no calories to a drink.

    At the start of the treatment procedure, participants completed magnetic resonance imaging scans of their brains and of their stomachs. They also answered questions about appetite and well-being verbally. After this, they drank the drink assigned to them on the occasion. This was followed by two more scans of their brains and of their stomachs at different times up to 45 minutes after drinking.

    Participants gave blood samples at the start and five more times up to an hour after drinking their assigned beverage (except on the day they received water). After the first sip, participants rated the tastiness and sweetness of the drink they consumed. All participants consumed their drinks within five minutes. Sixty minutes after drinking, after all the procedures were completed, participants were offered a takeaway breakfast.

    Results showed that all sweet drinks were liked equally, except monk fruit, which was liked modestly less than the sucrose-sweetened drink. All sweetened drinks except the one with monk fruit were liked more than water. All sweetened drinks were perceived as sweeter than water. The monk fruit-sweetened drink and the drink sweetened with allulose+stevia were rated modestly less sweet than the sucrose-sweetened drink.

    Cerebral blood flow in the hypothalamus was similarly affected by all sweet drinks. Cerebral blood flow is an indirect indicator of activity in a particular region of the brain, with higher cerebral blood flow generally suggesting higher neural activity.

    In the ventral tegmental area, the change in the cerebral blood flow was lower after sucrose than after water, sucralose, and monk fruit drink 30 minutes after ingestion. This suggests that neural activity in that region of the brain was lower after ingesting the sucrose-sweetened drink than after water, and drinks sweetened with sucralose and monk fruit extract.

    Exploratory analyses showed increased cerebral blood flow (and thus increased neural activity) after consumption of the allulose+stevia-sweetened drink in the amygdala region of the brain and after the stevia-sweetened drink in the putamen region of the brain compared to the sucrose-sweetened drink. Despite its low energy content, the allulose+stevia-sweetened drink delayed gastric emptying (the speed at which food leaves the stomach) similar to the sucrose-sweetened drink, whereas only the sucrose-sweetened drink increased glucose and insulin concentrations.

    “Although flavored waters with LNCS [low or no calorie sweeteners] mostly elicit similar neural and gastrointestinal responses as water, they have some distinct effects on the brain compared with 25 g of sucrose, particularly in reward-related brain areas,” study authors concluded.

    The study contributes to the scientific knowledge about brain reactions to sweetened beverages. However, it should be noted that the study was conducted on a very small group of participants, which may have made some differences in brain reactions undetectable using usual statistical procedures. Also, participants were young people and results may not generalize to other age groups.

    The paper, “Brain and physiological responses to flavored waters with different sweeteners: a randomized crossover study in healthy young adults,” was authored by Paul AM Smeets, Ralf Veit, Els Oosterink, Saskia Meijboom, Davide Risso, Hubert Preissl, and Stephanie Kullmann.

    URL: psypost.org/brain-scans-reveal

    -------------------------------------------------

    Private, vetted email list for mental health professionals: clinicians-exchange.org

    Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot

    -------------------------------------------------

    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #BrainImaging #SweetenersVsSugar #VTA #Hypothalamus #Neuroscience #FlavorBevStudy #LowCalorieSweeteners #SucroseContrast #NeuralReward #FoodScience

    #foodscience #neuralreward #sucrosecontrast #lowcaloriesweeteners #flavorbevstudy #neuroscience
  3. Psychology News Robot @[email protected] ·

    DATE: August 29, 2026 at 07:00AM
    SOURCE: PSYPOST.ORG

    ** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
    -------------------------------------------------

    TITLE: Brain scans reveal how artificial sweeteners affect our reward circuits differently than sugar

    URL: psypost.org/brain-scans-reveal

    An experimental study compared changes in brain activity after ingestion of water and different types of flavored waters. Results showed that cerebral blood flow in the hypothalamus (a brain region that controls homeostatic processes like hunger and thirst) was not differentially affected by any of the drinks. However, the ventral tegmental area (a midbrain region involved in reward and motivation) showed lower changes in cerebral blood flow after sucrose than after water, sucralose, or monk fruit drink ingestion. The paper was published in The American Journal of Clinical Nutrition.

    As obesity rates have risen worldwide, reducing excessive energy intake has become an important goal for both individuals and public health. One widely used strategy is to replace sugar with low- or no-calorie sweeteners, particularly in beverages, where added sugars can contribute substantially to daily calorie intake. Although concerns are often raised that exposure to sweetness might increase cravings for sweet foods, current evidence does not consistently support this idea.

    At the same time, low- and no-calorie sweeteners should not necessarily be viewed as a single, uniform group. Different sweeteners can vary in taste, metabolic effects, effects on the gut microbiome, and the physiological responses they produce after consumption. Sugars themselves also differ in how they are processed by the body and in their effects on blood glucose and other metabolic processes.

    Because the brain plays a central role in hunger, satiety, reward, and energy regulation, researchers are increasingly interested in how different sweeteners influence brain activity after consumption. Brain-imaging research suggests that caloric sugars and non-caloric sweeteners may sometimes produce different responses in regions involved in appetite regulation, including the hypothalamus, although findings remain inconsistent.

    Study author Paul AM Smeets and his colleagues conducted a study in which they examined changes in brain activity and physiological markers after the ingestion of flavored waters sweetened with the sugar sucrose or various low-no-calorie sweeteners. They hypothesized that sugar sucrose would elicit decreased cerebral blood flow (indicating decreased neural activity) in brain areas related to food intake regulation and reward 30 minutes after ingestion. They expected that low- or no-calorie sweeteners and water would not produce such effects due to their low or absent energy content.

    Study participants were 30 healthy individuals. Fifteen of them were men. Their average age was 23 years. They completed six treatment sessions between February 2023 and March 2024.

    The treatment consisted of ingestion of 500 milliliters of either water or one of five equally sweet, lemon-lime flavored waters sweetened with sucrose (25 grams, 97 kcal) or sucralose, stevia extract, monk fruit extract, or allulose + stevia extract.

    Sucralose is a high-intensity artificial sweetener made from modified sucrose that provides sweetness with virtually no calories. Stevia extract is a plant-derived sweetener obtained from Stevia rebaudiana and contains sweet compounds called steviol glycosides. Monk fruit extract is a natural high-intensity sweetener derived from Siraitia grosvenorii fruit. Allulose is a rare low-calorie sugar with properties similar to ordinary sugar. Stevia is mixed with allulose to increase sweetness while keeping calorie content low. These sweeteners add little or no calories to a drink.

    At the start of the treatment procedure, participants completed magnetic resonance imaging scans of their brains and of their stomachs. They also answered questions about appetite and well-being verbally. After this, they drank the drink assigned to them on the occasion. This was followed by two more scans of their brains and of their stomachs at different times up to 45 minutes after drinking.

