Articles tagged with Hypothalamus
Research in mice reveals that coordinated clock-gene and neuronal activity rhythms are necessary for daily hormone release, with the suprachiasmatic nucleus (SCN) and paraventricular nucleus (PVN) working together to generate circadian rhythms. Disruption of these clocks can lead to various pathologies.
Researchers at Baylor College of Medicine discovered two distinct brain circuits that regulate hunger-driven and non-hunger driven feeding behaviors. The study identified serotonin receptors and ion channels as potential molecular targets to suppress overeating and improve treatment options for obesity.
New research reveals that obese mice do not increase the density of blood vessels in the hypothalamus when leptin is absent. However, increasing leptin levels promotes vessel growth via astrocyte activity. This study provides a paradigm shift in understanding how the hypothalamus controls blood pressure in obesity.
A recent study has identified a constellation of genetic variants in the FTO gene that correlate with metabolic and behavioral changes linked to obesity. The research found that these variants influence the expression of IRX3 and IRX5, which collectively mediate risk of obesity.
Researchers at EPFL discovered that bile acids can trigger satiety in the brain by activating specific receptors. Bile acids reach the brain shortly after a meal and suppress food intake by blocking appetite-stimulating signals. This study suggests a new role for bile acids in regulating eating behavior.
The researchers generated human brain organoids of the arcuate nucleus, which exhibits high cell diversity, to model development and disease. The organoids maintained disease-specific gene signatures, including those related to Prader-Willi syndrome, a genetic disorder causing hunger and obesity.
Researchers mapped the developmental landscape of the mouse hypothalamus, revealing a stepwise strategy for neural progenitors to generate extreme neuronal diversity. The study provides insights into hypothalamic plasticity and potential therapeutic targets for diseases such as anorexia and narcolepsy.
Researchers at Nagoya University found that KNDy neurons, expressing kisspeptin, neurokinin-B, and dynorphin-A, are responsible for GnRH pulses, enabling ovarian function in mammals. Rescuing just 20% of these neurons is sufficient to restart GnRH and gonadotropin pulses and maintain fertility.
Genetic correlations between IBD, stress, and depression have been uncovered through 3D genomic mapping, implicating the hypothalamus in IBD pathogenesis. The study found enrichment of IBD-associated genetic variants in hypothalamic-like neurons and colonoids.
Researchers at RIKEN Center for Brain Science discovered a brain region called the SuM that detects new social experiences and segregates them from unfamiliar places. This finding can help understand normal memory and conditions where recognizing new information is impaired.
Researchers at Harvard Medical School have identified a population of neurons in the hypothalamus that controls hibernation-like behavior in mice. Stimulating these neurons induces torpor, while blocking their activity disrupts natural torpor, offering insights into the neural mechanisms underlying this state.
Researchers discovered that nociceptin neurons in the hypothalamus of mice promote consumption of high-fat food. Removing these neurons from the brain eliminated overeating in mice.
A new UCLA study has identified a key gene, reprimo, which regulates body temperature and may contribute to menopause-related weight gain. The research suggests that manipulating this gene could provide a safer alternative to hormone replacement therapy for alleviating symptoms.
A team of researchers found a specific brain region responsible for influencing social behaviors and reward valuations in monkeys. They discovered that this region, the lateral hypothalamus, plays a crucial role in shaping socially motivated behavior.
Researchers created a human model of congenital pituitary hypoplasia using patient-derived iPS cells to illuminate the underlying mechanisms. The model revealed that a deficiency in FGF10 from the neighboring hypothalamus caused CPH, highlighting the importance of interactions between the pituitary and hypothalamus.
Researchers found soybean oil causes genetic changes in the brain, affecting obesity, diabetes, and neurological conditions. The study discovered 100 genes not functioning correctly, including a gene that produces oxytocin, leading to potential ramifications for brain function and diseases.
A study by Dr. Michael L. Lipton and colleagues discovered a significant correlation between oral contraceptive use and reduced hypothalamic volume in 50 healthy women. The findings suggest potential effects on mood regulation and emotional processing.
Scientists have identified a previously unknown pathway connecting the hypothalamus and midbrain that drives defensive behaviors in mice. Further research on this pathway could increase understanding of anxiety disorders.
A newly identified hunger pathway in the brain can quickly modify food intake in response to food cues. The discovery improves understanding of how the brain controls energy balance and may lead to new treatments for eating disorders.
