#mitochondria — Public Fediverse posts

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: https://www.psypost.org/mitochondrial-protein-in-the-brain-regulates-dietary-fat-intake-and-body-weight/

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: https://www.psypost.org/mitochondrial-protein-in-the-brain-regulates-dietary-fat-intake-and-body-weight/

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

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

#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

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: https://www.psypost.org/mitochondrial-protein-in-the-brain-regulates-dietary-fat-intake-and-body-weight/

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: https://www.psypost.org/mitochondrial-protein-in-the-brain-regulates-dietary-fat-intake-and-body-weight/

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

Private, vetted email list for mental health professionals: https://www.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

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: https://www.psypost.org/mitochondrial-protein-in-the-brain-regulates-dietary-fat-intake-and-body-weight/

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: https://www.psypost.org/mitochondrial-protein-in-the-brain-regulates-dietary-fat-intake-and-body-weight/

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

Private, vetted email list for mental health professionals: https://www.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

https://www.europesays.com/ie/653960/ New study makes progress in understanding the mechanisms behind severity of HFpEF #Aging #blood #BloodPressure #diabetes #Éire #Genes #Health #Heart #HeartFailure #IE #Ireland #Lungs #Metabolism #Mitochondria #Mortality #Muscle #Obesity #pH #PulmonaryArtery #PulmonaryHypertension #Research #RNA #RNASequencing #Vasculature #Walking

📰 "Mapping subcellular H2O2 dynamics reveals tissue specific redox patterns in Drosophila"
https://www.biorxiv.org/content/10.64898/2026.08.21.745691v1?rss=1
#DrosophilaMelanogaster
#Mitochondria #Drosophila #Metabolism #WingDisc

📰 "Mapping subcellular H2O2 dynamics reveals tissue specific redox patterns in Drosophila"
https://www.biorxiv.org/content/10.64898/2026.08.21.745691v1?rss=1
#DrosophilaMelanogaster
#Mitochondria #Drosophila #Metabolism #WingDisc

📰 "Mapping subcellular H2O2 dynamics reveals tissue specific redox patterns in Drosophila"
https://www.biorxiv.org/content/10.64898/2026.08.21.745691v1?rss=1
#DrosophilaMelanogaster
#Mitochondria #Drosophila #Metabolism #WingDisc

📰 "Mapping subcellular H2O2 dynamics reveals tissue specific redox patterns in Drosophila"
https://www.biorxiv.org/content/10.64898/2026.08.21.745691v1?rss=1
#DrosophilaMelanogaster
#Mitochondria #Drosophila #Metabolism #WingDisc

📰 "Glycolytic compensation rather than NAD+/NADH balance sustains neuronal function during mitochondrial stress"
https://www.biorxiv.org/content/10.64898/2026.08.20.746069v1?rss=1
#Mitochondria #Drosophila #Metabolism

📰 "Glycolytic compensation rather than NAD+/NADH balance sustains neuronal function during mitochondrial stress"
https://www.biorxiv.org/content/10.64898/2026.08.20.746069v1?rss=1
#Mitochondria #Drosophila #Metabolism

📰 "Glycolytic compensation rather than NAD+/NADH balance sustains neuronal function during mitochondrial stress"
https://www.biorxiv.org/content/10.64898/2026.08.20.746069v1?rss=1
#Mitochondria #Drosophila #Metabolism

📰 "Glycolytic compensation rather than NAD+/NADH balance sustains neuronal function during mitochondrial stress"
https://www.biorxiv.org/content/10.64898/2026.08.20.746069v1?rss=1
#Mitochondria #Drosophila #Metabolism

#MetabolicHealth #Mitochondria #EnergyBoost #HealthTips #NutritionMatters #ModernLifestyle #WellnessJourney #HealthyLiving #wellnessthatworks #wellnessblogger #emotionalwellbeing #wellnesslifestyle #wellnesswarrior #healthandwellbeing #CellularEnergy #Vitality https://mastodon.social/@biohackingpathway/117141011274459244

More and more recognition that mitochondria matter an awful lot:

"Brain mitochondria as key drivers of cognition and behaviour", Carmen Sandi et al. 2026, a review.
https://www.nature.com/articles/s41583-026-01061-1

#neuroscience #mitochondria

More and more recognition that mitochondria matter an awful lot:

"Brain mitochondria as key drivers of cognition and behaviour", Carmen Sandi et al. 2026, a review.
https://www.nature.com/articles/s41583-026-01061-1

#neuroscience #mitochondria

More and more recognition that mitochondria matter an awful lot:

"Brain mitochondria as key drivers of cognition and behaviour", Carmen Sandi et al. 2026, a review.
https://www.nature.com/articles/s41583-026-01061-1

#neuroscience #mitochondria

More and more recognition that mitochondria matter an awful lot:

"Brain mitochondria as key drivers of cognition and behaviour", Carmen Sandi et al. 2026, a review.
https://www.nature.com/articles/s41583-026-01061-1

#neuroscience #mitochondria

More and more recognition that mitochondria matter an awful lot:

"Brain mitochondria as key drivers of cognition and behaviour", Carmen Sandi et al. 2026, a review.
https://www.nature.com/articles/s41583-026-01061-1

#neuroscience #mitochondria

📰 "Therapeutic potential of the Nrf2 activator omaveloxolone in spinocerebellar ataxia type 3 in cellular and Drosophila models"
https://doi.org/doi:10.3389/fphar.2026.1872142
https://pubmed.ncbi.nlm.nih.gov/42621215/
#Mitochondria #Drosophila

📰 "Therapeutic potential of the Nrf2 activator omaveloxolone in spinocerebellar ataxia type 3 in cellular and Drosophila models"
https://doi.org/doi:10.3389/fphar.2026.1872142
https://pubmed.ncbi.nlm.nih.gov/42621215/
#Mitochondria #Drosophila

📰 "Therapeutic potential of the Nrf2 activator omaveloxolone in spinocerebellar ataxia type 3 in cellular and Drosophila models"
https://doi.org/doi:10.3389/fphar.2026.1872142
https://pubmed.ncbi.nlm.nih.gov/42621215/
#Mitochondria #Drosophila

📰 "Therapeutic potential of the Nrf2 activator omaveloxolone in spinocerebellar ataxia type 3 in cellular and Drosophila models"
https://doi.org/doi:10.3389/fphar.2026.1872142
https://pubmed.ncbi.nlm.nih.gov/42621215/
#Mitochondria #Drosophila

📰 "Ringer Loss in Drosophila Uncovers Mitochondrial Complex I Deficits Characteristic of Human Parkinson's Disease"
https://doi.org/doi:10.64898/2026.07.27.741040
https://pubmed.ncbi.nlm.nih.gov/42619695/
#Mitochondria #Drosophila

📰 "Ringer Loss in Drosophila Uncovers Mitochondrial Complex I Deficits Characteristic of Human Parkinson's Disease"
https://doi.org/doi:10.64898/2026.07.27.741040
https://pubmed.ncbi.nlm.nih.gov/42619695/
#Mitochondria #Drosophila

📰 "Ringer Loss in Drosophila Uncovers Mitochondrial Complex I Deficits Characteristic of Human Parkinson's Disease"
https://doi.org/doi:10.64898/2026.07.27.741040
https://pubmed.ncbi.nlm.nih.gov/42619695/
#Mitochondria #Drosophila

📰 "Ringer Loss in Drosophila Uncovers Mitochondrial Complex I Deficits Characteristic of Human Parkinson's Disease"
https://doi.org/doi:10.64898/2026.07.27.741040
https://pubmed.ncbi.nlm.nih.gov/42619695/
#Mitochondria #Drosophila

📰 "NADH FLIM reveals cellular bioenergetics and mitochondrial morphology during Drosophila convergent extension"
https://doi.org/doi:10.1016/j.ydbio.2026.08.011
https://pubmed.ncbi.nlm.nih.gov/42617721/
#Mitochondria #Drosophila #Germband #Embryo