    Participants gave blood samples at the start and five more times up to an hour after drinking their assigned beverage (except on the day they received water). After the first sip, participants rated the tastiness and sweetness of the drink they consumed. All participants consumed their drinks within five minutes. Sixty minutes after drinking, after all the procedures were completed, participants were offered a takeaway breakfast.

    Results showed that all sweet drinks were liked equally, except monk fruit, which was liked modestly less than the sucrose-sweetened drink. All sweetened drinks except the one with monk fruit were liked more than water. All sweetened drinks were perceived as sweeter than water. The monk fruit-sweetened drink and the drink sweetened with allulose+stevia were rated modestly less sweet than the sucrose-sweetened drink.

    Cerebral blood flow in the hypothalamus was similarly affected by all sweet drinks. Cerebral blood flow is an indirect indicator of activity in a particular region of the brain, with higher cerebral blood flow generally suggesting higher neural activity.

    In the ventral tegmental area, the change in the cerebral blood flow was lower after sucrose than after water, sucralose, and monk fruit drink 30 minutes after ingestion. This suggests that neural activity in that region of the brain was lower after ingesting the sucrose-sweetened drink than after water, and drinks sweetened with sucralose and monk fruit extract.

    Exploratory analyses showed increased cerebral blood flow (and thus increased neural activity) after consumption of the allulose+stevia-sweetened drink in the amygdala region of the brain and after the stevia-sweetened drink in the putamen region of the brain compared to the sucrose-sweetened drink. Despite its low energy content, the allulose+stevia-sweetened drink delayed gastric emptying (the speed at which food leaves the stomach) similar to the sucrose-sweetened drink, whereas only the sucrose-sweetened drink increased glucose and insulin concentrations.

    “Although flavored waters with LNCS [low or no calorie sweeteners] mostly elicit similar neural and gastrointestinal responses as water, they have some distinct effects on the brain compared with 25 g of sucrose, particularly in reward-related brain areas,” study authors concluded.

    The study contributes to the scientific knowledge about brain reactions to sweetened beverages. However, it should be noted that the study was conducted on a very small group of participants, which may have made some differences in brain reactions undetectable using usual statistical procedures. Also, participants were young people and results may not generalize to other age groups.

    The paper, “Brain and physiological responses to flavored waters with different sweeteners: a randomized crossover study in healthy young adults,” was authored by Paul AM Smeets, Ralf Veit, Els Oosterink, Saskia Meijboom, Davide Risso, Hubert Preissl, and Stephanie Kullmann.

    URL: psypost.org/brain-scans-reveal

    -------------------------------------------------

    Private, vetted email list for mental health professionals: clinicians-exchange.org

    Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot

    -------------------------------------------------

    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #BrainImaging #SweetenersVsSugar #VTA #Hypothalamus #Neuroscience #FlavorBevStudy #LowCalorieSweeteners #SucroseContrast #NeuralReward #FoodScience

    #psychology #counseling #socialwork #psychotherapy #mentalhealth #psychiatry
  4. Österreich @[email protected] ·

    europesays.com/at/353975/ OPA1 in MC4R-Neuronen steuert Fetthunger und Körpergewicht – mit deutlichen Geschlechtsunterschieden #Adipositas #AI #Appetit #ARTIFICIALINTELLIGENCE #AT #Austria #Fett #Gehirn #Geist #Geschlechtsunterschiede #Gesundheit #Health #Hypothalamus #KI #KünstlicheIntelligenz #Mausmodell #Mc4r #MenschlicheErnährung #Mitochondrien #Neurologie #Neuroscience #Neurowissenschaften #Opa1 #Österreich #Setmelanotid

    #setmelanotid #osterreich #opa1 #neurowissenschaften #neuroscience #neurologie
  5. Psychology News Robot @[email protected] ·

    DATE: August 24, 2026 at 04:00PM
    SOURCE: PSYPOST.ORG

    ** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
    -------------------------------------------------

    TITLE: Mitochondrial protein in the brain regulates dietary fat intake and body weight

    URL: psypost.org/mitochondrial-prot

    A recent study published in The FASEB Journal provides evidence that a specific mitochondrial protein in the brain helps regulate appetite and body weight in response to dietary fat. The research indicates that lacking this protein in a specific group of appetite-controlling neurons leads to increased fat consumption and obesity in mice, with the effects being especially pronounced in females.

    “I think the important message is that the brain does not simply respond to how much we eat, but also responds differently depending on the type of food we consume,” said Shigenobu Matsumura, a researcher in the Department of Nutrition at Osaka Metropolitan University. “Our study suggests that mitochondria in a specific population of neurons, MC4R neurons, are important for controlling the appetite for dietary fat and body weight.”

    The melanocortin 4 receptor, often abbreviated as MC4R, is a signaling protein located in the hypothalamus, a brain region that manages hunger and energy balance. A 1997 study published in Cell demonstrated that disrupting the MC4R pathway in mice leads to severe obesity and overeating. Building on this foundation, a 2019 review in Trends in Molecular Medicine discussed how MC4R signaling is a major target for human obesity treatments.

    Brain cells demand massive amounts of energy, making them heavily reliant on mitochondria, the energy-producing structures inside cells. These structures constantly merge and divide to adapt to metabolic needs. Optic atrophy protein 1, or OPA1, is a protein that manages the fusion of the inner mitochondrial membrane and maintains its internal structure.

    The importance of MC4R and mitochondria in metabolism is well documented, but how dietary fat directly influences these cellular dynamics was not fully understood. A 2022 review in the International Journal of Molecular Sciences detailed how the hormone estrogen regulates mitochondrial fusion and division, pointing to potential biological sex differences in metabolic stress responses. This gap in knowledge motivated the current research team to explore how OPA1 inside MC4R neurons responds to fat consumption and influences body weight across both sexes.

    “We have been interested in whether neuronal energy metabolism is affected by the type of food we eat and, if so, how important this is for appetite and body weight regulation,” Matsumura explained.

    The researchers first looked at how dietary fat affects normal, wild-type mice. They provided eight-week-old mice with voluntary access to liquid soybean oil alongside a standard chow diet. After six weeks of this feeding regimen, the scientists examined the animals’ brains.

    They found that male mice showed a 1.6-fold relative increase in hypothalamic OPA1 gene expression compared to male mice kept strictly on a standard diet. Female mice did not experience this increase in OPA1 expression. Brain cells typically rely on sugars for fuel, making this lipid-driven genetic response an unexpected result.

