#hypothalamus — 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. **
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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 5, 2026 at 06:00PM
SOURCE: PSYPOST.ORG

** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
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TITLE: Animal studies suggest that reproductive behavior fully recovers after puberty-blocking treatment ends

URL: https://www.psypost.org/animal-studies-suggest-that-reproductive-behavior-fully-recovers-after-puberty-blocking-treatment-ends/

Recent research provides evidence that temporarily pausing puberty with the drug leuprolide delays reproductive development in adolescent rats but allows for full physical and behavioral maturation after the treatment stops. The findings suggest that the brain and body adjust to the medication through specific genetic changes, enabling normal reproductive function to eventually emerge. These two related studies were published in the journals Biology of Sex Differences and Hormones and Behavior.

Adolescents who experience distress because their gender identity does not match their sex assigned at birth are sometimes prescribed puberty-blocking medications. These drugs, known as gonadotropin-releasing hormone agonists, temporarily pause physical changes like breast development or facial hair growth. Leuprolide is one commonly used medication in this category. Delaying these physical changes gives young people time to explore their gender identity without the stress of developing unwanted physical traits.

A research team led by Fay Guarraci at Southwestern University initiated a series of experiments to understand how protracted puberty suppression affects brain and reproductive development. The researchers wanted to track both the behavioral and biological changes that occur during and after leuprolide administration. Because long-term physiological studies on human adolescents are limited, animal models help scientists observe how the brain and reproductive systems respond to these hormone-altering drugs over time.

In the first study, published in 2023, Guarraci and her colleagues tested how leuprolide affected the physical and behavioral development of 40 adolescent Long-Evans rats. The sample included 24 female rats and 16 male rats. Starting on postnatal day 25, which corresponds to early adolescence in rats, the scientists administered daily injections of either 50 micrograms per kilogram of leuprolide or a neutral saltwater solution for 25 days. The researchers monitored the rats daily for physical signs of puberty, such as vaginal opening in females and penile development in males.

Following the treatment period, the authors placed the rats in specialized chambers to observe their sexual motivation and mating behaviors. They recorded how much time the subjects chose to spend with male or female stimulus rats and tracked specific reproductive actions. The female subjects were tested during their first reproductive cycle after the drug was stopped. The male subjects underwent weekly behavioral tests for a month to track their development over a longer timeframe.

The researchers observed that leuprolide delayed the physical onset of puberty. Female rats receiving the drug reached puberty at an average of 45.9 days of age, compared to 38.1 days for those receiving the saltwater solution. Male rats receiving the drug reached puberty at an average of 45.0 days, compared to 39.0 days for the control group. During the treatment window, the female rats did not experience normal reproductive cycles.

Once the leuprolide injections ended, the female rats rapidly resumed normal reproductive function. Within a week, they displayed typical mating behaviors and became pregnant at absolute rates comparable to the control group. The male rats took longer to recover from the puberty-blocking effects. During the initial post-treatment tests, the leuprolide-treated males showed reduced sexual motivation toward females and engaged in fewer mating behaviors. By the fourth week after treatment ended, the treated males exhibited sexual behavior that matched the control group.

To understand the biological mechanisms driving these behavioral changes, the researchers conducted a second study, published in 2025. This experiment involved 16 female and 17 male adolescent rats, using the exact same 25-day leuprolide treatment protocol. Instead of observing behavior after the drug was stopped, the scientists analyzed the rats’ brains and blood hormone levels on the final day of treatment. They specifically measured the activity of genes related to reproduction in the pituitary gland and the hypothalamus, two brain regions that control hormone production.

Leuprolide once again delayed physical puberty, pushing the onset back by about five days in females (from 37.25 to 42.25 days) and ten days in males (from 39.50 to 49.67 days). Blood tests indicated that the circulating levels of sex hormones like testosterone and estrogen were not statistically significantly different between the treated and untreated rats at the end of the 25-day window. However, the genetic analysis showed distinct changes in how the brain was preparing for reproduction.