📰 "NADH FLIM reveals cellular bioenergetics and mitochondrial morphology during Drosophila convergent extension"
https://doi.org/doi:10.1016/j.ydbio.2026.08.011
https://pubmed.ncbi.nlm.nih.gov/42617721/
#Mitochondria #Drosophila #Germband #Embryo

📰 "NADH FLIM reveals cellular bioenergetics and mitochondrial morphology during Drosophila convergent extension"
https://doi.org/doi:10.1016/j.ydbio.2026.08.011
https://pubmed.ncbi.nlm.nih.gov/42617721/
#Mitochondria #Drosophila #Germband #Embryo

📰 "NADH FLIM reveals cellular bioenergetics and mitochondrial morphology during Drosophila convergent extension"
https://doi.org/doi:10.1016/j.ydbio.2026.08.011
https://pubmed.ncbi.nlm.nih.gov/42617721/
#Mitochondria #Drosophila #Germband #Embryo

📰 "Developmental susceptibility to PFOS toxicity in Drosophila shows genetic variation in toxicodynamics and rescue via enhanced muscle mitochondrial function"
https://doi.org/doi:10.1093/toxsci/kfag102
https://pubmed.ncbi.nlm.nih.gov/42615982/
#DrosophilaMelanogaster
#Mitochondria #Drosophila

📰 "Developmental susceptibility to PFOS toxicity in Drosophila shows genetic variation in toxicodynamics and rescue via enhanced muscle mitochondrial function"
https://doi.org/doi:10.1093/toxsci/kfag102
https://pubmed.ncbi.nlm.nih.gov/42615982/
#DrosophilaMelanogaster
#Mitochondria #Drosophila

📰 "Developmental susceptibility to PFOS toxicity in Drosophila shows genetic variation in toxicodynamics and rescue via enhanced muscle mitochondrial function"
https://doi.org/doi:10.1093/toxsci/kfag102
https://pubmed.ncbi.nlm.nih.gov/42615982/
#DrosophilaMelanogaster
#Mitochondria #Drosophila

📰 "Developmental susceptibility to PFOS toxicity in Drosophila shows genetic variation in toxicodynamics and rescue via enhanced muscle mitochondrial function"
https://doi.org/doi:10.1093/toxsci/kfag102
https://pubmed.ncbi.nlm.nih.gov/42615982/
#DrosophilaMelanogaster
#Mitochondria #Drosophila

📰 "Deficiency in MICOS component Chchd3 Compromises Drosophila Heart Function via mitophagy, ROS and ER Stress"
https://www.biorxiv.org/content/10.64898/2026.08.14.744045v1?rss=1
#Mitochondria #Drosophila

📰 "Deficiency in MICOS component Chchd3 Compromises Drosophila Heart Function via mitophagy, ROS and ER Stress"
https://www.biorxiv.org/content/10.64898/2026.08.14.744045v1?rss=1
#Mitochondria #Drosophila

📰 "Deficiency in MICOS component Chchd3 Compromises Drosophila Heart Function via mitophagy, ROS and ER Stress"
https://www.biorxiv.org/content/10.64898/2026.08.14.744045v1?rss=1
#Mitochondria #Drosophila

📰 "Deficiency in MICOS component Chchd3 Compromises Drosophila Heart Function via mitophagy, ROS and ER Stress"
https://www.biorxiv.org/content/10.64898/2026.08.14.744045v1?rss=1
#Mitochondria #Drosophila

https://www.europesays.com/ie/644205/ UC Irvine researchers develop framework to make CAR T-cell therapy safer #blood #Brain #cancer #CancerTreatment #CARTCell #Cell #ClinicalTesting #Drugs #Éire #Health #IE #immunotherapy #inflammation #Ireland #Mitochondria #oncology #Pharmacology #pharmacy #Research #Syndrome #TCell #therapy

The Shocking Truth About Sugar & Energy 😮⁣
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#sugar #energy #dopamine #healthtips #nutrition #mitochondria #sugarfacts #wellness #healthychoices #sciencefacts #healthyliving #foodscience #shorts #shortsvideo ⁣