    “The most surprising finding was that dietary fat intake changed the expression of genes related to neuronal mitochondria,” Matsumura told PsyPost. “In general, neurons mainly use carbohydrates as an energy source, and when fatty acid use increases, mitochondrial activity should also increase. Considering these facts, we did not expect that increased fat intake would affect the expression of mitochondrial genes in this way.”

    Next, the team genetically engineered mice to lack the OPA1 protein specifically within their MC4R-expressing neurons. They tracked the body weight and food intake of these knockout mice, alongside normal control mice, over several months. Using specialized metabolic cages, they also measured the animals’ oxygen consumption, carbon dioxide production, and daily physical activity.

    Even when fed a standard chow diet, the OPA1 knockout mice of both sexes gradually grew heavier than the control animals. Noticeable weight differences began to appear around 18 to 20 weeks of age. At this point, the knockout mice began consuming more food than the controls, suggesting that OPA1 helps these neurons properly regulate appetite even in the absence of high-fat foods.

    The researchers then introduced voluntary soybean oil ingestion to another group of eight-week-old mice. The control mice maintained a relatively stable body weight trajectory when given the oil. In contrast, the OPA1 knockout mice consumed higher amounts of the soybean oil and experienced progressive, rapid obesity. This weight gain was highly pronounced in the female knockout mice. By 22 weeks of age, the female knockout mice reached an average body weight of nearly 50 grams, compared to about 35 grams for the control females.

    The finding reframes how researchers might view weight gain on a cellular level. “I think one interesting point of this study is that it connects dietary fat, neuronal energy metabolism, and the regulation of appetite,” Matsumura noted. “Obesity is often discussed mainly in terms of how much people eat, but our findings suggest that the energy metabolism of specific neurons may also influence how strongly the brain responds to dietary fat.”

    To check if the MC4R signaling pathway was completely broken in these engineered mice, the researchers administered setmelanotide, a drug that activates MC4R. After a 24-hour fasting period, they injected groups of six to seven mice with either a placebo or the drug and measured their food intake. In control mice and male knockout mice, the drug successfully suppressed feeding over the following four hours.

    In the female knockout mice, the appetite-suppressing effect of the setmelanotide was blunted. This indicates that the loss of OPA1 disrupts the metabolic outcomes of MC4R signaling more severely in females, rather than simply turning the receptor off entirely. The researchers also measured gene expression and found that male mice eating soybean oil had coordinated changes in appetite-related genes. The female mice showed far less consistent genetic responses to the fat intake.

    “Interestingly, we found a clear sex difference, suggesting that the mechanisms regulating dietary fat intake may be different between males and females,” Matsumura added. “In addition, the sex difference we observed may be important for understanding why the mechanisms underlying obesity can differ between men and women.”

    Mouse models of metabolism do not entirely replicate human metabolic disorders, meaning these mechanisms require further validation. The study relied on analyzing bulk tissue from the hypothalamus to measure gene expression, which might mask subtle changes happening in individual cell types.

    “The most important caveat is that these findings were obtained in mice, so we do not yet know whether the same mechanism occurs in humans,” Matsumura said. “We also used soybean oil as the dietary fat source, and it remains to be determined whether different types of dietary fat have the same effects. In addition, we do not yet fully understand the mechanism responsible for the sex difference.”

    Future research is needed to isolate these specific neurons to get an exact picture of their internal workings. “We would like to understand how dietary fat regulates OPA1 and mitochondrial function in MC4R neurons, and why this regulation differs between males and females,” Matsumura explained.

    “We are also interested in determining whether different types of dietary fat produce different responses. Ultimately, we hope to determine whether this mechanism is relevant to human obesity and whether mitochondrial function could help explain differences in response to MC4R-targeted obesity treatments.”

    The study, “OPA1 in MC4R Neurons Regulates Dietary Fat Intake and Body Weight in Mice,” was authored by Shigenobu Matsumura, Mizuki Fujiwara, Soyoka Horie, Miona Marutani, Eri Nousou, Nanase Iki, Yuka Yamato, Yui Otonashi, Tsutomu Sasaki, Mina Fujitani, and Teppei Fujikawa.

    URL: psypost.org/mitochondrial-prot

    -------------------------------------------------

    Private, vetted email list for mental health professionals: clinicians-exchange.org

    Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot

    -------------------------------------------------

    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #OPA1 #MC4R #hypothalamus #mitochondria #dietaryfat #weightregulation #sexdifferences #obesityresearch #neuronenergymetabolism #setmelanotide

    #psychology #counseling #socialwork #psychotherapy #mentalhealth #psychiatry
  6. Psychology News Robot @[email protected] ·

    DATE: August 24, 2026 at 04:00PM
    SOURCE: PSYPOST.ORG

    ** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
    -------------------------------------------------

    TITLE: Mitochondrial protein in the brain regulates dietary fat intake and body weight

    URL: psypost.org/mitochondrial-prot

    A recent study published in The FASEB Journal provides evidence that a specific mitochondrial protein in the brain helps regulate appetite and body weight in response to dietary fat. The research indicates that lacking this protein in a specific group of appetite-controlling neurons leads to increased fat consumption and obesity in mice, with the effects being especially pronounced in females.

    “I think the important message is that the brain does not simply respond to how much we eat, but also responds differently depending on the type of food we consume,” said Shigenobu Matsumura, a researcher in the Department of Nutrition at Osaka Metropolitan University. “Our study suggests that mitochondria in a specific population of neurons, MC4R neurons, are important for controlling the appetite for dietary fat and body weight.”

    The melanocortin 4 receptor, often abbreviated as MC4R, is a signaling protein located in the hypothalamus, a brain region that manages hunger and energy balance. A 1997 study published in Cell demonstrated that disrupting the MC4R pathway in mice leads to severe obesity and overeating. Building on this foundation, a 2019 review in Trends in Molecular Medicine discussed how MC4R signaling is a major target for human obesity treatments.

    Brain cells demand massive amounts of energy, making them heavily reliant on mitochondria, the energy-producing structures inside cells. These structures constantly merge and divide to adapt to metabolic needs. Optic atrophy protein 1, or OPA1, is a protein that manages the fusion of the inner mitochondrial membrane and maintains its internal structure.

    The importance of MC4R and mitochondria in metabolism is well documented, but how dietary fat directly influences these cellular dynamics was not fully understood. A 2022 review in the International Journal of Molecular Sciences detailed how the hormone estrogen regulates mitochondrial fusion and division, pointing to potential biological sex differences in metabolic stress responses. This gap in knowledge motivated the current research team to explore how OPA1 inside MC4R neurons responds to fat consumption and influences body weight across both sexes.

    “We have been interested in whether neuronal energy metabolism is affected by the type of food we eat and, if so, how important this is for appetite and body weight regulation,” Matsumura explained.