In the pituitary gland, both male and female rats treated with leuprolide showed increased activity in genes responsible for producing estrogen receptors and gonadotropin-releasing hormone receptors. In the hypothalamus, the effects differed by sex. Male rats receiving the drug had lower activity of the Kiss1 gene in the preoptic area, a brain region involved in sexual behavior. This gene produces kisspeptin, a protein that helps trigger puberty.

In a different section of the hypothalamus called the mediobasal region, the Kiss1 gene was highly active in both treated males and females. The scientists note that this heightened gene activity likely represents the brain attempting to compensate for the drug’s suppressive effects. The brain continues to mature and build the necessary reproductive architecture even while the physical manifestation of puberty is stalled.

Applying findings from animal models to human biology requires noting that rats and humans mature on vastly different timelines. The precise brain mechanisms governing puberty also feature species-specific variations, meaning a one-week recovery period in rats does not correspond to a specific timeframe in human adolescents.

Animal studies remain highly useful, however, because they allow scientists to directly examine brain tissue and track genetic changes across a full developmental lifespan. Observing these molecular adaptations in a controlled environment provides evidence about how the mammalian brain responds to protracted puberty suppression that would be impossible to gather from human patients.

Drug doses used in experimental models do not always translate exactly to the proportional doses prescribed in clinical settings. Future research could isolate smaller, more specific clusters of cells within the hypothalamus to see exactly where these genetic changes originate. Tracking hormone and gene expression over a longer timeline after the medication is stopped would also help clarify how the brain readjusts. Testing different doses of the medication could provide additional context regarding how the body manages chemical puberty suppression.

The study, “Chronic periadolescent leuprolide exposure affects the development of reproductive physiology and behavior of female and male rats differently, but both mature after treatment termination,” was authored by Fay A. Guarraci, Layla Avendano, Megan Kelly, Cleriza Estoesta, Bernard Sencherey, Hannah S. Valdivia, Amanda Gale, Lily Yepez, Jasmine B. Belfield, Kristen M. Carter, Natalie Williams, and Andrea C. Gore.

The study, “Chronic periadolescent leuprolide exposure affects the expression of multiple genes in the hypothalamus and pituitary gland with a different pattern of expression in female and male Long-Evans rats,” was authored by Fay A. Guarraci, Ian M. Klepcyk, Lindsay M. Thompson, Madeline Streifer, Emily N. Hilz, Grace Hudson, Sarah H. Meerts, and Andrea C. Gore.

URL: https://www.psypost.org/animal-studies-suggest-that-reproductive-behavior-fully-recovers-after-puberty-blocking-treatment-ends/

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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #PubertyBlockers #Leuprolide #ReproductiveDevelopment #AdolescentResearch #AnimalStudy #HormonesAndBehavior #BiologyOfSexDifferences #Kiss1 #Hypothalamus #PituitaryGland

Threonic acid, an ascorbic acid metabolite, synergizes with intermittent fasting to ameliorate obesity [2026]
https://doi.org/10.1038/s12276-025-01613-y

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

🧠 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:

🌍 https://doi.org/10.1101/2025.10.16.682711

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

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. https://www.riffreporter.de/de/wissen/hypothalamus-stresshormone-cortisol-hormonregulation

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

https://www.scientificeuropean.co.uk/health/targeting-neurons-in-hypothalamus-for-stress-related-sleep-disorders/

#CarmineClemente - How Do #Human #Brains #Think and #Feel?

https://www.youtube.com/watch?v=GecPtAXpcJY

#Philosophy #PhilosophyOfScience #Science #PhilosophyOfMedicine #Medicine #Biology #PhilosophyOfBiology #Brain #Thinking #Feeling #Consciousness #PhilosophyOfConsciousness #Awareness #Learning #Pituitary #Hypothalamus #Hormone #Hormones #Appetite #CloserToTruth #RobertKuhn

Sleep normalizes #synapses in the cortex & hippocampus that have been potentiated during the daytime. This study shows that slow-wave #sleep also down-regulates #AMPAreceptor levels in the #hypothalamus, a brain region that regulates sleep #PLOSBiology https://plos.io/3MdTALe