The Shocking Truth About Sugar & Energy 😮⁣
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#sugar #energy #dopamine #healthtips #nutrition #mitochondria #sugarfacts #wellness #healthychoices #sciencefacts #healthyliving #foodscience #shorts #shortsvideo ⁣

The Shocking Truth About Sugar & Energy 😮⁣
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#sugar #energy #dopamine #healthtips #nutrition #mitochondria #sugarfacts #wellness #healthychoices #sciencefacts #healthyliving #foodscience #shorts #shortsvideo ⁣

The Shocking Truth About Sugar & Energy 😮⁣
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#sugar #energy #dopamine #healthtips #nutrition #mitochondria #sugarfacts #wellness #healthychoices #sciencefacts #healthyliving #foodscience #shorts #shortsvideo ⁣

The Shocking Truth About Sugar & Energy 😮⁣
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#sugar #energy #dopamine #healthtips #nutrition #mitochondria #sugarfacts #wellness #healthychoices #sciencefacts #healthyliving #foodscience #shorts #shortsvideo ⁣

📰 "Role of Early-Life Microbiome Colonization in Physiological Development of Drosophila melanogaster"
https://www.biorxiv.org/content/10.64898/2026.08.16.745128v1?rss=1
#DrosophilaMelanogaster
#Mitochondria #Drosophila #Metabolism #Immunity #Adult
#Embryo #Larva

📰 "Role of Early-Life Microbiome Colonization in Physiological Development of Drosophila melanogaster"
https://www.biorxiv.org/content/10.64898/2026.08.16.745128v1?rss=1
#DrosophilaMelanogaster
#Mitochondria #Drosophila #Metabolism #Immunity #Adult
#Embryo #Larva

📰 "Role of Early-Life Microbiome Colonization in Physiological Development of Drosophila melanogaster"
https://www.biorxiv.org/content/10.64898/2026.08.16.745128v1?rss=1
#DrosophilaMelanogaster
#Mitochondria #Drosophila #Metabolism #Immunity #Adult
#Embryo #Larva

📰 "Role of Early-Life Microbiome Colonization in Physiological Development of Drosophila melanogaster"
https://www.biorxiv.org/content/10.64898/2026.08.16.745128v1?rss=1
#DrosophilaMelanogaster
#Mitochondria #Drosophila #Metabolism #Immunity #Adult
#Embryo #Larva

📰 "Subarctic Drosophila species cold-acclimated in laboratory maintain full capacity for oxygen consumption in their flight muscle mitochondria"
https://doi.org/doi:10.1016/j.jinsphys.2026.105045
https://pubmed.ncbi.nlm.nih.gov/42603585/
#Mitochondria #Drosophila #Metabolism

📰 "Subarctic Drosophila species cold-acclimated in laboratory maintain full capacity for oxygen consumption in their flight muscle mitochondria"
https://doi.org/doi:10.1016/j.jinsphys.2026.105045
https://pubmed.ncbi.nlm.nih.gov/42603585/
#Mitochondria #Drosophila #Metabolism

📰 "Subarctic Drosophila species cold-acclimated in laboratory maintain full capacity for oxygen consumption in their flight muscle mitochondria"
https://doi.org/doi:10.1016/j.jinsphys.2026.105045
https://pubmed.ncbi.nlm.nih.gov/42603585/
#Mitochondria #Drosophila #Metabolism

📰 "Subarctic Drosophila species cold-acclimated in laboratory maintain full capacity for oxygen consumption in their flight muscle mitochondria"
https://doi.org/doi:10.1016/j.jinsphys.2026.105045
https://pubmed.ncbi.nlm.nih.gov/42603585/
#Mitochondria #Drosophila #Metabolism

🧬 New publication from the lab! 🎉

Timeless and mitochondria! 🧬⚡

Kalisse Horne, a PhD student, started this as a side project, and it grew into a full research project!
Many students in the lab, including Havya, Shriya, and Rhea, also contributed to this work, together with Chiaki Noguchi, Dr. Christian Sell, and Dr. Josh Mell 😊
Great teamwork! 👏🔬

https://www.mdpi.com/2218-273X/16/8/1177

#Timeless #Mitochondria #GenomeIntegrity #ReplicationStress #GraduateSchool #BiomedicalScience #Publication