    The researchers first looked at how dietary fat affects normal, wild-type mice. They provided eight-week-old mice with voluntary access to liquid soybean oil alongside a standard chow diet. After six weeks of this feeding regimen, the scientists examined the animals’ brains.

    They found that male mice showed a 1.6-fold relative increase in hypothalamic OPA1 gene expression compared to male mice kept strictly on a standard diet. Female mice did not experience this increase in OPA1 expression. Brain cells typically rely on sugars for fuel, making this lipid-driven genetic response an unexpected result.

    “The most surprising finding was that dietary fat intake changed the expression of genes related to neuronal mitochondria,” Matsumura told PsyPost. “In general, neurons mainly use carbohydrates as an energy source, and when fatty acid use increases, mitochondrial activity should also increase. Considering these facts, we did not expect that increased fat intake would affect the expression of mitochondrial genes in this way.”

    Next, the team genetically engineered mice to lack the OPA1 protein specifically within their MC4R-expressing neurons. They tracked the body weight and food intake of these knockout mice, alongside normal control mice, over several months. Using specialized metabolic cages, they also measured the animals’ oxygen consumption, carbon dioxide production, and daily physical activity.

    Even when fed a standard chow diet, the OPA1 knockout mice of both sexes gradually grew heavier than the control animals. Noticeable weight differences began to appear around 18 to 20 weeks of age. At this point, the knockout mice began consuming more food than the controls, suggesting that OPA1 helps these neurons properly regulate appetite even in the absence of high-fat foods.

    The researchers then introduced voluntary soybean oil ingestion to another group of eight-week-old mice. The control mice maintained a relatively stable body weight trajectory when given the oil. In contrast, the OPA1 knockout mice consumed higher amounts of the soybean oil and experienced progressive, rapid obesity. This weight gain was highly pronounced in the female knockout mice. By 22 weeks of age, the female knockout mice reached an average body weight of nearly 50 grams, compared to about 35 grams for the control females.

    The finding reframes how researchers might view weight gain on a cellular level. “I think one interesting point of this study is that it connects dietary fat, neuronal energy metabolism, and the regulation of appetite,” Matsumura noted. “Obesity is often discussed mainly in terms of how much people eat, but our findings suggest that the energy metabolism of specific neurons may also influence how strongly the brain responds to dietary fat.”

    To check if the MC4R signaling pathway was completely broken in these engineered mice, the researchers administered setmelanotide, a drug that activates MC4R. After a 24-hour fasting period, they injected groups of six to seven mice with either a placebo or the drug and measured their food intake. In control mice and male knockout mice, the drug successfully suppressed feeding over the following four hours.

    In the female knockout mice, the appetite-suppressing effect of the setmelanotide was blunted. This indicates that the loss of OPA1 disrupts the metabolic outcomes of MC4R signaling more severely in females, rather than simply turning the receptor off entirely. The researchers also measured gene expression and found that male mice eating soybean oil had coordinated changes in appetite-related genes. The female mice showed far less consistent genetic responses to the fat intake.

    “Interestingly, we found a clear sex difference, suggesting that the mechanisms regulating dietary fat intake may be different between males and females,” Matsumura added. “In addition, the sex difference we observed may be important for understanding why the mechanisms underlying obesity can differ between men and women.”

    Mouse models of metabolism do not entirely replicate human metabolic disorders, meaning these mechanisms require further validation. The study relied on analyzing bulk tissue from the hypothalamus to measure gene expression, which might mask subtle changes happening in individual cell types.

    “The most important caveat is that these findings were obtained in mice, so we do not yet know whether the same mechanism occurs in humans,” Matsumura said. “We also used soybean oil as the dietary fat source, and it remains to be determined whether different types of dietary fat have the same effects. In addition, we do not yet fully understand the mechanism responsible for the sex difference.”

    Future research is needed to isolate these specific neurons to get an exact picture of their internal workings. “We would like to understand how dietary fat regulates OPA1 and mitochondrial function in MC4R neurons, and why this regulation differs between males and females,” Matsumura explained.

    “We are also interested in determining whether different types of dietary fat produce different responses. Ultimately, we hope to determine whether this mechanism is relevant to human obesity and whether mitochondrial function could help explain differences in response to MC4R-targeted obesity treatments.”

    The study, “OPA1 in MC4R Neurons Regulates Dietary Fat Intake and Body Weight in Mice,” was authored by Shigenobu Matsumura, Mizuki Fujiwara, Soyoka Horie, Miona Marutani, Eri Nousou, Nanase Iki, Yuka Yamato, Yui Otonashi, Tsutomu Sasaki, Mina Fujitani, and Teppei Fujikawa.

    URL: psypost.org/mitochondrial-prot

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    #setmelanotide #neuronenergymetabolism #obesityresearch #sexdifferences #weightregulation #dietaryfat
  7. Psychology News Robot @[email protected] ·

    DATE: August 24, 2026 at 04:00PM
    SOURCE: PSYPOST.ORG

    ** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
    -------------------------------------------------

    TITLE: Mitochondrial protein in the brain regulates dietary fat intake and body weight

    URL: psypost.org/mitochondrial-prot

    A recent study published in The FASEB Journal provides evidence that a specific mitochondrial protein in the brain helps regulate appetite and body weight in response to dietary fat. The research indicates that lacking this protein in a specific group of appetite-controlling neurons leads to increased fat consumption and obesity in mice, with the effects being especially pronounced in females.

    “I think the important message is that the brain does not simply respond to how much we eat, but also responds differently depending on the type of food we consume,” said Shigenobu Matsumura, a researcher in the Department of Nutrition at Osaka Metropolitan University. “Our study suggests that mitochondria in a specific population of neurons, MC4R neurons, are important for controlling the appetite for dietary fat and body weight.”

    The melanocortin 4 receptor, often abbreviated as MC4R, is a signaling protein located in the hypothalamus, a brain region that manages hunger and energy balance. A 1997 study published in Cell demonstrated that disrupting the MC4R pathway in mice leads to severe obesity and overeating. Building on this foundation, a 2019 review in Trends in Molecular Medicine discussed how MC4R signaling is a major target for human obesity treatments.

    Brain cells demand massive amounts of energy, making them heavily reliant on mitochondria, the energy-producing structures inside cells. These structures constantly merge and divide to adapt to metabolic needs. Optic atrophy protein 1, or OPA1, is a protein that manages the fusion of the inner mitochondrial membrane and maintains its internal structure.

    The importance of MC4R and mitochondria in metabolism is well documented, but how dietary fat directly influences these cellular dynamics was not fully understood. A 2022 review in the International Journal of Molecular Sciences detailed how the hormone estrogen regulates mitochondrial fusion and division, pointing to potential biological sex differences in metabolic stress responses. This gap in knowledge motivated the current research team to explore how OPA1 inside MC4R neurons responds to fat consumption and influences body weight across both sexes.

