All articles tagged with #hypothalamus
Researchers found that aging-linked decline of the brain protein Menin in the ventromedial hypothalamus triggers inflammation, memory and physical aging signs in mice. Restoring Menin reversed several aging features, and dietary D-serine supplementation improved cognition in older mice, suggesting a brain-centered mechanism for aging with potential human relevance—but no human trials yet and safety remains uncertain.
UC Berkeley researchers mapped brain circuits that regulate growth hormone release during sleep and discovered a feedback loop with the locus coeruleus that balances sleep and wakefulness, linking deep sleep to metabolism and cognition and offering new targets for treating sleep-related metabolic and neurodegenerative conditions.
Scientists discovered that metformin lowers blood sugar not only via the liver and gut but also by acting in the brain. In mice, metformin inhibits Rap1 in the ventromedial hypothalamus, activating SF1 neurons and reducing glucose; surprisingly small brain doses produced effects, and removing Rap1 from VMH abolished metformin’s action, illustrating a distinct brain pathway that could enable lower-dose, brain-targeted diabetes therapies in the future.
Scientists reveal metformin lowers blood sugar by acting in the brain, specifically by suppressing Rap1 in the ventromedial hypothalamus and activating SF1 neurons, with brain effects at far lower drug levels than previously thought, opening possibilities for brain-targeted diabetes therapies and potential brain-health benefits.
New preclinical work links metformin’s metabolic effects to the brain, showing it acts in the hypothalamus via the Rap1 pathway to enhance central insulin signaling and reduce liver glucose production in mice. This brain-first mechanism could reshape diabetes and obesity therapies, informing drug combinations and trial endpoints, but human validation is needed and questions remain about dosing, blood–brain barrier crossing, and interactions with AMPK.
Researchers found that after meals ball pythons exhibit a 1000-fold rise in pTOS, a gut-bacteria–derived metabolite. In mice, high doses of pTOS reduced appetite and caused weight loss without typical GLP-1 drug side effects, likely by activating neurons in the ventromedial hypothalamus. While promising, translating this to humans is still early, and the study in Nature Metabolism notes many more metabolites to explore.
Researchers identified pTOS, a metabolite produced by python gut bacteria that surges after a meal (more than 1,000-fold); when given to obese mice, it suppressed appetite, leading to about 9% body weight loss over 28 days, without notable changes in energy expenditure or organ size. Unlike GLP-1 drugs that slow gastric emptying, pTOS appears to act on the hypothalamus to regulate hunger. The molecule also exists at low levels in human urine, suggesting potential safety, though clinical applicability requires more research; the findings were published in Nature Metabolism.
In a mouse study, early-life exposure to a high-fat, high-sugar diet permanently shifts hypothalamic appetite pathways and adult feeding behavior even after weight normalizes; however, interventions targeting the gut microbiome—probiotic Bifidobacterium longum APC1472 or prebiotic fibers FOS/GOS—can restore brain–gut signaling and mitigate these long-term effects, with some sex-specific vulnerabilities observed.
Researchers have discovered that metformin, a common diabetes drug, also acts in the brain, specifically in the ventromedial hypothalamus, by turning off the protein Rap1, which is essential for its blood sugar-lowering effects. This finding suggests new avenues for more targeted diabetes treatments and highlights the brain's role in metformin's mechanism of action.
A UC Berkeley study uncovers a neural feedback mechanism controlling growth hormone release during sleep, revealing how sleep quality influences muscle growth, fat burning, and brain function, with potential implications for treating sleep and metabolic disorders.
Researchers at the University of Michigan discovered that specific neurons in the hypothalamus help regulate blood sugar levels during routine activities like fasting, by promoting fat breakdown to maintain glucose and prevent hypoglycemia overnight, which could have implications for understanding prediabetes and diabetes management.
A study from the University of Michigan found that specific hypothalamic neurons, VMHCckbr, actively regulate blood glucose during routine conditions by promoting fat breakdown and glycerol production, which supports glucose stability overnight. Overactivity of these neurons may contribute to prediabetes, highlighting the brain's nuanced role in metabolic health.
Scientists have discovered that the brain, in addition to the pancreas, can produce insulin, with at least six different types of insulin-producing cells identified in the brain. This local insulin may play roles in cognitive function, growth regulation, and appetite suppression, and could be significant in understanding and treating conditions like Alzheimer's disease. However, much remains unknown about the functions and origins of brain insulin, and further research is needed.
Research in male mice identifies a stress-sensitive neural pathway between the paraventricular nucleus and lateral hypothalamus that disrupts sleep and impairs memory, suggesting potential targets for treating stress-related cognitive and sleep issues.
Researchers have discovered a new population of neurons in the hypothalamus that regulate appetite by expressing leptin receptors and the BNC2 gene. These neurons respond to hunger-suppressing signals and food-related cues. Disrupting these neurons in mice led to increased food intake and weight gain, highlighting their role in energy balance. This finding offers a potential new target for obesity treatments, providing hope for more effective therapies against the obesity epidemic.