🧬 New publication from the lab! 🎉

Timeless and mitochondria! 🧬⚡

Kalisse Horne, a PhD student, started this as a side project, and it grew into a full research project!
Many students in the lab, including Havya, Shriya, and Rhea, also contributed to this work, together with Chiaki Noguchi, Dr. Christian Sell, and Dr. Josh Mell 😊
Great teamwork! 👏🔬

https://www.mdpi.com/2218-273X/16/8/1177

#Timeless #Mitochondria #GenomeIntegrity #ReplicationStress #GraduateSchool #BiomedicalScience #Publication

🧬 New publication from the lab! 🎉

Timeless and mitochondria! 🧬⚡

Kalisse Horne, a PhD student, started this as a side project, and it grew into a full research project!
Many students in the lab, including Havya, Shriya, and Rhea, also contributed to this work, together with Chiaki Noguchi, Dr. Christian Sell, and Dr. Josh Mell 😊
Great teamwork! 👏🔬

https://www.mdpi.com/2218-273X/16/8/1177

#Timeless #Mitochondria #GenomeIntegrity #ReplicationStress #GraduateSchool #BiomedicalScience #Publication

🧬 New publication from the lab! 🎉

Timeless and mitochondria! 🧬⚡

Kalisse Horne, a PhD student, started this as a side project, and it grew into a full research project!
Many students in the lab, including Havya, Shriya, and Rhea, also contributed to this work, together with Chiaki Noguchi, Dr. Christian Sell, and Dr. Josh Mell 😊
Great teamwork! 👏🔬

https://www.mdpi.com/2218-273X/16/8/1177

#Timeless #Mitochondria #GenomeIntegrity #ReplicationStress #GraduateSchool #BiomedicalScience #Publication

🧬 New publication from the lab! 🎉

Timeless and mitochondria! 🧬⚡

Kalisse Horne, a PhD student, started this as a side project, and it grew into a full research project!
Many students in the lab, including Havya, Shriya, and Rhea, also contributed to this work, together with Chiaki Noguchi, Dr. Christian Sell, and Dr. Josh Mell 😊
Great teamwork! 👏🔬

https://www.mdpi.com/2218-273X/16/8/1177

#Timeless #Mitochondria #GenomeIntegrity #ReplicationStress #GraduateSchool #BiomedicalScience #Publication

Probiotics may help protect against sarcopenia in older adults

Researchers used three approaches to study whether probiotics could help prevent sarcopenia (age-related loss of muscle mass, strength…
#NewsBeep #News #US #USA #UnitedStates #UnitedStatesOfAmerica #Nutrition #3dimensional #3D #cellbiology #cristae #cytological #cytology #energy #eukaryotic #Health #HumanBiology #Intracellular #Mitochondria #organelle #respiration
https://www.newsbeep.com/us/812287/

Probiotics may help protect against sarcopenia in older adults

Researchers used three approaches to study whether probiotics could help prevent sarcopenia (age-related loss of muscle mass, strength…
#NewsBeep #News #US #USA #UnitedStates #UnitedStatesOfAmerica #Nutrition #3dimensional #3D #cellbiology #cristae #cytological #cytology #energy #eukaryotic #Health #HumanBiology #Intracellular #Mitochondria #organelle #respiration
https://www.newsbeep.com/us/812287/

Probiotics may help protect against sarcopenia in older adults

Researchers used three approaches to study whether probiotics could help prevent sarcopenia (age-related loss of muscle mass, strength…
#NewsBeep #News #US #USA #UnitedStates #UnitedStatesOfAmerica #Nutrition #3dimensional #3D #cellbiology #cristae #cytological #cytology #energy #eukaryotic #Health #HumanBiology #Intracellular #Mitochondria #organelle #respiration
https://www.newsbeep.com/us/812287/