    “We have been interested in whether neuronal energy metabolism is affected by the type of food we eat and, if so, how important this is for appetite and body weight regulation,” Matsumura explained.

    The researchers first looked at how dietary fat affects normal, wild-type mice. They provided eight-week-old mice with voluntary access to liquid soybean oil alongside a standard chow diet. After six weeks of this feeding regimen, the scientists examined the animals’ brains.

    They found that male mice showed a 1.6-fold relative increase in hypothalamic OPA1 gene expression compared to male mice kept strictly on a standard diet. Female mice did not experience this increase in OPA1 expression. Brain cells typically rely on sugars for fuel, making this lipid-driven genetic response an unexpected result.

    “The most surprising finding was that dietary fat intake changed the expression of genes related to neuronal mitochondria,” Matsumura told PsyPost. “In general, neurons mainly use carbohydrates as an energy source, and when fatty acid use increases, mitochondrial activity should also increase. Considering these facts, we did not expect that increased fat intake would affect the expression of mitochondrial genes in this way.”

    Next, the team genetically engineered mice to lack the OPA1 protein specifically within their MC4R-expressing neurons. They tracked the body weight and food intake of these knockout mice, alongside normal control mice, over several months. Using specialized metabolic cages, they also measured the animals’ oxygen consumption, carbon dioxide production, and daily physical activity.

    Even when fed a standard chow diet, the OPA1 knockout mice of both sexes gradually grew heavier than the control animals. Noticeable weight differences began to appear around 18 to 20 weeks of age. At this point, the knockout mice began consuming more food than the controls, suggesting that OPA1 helps these neurons properly regulate appetite even in the absence of high-fat foods.

    The researchers then introduced voluntary soybean oil ingestion to another group of eight-week-old mice. The control mice maintained a relatively stable body weight trajectory when given the oil. In contrast, the OPA1 knockout mice consumed higher amounts of the soybean oil and experienced progressive, rapid obesity. This weight gain was highly pronounced in the female knockout mice. By 22 weeks of age, the female knockout mice reached an average body weight of nearly 50 grams, compared to about 35 grams for the control females.

    The finding reframes how researchers might view weight gain on a cellular level. “I think one interesting point of this study is that it connects dietary fat, neuronal energy metabolism, and the regulation of appetite,” Matsumura noted. “Obesity is often discussed mainly in terms of how much people eat, but our findings suggest that the energy metabolism of specific neurons may also influence how strongly the brain responds to dietary fat.”

    To check if the MC4R signaling pathway was completely broken in these engineered mice, the researchers administered setmelanotide, a drug that activates MC4R. After a 24-hour fasting period, they injected groups of six to seven mice with either a placebo or the drug and measured their food intake. In control mice and male knockout mice, the drug successfully suppressed feeding over the following four hours.

    In the female knockout mice, the appetite-suppressing effect of the setmelanotide was blunted. This indicates that the loss of OPA1 disrupts the metabolic outcomes of MC4R signaling more severely in females, rather than simply turning the receptor off entirely. The researchers also measured gene expression and found that male mice eating soybean oil had coordinated changes in appetite-related genes. The female mice showed far less consistent genetic responses to the fat intake.

    “Interestingly, we found a clear sex difference, suggesting that the mechanisms regulating dietary fat intake may be different between males and females,” Matsumura added. “In addition, the sex difference we observed may be important for understanding why the mechanisms underlying obesity can differ between men and women.”

    Mouse models of metabolism do not entirely replicate human metabolic disorders, meaning these mechanisms require further validation. The study relied on analyzing bulk tissue from the hypothalamus to measure gene expression, which might mask subtle changes happening in individual cell types.

    “The most important caveat is that these findings were obtained in mice, so we do not yet know whether the same mechanism occurs in humans,” Matsumura said. “We also used soybean oil as the dietary fat source, and it remains to be determined whether different types of dietary fat have the same effects. In addition, we do not yet fully understand the mechanism responsible for the sex difference.”

    Future research is needed to isolate these specific neurons to get an exact picture of their internal workings. “We would like to understand how dietary fat regulates OPA1 and mitochondrial function in MC4R neurons, and why this regulation differs between males and females,” Matsumura explained.

    “We are also interested in determining whether different types of dietary fat produce different responses. Ultimately, we hope to determine whether this mechanism is relevant to human obesity and whether mitochondrial function could help explain differences in response to MC4R-targeted obesity treatments.”

    The study, “OPA1 in MC4R Neurons Regulates Dietary Fat Intake and Body Weight in Mice,” was authored by Shigenobu Matsumura, Mizuki Fujiwara, Soyoka Horie, Miona Marutani, Eri Nousou, Nanase Iki, Yuka Yamato, Yui Otonashi, Tsutomu Sasaki, Mina Fujitani, and Teppei Fujikawa.

    URL: psypost.org/mitochondrial-prot

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    Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot

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    #psychology #counseling #socialwork #psychotherapy #mentalhealth #psychiatry
  8. France | République française @[email protected] ·

    europesays.com/fr/1124553/ Les troubles du sommeil précéderaient de plusieurs années les premiers symptômes de la maladie de Charcot #CellulesNerveuses #cerveau #FR #France #Health #hypothalamus #MaladieDeCharcot #MaladieNeuroDégénérative #Motoneurones #MuscleRespiratoire #neurone #NeuroneàOrexine #Santé #sommeil #TroublesDuSommeil #TroublesMoteurs

    #troublesmoteurs #troublesdusommeil #sommeil #sante #neuroneaorexine #neurone
  9. Suisse @[email protected] ·

    europesays.com/ch-fr/258247/ Les troubles du sommeil précéderaient de plusieurs années les premiers symptômes de la maladie de Charcot #CellulesNerveuses #cerveau #Health #Hypothalamus #MaladieDeCharcot #MaladieNeuroDégénérative #Motoneurones #MuscleRespiratoire #Neurone #NeuroneàOrexine #Santé #sommeil #Suisse #TroublesDuSommeil #TroublesMoteurs

    #troublesmoteurs #troublesdusommeil #suisse #sommeil #sante #neuroneaorexine
  10. Belgique @[email protected] ·

    europesays.com/be-fr/210758/ Les troubles du sommeil précéderaient de plusieurs années les premiers symptômes de la maladie de Charcot #BE #BEFr #Belgique #Belgium #CellulesNerveuses #Cerveau #Health #Hypothalamus #MaladieDeCharcot #MaladieNeuroDégénérative #Motoneurones #MuscleRespiratoire #Neurone #NeuroneàOrexine #Santé #Sommeil #TroublesDuSommeil #TroublesMoteurs