Should I stay or should I go? Animal studies suggest the hypothalamus helps switching between survival behaviors (hunt vs escape). @fearlab &co use #neuroimaging & computational modeling to show that the #hypothalamus also modulates switching between survival actions in humans #PLOSBiology https://plos.io/4bq8JmH

Obese and overweight people's brains 'are different'
https://www.msn.com/en-gb/health/nutrition/obese-and-overweight-people-s-brains-are-different/ar-AA1eVEKC?cvid=98f061cb29964418db681d6cbc64daf1&ocid=winp2fptaskbarhover&ei=24

#Obesity
#Overweight
#Brain
#Hypothalamus

#Cannabis activates specific #hunger #neurons in #brain
The study was conducted on mice and found that cannabis activates neurons located in the #hypothalamus, the area of the brain that controls vital functions, such as heart rate, hunger, and the release of hormones. Cannabis specifically enhances activity in the mediobasal hypothalamus, the brain region that regulates hunger.
https://news.wsu.edu/press-release/2024/01/16/cannabis-activates-specific-hunger-neurons-in-brain/

Obese and overweight people's brains 'are different'
https://www.msn.com/en-gb/health/nutrition/obese-and-overweight-people-s-brains-are-different/ar-AA1eVEKC?cvid=a87d9307e4964339bb1dd7ff47b913c5&ocid=winp2fptaskbarhover&ei=22

#Obesity
#Brain
#Hypothalamus

"Our data indicate that #cannabis vapor increased meal frequency and food seeking behavior without altering locomotor activity. Importantly, we observed augmented mediobasal #hypothalamus activity within distinct neuronal populations when mice anticipated or consumed #food."

https://www.nature.com/articles/s41598-023-50112-5

#Hyperglycemia activates glucose sensing & feeding behavior in #hypothalamus via CSF. @katterineSalaz2 @FranciscoNuala2 &co show that raised CSF glucose induces SCO-spondin & Wnt5a release, controlling ciliary beating in #EpendymalCells. #PLOSBiology https://plos.io/3Rsb8qV

Subset of neurons in #hypothalamus increases appetite & decreases #thermogenesis. @JongSohn &co show that ion channel GIRK2 functions in hypothalamic NPY/AgRP neurons to increase energy expenditure in mice and may control body weight @kaistpr #PLOSBiology https://plos.io/3qGa8Ev

Healing from the hypothalamus –

To survive an infection, our body must recognize and respond to invading pathogens. This is the job of the immune system. When the first few immune cells encounter a pathogen, especially one that they haven’t seen before, they start releasing #cytokines like #interleukin-1 (IL-1).

These cytokines are the messengers of the immune system. They race through the body via the bloodstream, summoning immune troops to push back the invading pathogen.

When they reach the central nervous system, cytokines must cross the #blood-#brain #barrier to alert and recruit a brain response. The blood-brain barrier has only a handful of entry points, called #circumventricular #organs, where traffic can pass between the central nervous system and the bloodstream with relative ease.

One of these sits at the base of the #hypothalamus in a structure called the #Vascular #Organ of the #Lamina #Terminalis (VOLT for short). The #VOLT is filled with receptors that detect IL-1 and other cytokines.

That, along with its proximity to our #homeostat hypothalamus, means it’s positioned perfectly to sense an ongoing immune response and initiate our brain and body’s many defensive tactics.

After receiving signals from the VOLT, the hypothalamus creates many of the familiar experiences of sickness

https://pennneuroknow.com/2023/06/27/healing-from-the-hypothalamus/

When we get an infection, the reaction of a brain structure called the hypothalamus makes us feel sick – but its responses are also important steps on the way to healing. Read about how we heal from the hypothalamus in this week's post by Lisa Wooldridge.

https://pennneuroknow.com/2023/06/27/healing-from-the-hypothalamus/

#neuroscience #sciComm #hypothalamus #brain #illness #health #immuneSystem