    #troublesmoteurs #troublesdusommeil #sommeil #sante #neuroneaorexine #neurone
  11. Österreich @[email protected] ·

    europesays.com/at/313423/ Metformin senkt Blutzucker offenbar auch über das Gehirn #AT #Austria #BaylorCollegeOfMedicine #Blutzucker #Diabetesforschung #Diabetesmedikamente #Gehirn #Gesundheit #Health #Hypothalamus #Insulinresistenz #Metformin #Neurowissenschaften #Österreich #Rap1 #SmartUpNews #Typ2Diabetes #Zuckerstoffwechsel

    #zuckerstoffwechsel #typ2diabetes #smartupnews #rap1 #osterreich #neurowissenschaften
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    Diabetes News: Metformin’s Brain Action

    I can’t take Metformin because it gives me severe diarrhea, but for others, it is good news that…
    #NewsBeep #News #US #USA #UnitedStates #UnitedStatesOfAmerica #Health #hypothalamus #kosdiabetesgroup #metformin #rap1 #Recommended
    newsbeep.com/us/787681/

    #newsbeep #news #us #usa #unitedstates #unitedstatesofamerica
  13. United States News Beep @[email protected] ·

    Diabetes News: Metformin’s Brain Action

    I can’t take Metformin because it gives me severe diarrhea, but for others, it is good news that…
    #NewsBeep #News #US #USA #UnitedStates #UnitedStatesOfAmerica #Health #hypothalamus #kosdiabetesgroup #metformin #rap1 #Recommended
    newsbeep.com/us/787681/

    #recommended #rap1 #metformin #kosdiabetesgroup #hypothalamus #health
  14. Österreich @[email protected] ·

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    #wacht #wachstumshormon #therapie #stoffwechsel #schlaf #rueckkopplung
  15. Rhyothemis @[email protected] ·

    Threonic acid, an ascorbic acid metabolite, synergizes with intermittent fasting to ameliorate obesity [2026]
    doi.org/10.1038/s12276-025-016

    #obesity #neuroscience #neuropeptides #fasting #appetite #hypothalamus #metabolism #VitaminC

    #obesity #neuroscience #neuropeptides #fasting #appetite #hypothalamus
  16. Rhyothemis @[email protected] ·

    Threonic acid, an ascorbic acid metabolite, synergizes with intermittent fasting to ameliorate obesity [2026]
    doi.org/10.1038/s12276-025-016

    #obesity #neuroscience #neuropeptides #fasting #appetite #hypothalamus #metabolism #VitaminC

    #obesity #neuroscience #neuropeptides #fasting #appetite #hypothalamus
  17. Rhyothemis @[email protected] ·

    Threonic acid, an ascorbic acid metabolite, synergizes with intermittent fasting to ameliorate obesity [2026]
    doi.org/10.1038/s12276-025-016

    #obesity #neuroscience #neuropeptides #fasting #appetite #hypothalamus #metabolism #VitaminC

    #obesity #neuroscience #neuropeptides #fasting #appetite #hypothalamus
  18. Rhyothemis @[email protected] ·

    Threonic acid, an ascorbic acid metabolite, synergizes with intermittent fasting to ameliorate obesity [2026]
    doi.org/10.1038/s12276-025-016

    #obesity #neuroscience #neuropeptides #fasting #appetite #hypothalamus #metabolism #VitaminC

    #vitaminc #metabolism #hypothalamus #appetite #fasting #neuropeptides
  19. Rhyothemis @[email protected] ·

    Threonic acid, an ascorbic acid metabolite, synergizes with intermittent fasting to ameliorate obesity [2026]
    doi.org/10.1038/s12276-025-016

    #obesity #neuroscience #neuropeptides #fasting #appetite #hypothalamus #metabolism #VitaminC

    #obesity #neuroscience #neuropeptides #fasting #appetite #hypothalamus
  20. Belgique @[email protected] ·

    europesays.com/be-fr/109374/ Ce n’est pas votre excès de poids qui menace votre cerveau, mais ce bourrelet précis, révèle une étude inédite #BE #BEFr #Belgique #Belgium #Cerveau #DéclinCognitif #DégénérescenceCérébrale #GraisseAbdominale #Health #Hypothalamus #IMC #Obésité #Santé #SubstanceGrise #vieillissement

    #vieillissement #substancegrise #sante #obesite #imc #hypothalamus
  21. France | République française @[email protected] ·

    europesays.com/fr/937552/ Ce n’est pas votre excès de poids qui menace votre cerveau, mais ce bourrelet précis, révèle une étude inédite #cerveau #DéclinCognitif #DégénérescenceCérébrale #FR #France #GraisseAbdominale #Health #hypothalamus #IMC #obésité #Santé #SubstanceGrise #vieillissement

    #vieillissement #substancegrise #sante #obesite #imc #hypothalamus
  22. Suisse @[email protected] ·

    europesays.com/ch-fr/133887/ Ce n’est pas votre excès de poids qui menace votre cerveau, mais ce bourrelet précis, révèle une étude inédite #cerveau #DéclinCognitif #DégénérescenceCérébrale #GraisseAbdominale #Health #Hypothalamus #IMC #Obésité #Santé #SubstanceGrise #Suisse #vieillissement

    #vieillissement #suisse #substancegrise #sante #obesite #imc
  23. France | République française @[email protected] ·

    europesays.com/fr/784124/ Et si vos nuits révélaient la maladie de Charcot des années avant les symptômes ? #CellulesNerveuses #cerveau #charcot #FR #France #Health #hypothalamus #MaladieDeCharcot #MaladieNeuroDégénérative #Motoneurones #MuscleRespiratoire #neurone #NeuroneàOrexine #Santé #SLA #sommeil #TroubleMoteur #TroublesDuSommeil

    #troublesdusommeil #troublemoteur #sommeil #sla #sante #neuroneaorexine
  24. Suisse @[email protected] ·

    europesays.com/ch-fr/38070/ Et si vos nuits révélaient la maladie de Charcot des années avant les symptômes ? #CellulesNerveuses #cerveau #Charcot #Health #Hypothalamus #MaladieDeCharcot #MaladieNeuroDégénérative #Motoneurones #MuscleRespiratoire #Neurone #NeuroneàOrexine #Santé #SLA #sommeil #Suisse #TroubleMoteur #TroublesDuSommeil

    #troublesdusommeil #troublemoteur #suisse #sommeil #sla #sante
  25. Belgique @[email protected] ·

    europesays.com/be-fr/32688/ Et si vos nuits révélaient la maladie de Charcot des années avant les symptômes ? #BE #BEFr #Belgique #Belgium #CellulesNerveuses #Cerveau #charcot #Health #Hypothalamus #MaladieDeCharcot #MaladieNeuroDégénérative #Motoneurones #MuscleRespiratoire #Neurone #NeuroneàOrexine #Santé #SLA #Sommeil #TroubleMoteur #TroublesDuSommeil

    #troublesdusommeil #troublemoteur #sommeil #sla #sante #neuroneaorexine
  26. CD Castillo @[email protected] ·
    La oxitocina tiene efectos distintos dependiendo de que neuronas la liberen (NPV posterior, NPV anterior, extensión amigdalina, etc) y en que patrón lo hagan (el patrón electrofisiológico de las neuronas es muy distinto!!)

    https://www.nature.com/articles/s41386-026-02352-y

    #Oxytocin #Anxiety #Socialisolation #SocialAffiliation #Neurophysiology #Hypothalamus #Neuropeptides
    #anxiety #hypothalamus #neuropeptides #neurophysiology #oxytocin #socialaffiliation
  27. CD Castillo @[email protected] ·
    La oxitocina tiene efectos distintos dependiendo de que neuronas la liberen (NPV posterior, NPV anterior, extensión amigdalina, etc) y en que patrón lo hagan (el patrón electrofisiológico de las neuronas es muy distinto!!)

    https://www.nature.com/articles/s41386-026-02352-y

    #Oxytocin #Anxiety #Socialisolation #SocialAffiliation #Neurophysiology #Hypothalamus #Neuropeptides
    #anxiety #hypothalamus #neuropeptides #neurophysiology #oxytocin #socialaffiliation
  28. CD Castillo @[email protected] ·
    La oxitocina tiene efectos distintos dependiendo de que neuronas la liberen (NPV posterior, NPV anterior, extensión amigdalina, etc) y en que patrón lo hagan (el patrón electrofisiológico de las neuronas es muy distinto!!)

    https://www.nature.com/articles/s41386-026-02352-y

    #Oxytocin #Anxiety #Socialisolation #SocialAffiliation #Neurophysiology #Hypothalamus #Neuropeptides
    #anxiety #hypothalamus #neuropeptides #neurophysiology #oxytocin #socialaffiliation
  29. CD Castillo @[email protected] ·
    La oxitocina tiene efectos distintos dependiendo de que neuronas la liberen (NPV posterior, NPV anterior, extensión amigdalina, etc) y en que patrón lo hagan (el patrón electrofisiológico de las neuronas es muy distinto!!)

    https://www.nature.com/articles/s41386-026-02352-y

    #Oxytocin #Anxiety #Socialisolation #SocialAffiliation #Neurophysiology #Hypothalamus #Neuropeptides
    #socialisolation #socialaffiliation #oxytocin #neurophysiology #neuropeptides #hypothalamus
  30. CD Castillo @[email protected] ·
    La oxitocina tiene efectos distintos dependiendo de que neuronas la liberen (NPV posterior, NPV anterior, extensión amigdalina, etc) y en que patrón lo hagan (el patrón electrofisiológico de las neuronas es muy distinto!!)

    https://www.nature.com/articles/s41386-026-02352-y

    #Oxytocin #Anxiety #Socialisolation #SocialAffiliation #Neurophysiology #Hypothalamus #Neuropeptides
    #anxiety #hypothalamus #neuropeptides #neurophysiology #oxytocin #socialaffiliation
  31. United States News Beep @[email protected] ·

    Gut-Brain-Heart Axis: How Microbes Control Your Blood Pressure

    Sumary: High blood pressure and heart failure might be managed through the gut. New research has identified a…
    #NewsBeep #News #US #USA #UnitedStates #UnitedStatesOfAmerica #Health #DiastolicDysfunction #Gut-Brain-HeartAxis #heartfailure #hypertension #hypothalamus #Indole-3AceticAcid #MaxDelbrückCenter #Microbiome #Neuroscience
    newsbeep.com/us/492103/

    #newsbeep #news #us #usa #unitedstates #unitedstatesofamerica
  32. United States News Beep @[email protected] ·

    Gut-Brain-Heart Axis: How Microbes Control Your Blood Pressure

    Sumary: High blood pressure and heart failure might be managed through the gut. New research has identified a…
    #NewsBeep #News #US #USA #UnitedStates #UnitedStatesOfAmerica #Health #DiastolicDysfunction #Gut-Brain-HeartAxis #heartfailure #hypertension #hypothalamus #Indole-3AceticAcid #MaxDelbrückCenter #Microbiome #Neuroscience
    newsbeep.com/us/492103/

    #neuroscience #microbiome #maxdelbruckcenter #indole #hypothalamus #hypertension
  33. Ireland @[email protected] ·

    europesays.com/ie/353120/ Obesogenic effects of warm temperature involve feeding adaptation by preoptic area leptin receptor neurons #Éire #general #Hypothalamus #IE #Ireland #LifeSciences #Obesity #Science

    #science #obesity #lifesciences #ireland #ie #hypothalamus
  34. Ireland @[email protected] ·

    europesays.com/ie/345742/ Brain neurons after exercise drive long-term endurance gains #Brain #Éire #Exercise #Health #Hypothalamus #IE #Ireland #Laboratory #Muscle #Neuron #Neurons #PhysicalActivity #Research #Running

    #running #research #physicalactivity #neurons #neuron #muscle
  35. Ireland @[email protected] ·

    europesays.com/ie/335667/ Neural Afterburn: Brain Rewires Itself to Boost Endurance #BrainPlasticity #Éire #EnduranceTraining #Exercise #Fitness #Health #Hypothalamus #IE #Ireland #MetabolicHealth #NeuralCircuits #neuroplasticity #Neuroscience #SF1Neurons #SynapticPlasticity #UniversityOfPennsylvania

    #universityofpennsylvania #synapticplasticity #sf1neurons #neuroscience #neuroplasticity #neuralcircuits
  36. France | République française @[email protected] ·

    europesays.com/fr/672086/ Et si vos nuits révélaient la maladie de Charcot des années à l’avance ? #CellulesNerveuses #cerveau #charcot #FR #France #Health #hypothalamus #MaladieDeCharcot #MaladieNeuroDégénérative #Motoneurones #MuscleRespiratoire #neurone #NeuroneàOrexine #Santé #SLA #sommeil #TroubleMoteur #TroublesDuSommeil

    #troublesdusommeil #troublemoteur #sommeil #sla #sante #neuroneaorexine
  37. France | République française @[email protected] ·

    europesays.com/fr/632026/ ce signe précoce qui change tout pour la maladie de Charcot #CellulesNerveuses #cerveau #FR #France #Health #hypothalamus #MaladieDeCharcot #MaladieNeuroDégénérative #Motoneurones #MuscleRespiratoire #neurone #NeuroneàOrexine #Santé #sommeil #TroublesDuSommeil #TroublesMoteurs

    #troublesmoteurs #troublesdusommeil #sommeil #sante #neuroneaorexine #neurone
  38. España @[email protected] ·

    europesays.com/es/291823/ Cáncer de mama: cómo se altera el reloj biológico del organismo antes de que el tumor sea detectable #AdrenalGland #anxiety #BreastCancer #cáncer #corticosterone #DayNightRhythms #diurnal #ES #España #FeedbackLoop #Health #HpaAxis #hypothalamus #insomnia #JeremyBorniger #neurons #neuroscience #ParaventricularNucleus #PituitaryGland #pvn #rhythm #Salud #Spain #StressHormone

    #stresshormone #spain #salud #rhythm #pvn #pituitarygland
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    europesays.com/ie/186314/ Tirzepatide may only temporarily suppress brain activity involved in “food noise” #Agonist #BingeEatingDisorder #Brain #BrainSurgery #CT #diabetes #Drugs #EatingDisorder #Éire #food #Frequency #Glucagon #GlucagonLikePeptide1 #Glucose #Health #hospital #Hypothalamus #IE #Ireland #medicine #Neurosurgery #Obesity #Receptor #Research #Surgery #therapy #Type2Diabetes #WeightLoss

    #weightloss #type2diabetes #therapy #surgery #research #receptor
  40. Fabrizio Musacchio @[email protected] ·

    🧠 New preprint by Kim et al. (2025) from David Anderson’s lab: A line #attractor maintains aggressiveness during feeding in “hangry” mice 🍔🐁. Using in vivo #CalciumImaging and #rSLDS modeling, they show how moderate fasting stabilizes an aggression-related attractor in #VMHvl, while prolonged fasting collapses it, linking hunger, motivation, and aggression through #PopulationDynamics:

    🌍 doi.org/10.1101/2025.10.16.682

    #Neuroscience #CompNeuro #Behavior #AttractorDynamics #Hypothalamus #2p #imaging

    #attractor #calciumimaging #rslds #vmhvl #populationdynamics #neuroscience
  41. Fabrizio Musacchio @[email protected] ·

    🧠 New preprint by Kim et al. (2025) from David Anderson’s lab: A line #attractor maintains aggressiveness during feeding in “hangry” mice 🍔🐁. Using in vivo #CalciumImaging and #rSLDS modeling, they show how moderate fasting stabilizes an aggression-related attractor in #VMHvl, while prolonged fasting collapses it, linking hunger, motivation, and aggression through #PopulationDynamics:

    🌍 doi.org/10.1101/2025.10.16.682

    #Neuroscience #CompNeuro #Behavior #AttractorDynamics #Hypothalamus #2p #imaging

    #attractor #calciumimaging #rslds #vmhvl #populationdynamics #neuroscience
  42. Fabrizio Musacchio @[email protected] ·

    🧠 New preprint by Kim et al. (2025) from David Anderson’s lab: A line #attractor maintains aggressiveness during feeding in “hangry” mice 🍔🐁. Using in vivo #CalciumImaging and #rSLDS modeling, they show how moderate fasting stabilizes an aggression-related attractor in #VMHvl, while prolonged fasting collapses it, linking hunger, motivation, and aggression through #PopulationDynamics:

    🌍 doi.org/10.1101/2025.10.16.682

    #Neuroscience #CompNeuro #Behavior #AttractorDynamics #Hypothalamus #2p #imaging

    #attractor #calciumimaging #rslds #vmhvl #populationdynamics #neuroscience
  43. RiffReporter @[email protected] ·

    Ob wir schlafen, frieren oder gestresst sind – der kleine #Hypothalamus im #Gehirn hat alles im Griff. Teil 3 der 5-teiligen Serie über #Hormone von Sigrid März. riffreporter.de/de/wissen/hypo

    #hypothalamus #gehirn #hormone
  44. RiffReporter @[email protected] ·

    Ob wir schlafen, frieren oder gestresst sind – der kleine #Hypothalamus im #Gehirn hat alles im Griff. Teil 3 der 5-teiligen Serie über #Hormone von Sigrid März. riffreporter.de/de/wissen/hypo

    #hypothalamus #gehirn #hormone
  45. RiffReporter @[email protected] ·

    Ob wir schlafen, frieren oder gestresst sind – der kleine #Hypothalamus im #Gehirn hat alles im Griff. Teil 3 der 5-teiligen Serie über #Hormone von Sigrid März. riffreporter.de/de/wissen/hypo

    #hypothalamus #gehirn #hormone
  46. RiffReporter @[email protected] ·

    Ob wir schlafen, frieren oder gestresst sind – der kleine #Hypothalamus im #Gehirn hat alles im Griff. Teil 3 der 5-teiligen Serie über #Hormone von Sigrid März. riffreporter.de/de/wissen/hypo

    #hypothalamus #gehirn #hormone
  47. Scientific European @[email protected] ·

    Targeting Neurons in Hypothalamus for Stress-related Sleep disorders
    Stress-related sleep and memory disorders are important health problem facing many people............
    #brain #Hypothalamus #memory #neurons #Sleep #sleepdisorder #Stress #Stressrelatedsleepdisorder
    Umesh Prasad

    scientificeuropean.co.uk/healt

    #brain #hypothalamus #memory #neurons #sleep #sleepdisorder
  48. Scientific European @[email protected] ·

    Targeting Neurons in Hypothalamus for Stress-related Sleep disorders
    Stress-related sleep and memory disorders are important health problem facing many people............
    #brain #Hypothalamus #memory #neurons #Sleep #sleepdisorder #Stress #Stressrelatedsleepdisorder
    Umesh Prasad

    scientificeuropean.co.uk/healt

    #brain #hypothalamus #memory #neurons #sleep #sleepdisorder
  49. Scientific European @[email protected] ·

    Targeting Neurons in Hypothalamus for Stress-related Sleep disorders
    Stress-related sleep and memory disorders are important health problem facing many people............
    #brain #Hypothalamus #memory #neurons #Sleep #sleepdisorder #Stress #Stressrelatedsleepdisorder
    Umesh Prasad

    scientificeuropean.co.uk/healt

    #brain #hypothalamus #memory #neurons #sleep #sleepdisorder
  50. Scientific European @[email protected] ·

    Targeting Neurons in Hypothalamus for Stress-related Sleep disorders
    Stress-related sleep and memory disorders are important health problem facing many people............
    #brain #Hypothalamus #memory #neurons #Sleep #sleepdisorder #Stress #Stressrelatedsleepdisorder
    Umesh Prasad

    scientificeuropean.co.uk/healt

    #brain #hypothalamus #memory #neurons #sleep #sleepdisorder