A new study suggests that the brain uses sensory signals from the mouth and throat to temporarily quench thirst, but also relies on gut sensors to review this decision based on a drink's hydration potential. This helps regulate fluid balance within the body and may provide insights into diseases like high blood pressure.
A USC Dornsife-led study has provided the first global network model of the inner workings of the hypothalamus, a critical part of the brain that controls fundamental behaviors and physiology. The study reveals novel associations with several diseases, including neurodegenerative diseases and behavioral disorders.
A multidisciplinary team has found a new connection between the lateral hypothalamus, a feeding center, and the hippocampus, a memory center, revealing how the protein complex NCOR1/2 regulates memory. The study sheds light on potential links to autism, intellectual disabilities, and neurodegenerative diseases.
Researchers at Children's Hospital Los Angeles have identified a set of molecules that wire the body weight center of the brain. Blocking these signals causes connections to fail and leads to elevated body weight.
Undernutrition delays puberty onset by enhancing AMPK levels in the hypothalamus of female rodents. Overexpressing active AMPK also delays puberty, implying its role in regulating female puberty via kisspeptin signaling.
Researchers at the Max Planck Institute discovered that individuals with depression have a larger left hypothalamus than those without the disorder. The study found a correlation between the severity of depression and the size of the brain region, but no effect from medication.
Researchers at University of Tsukuba identified two molecules, Ptf1a and Meis, that specify the development of a hypothalamus-like region in sea squirt embryos. These findings have implications for understanding brain development and potentially treating diseases like Parkinson's disease.
A study by Takeo Nakanishi at Kanazawa University found that fever is regulated by prostaglandin E2 and OATP2A1 transporters, suggesting these as potential therapeutic targets for treating fever-related conditions.
A newly discovered neural circuit in mice regulates feeding behavior, with SST neurons playing a central role. The study reveals that activating these neurons increases eating behavior, while inhibiting them reduces it.
A study published in PLOS Biology found that exercise-induced appetite suppression is linked to the activation of temperature-sensitive TRPV1-like receptors in hypothalamic arcuate nucleus cells. These cells respond to heat and play a role in suppressing food intake in response to exercise.
Scientists discovered an anorexigenic neural circuit involving medial septal complex and paraventricular hypothalamus projections, associated with reduced nighttime and daytime food intake in mice. The study suggests a potential new approach to treating eating disorders without inducing maladaptive behaviors.
Scientists have identified a new group of cells responsible for keeping humans awake. The supramammillary nucleus is part of the caudal hypothalamus and plays a crucial role in maintaining wakefulness. When activated, it promotes prolonged wakefulness during normal sleep periods.
Researchers found that a diet rich in saturated fats damages the brain's hunger control system within days, while gut bacteria changes occur weeks later. The study suggests that this sequence of events may contribute to weight gain and obesity.
A study found that protein tyrosine phosphatase receptor type J (PTPRJ) inhibits leptin signaling, leading to leptin resistance. PTPRJ expression in the hypothalamus is up-regulated by diet-induced obesity, making it a potential target for improving obesity treatment.
Researchers at Albert Einstein College of Medicine found that adult neural stem cells in the hypothalamus govern how fast aging occurs in the body. By replenishing these stem cells or the molecules they produce, it's possible to slow and even reverse various aspects of aging throughout the body.
Researchers found that intranasal insulin improves functional connectivity in brain regions involved in cognitive processes and appetite regulation. The study suggests that insulin in the brain may help regulate eating behavior and facilitate weight loss by suppressing the relationship between adiposity and hunger sensation.
Researchers discovered that a small group of hypothalamus neurons, called POMC, modulate the amount of insulin produced by the pancreas. The study reveals new molecular mechanisms involved in this connection and highlights the importance of mitochondrial dynamics in glucose sensing and insulin release control.
Researchers at Japan's National Institute of Genetics discovered a direct neural link connecting the brain's visual system to its feeding center, linking visual perception of food to feeding motivation. This study, using genetically engineered zebrafish, shows that 'eating with the eyes' is deeply rooted in evolution.
A mouse study found that prenatal BPA exposure weakens the body's fullness cues by reducing sensitivity to leptin, a hormone controlling appetite. This altered response can lead to increased obesity risk in offspring, supporting concerns about the potential impact of environmental endocrine disruptors on human health.
Researchers at Nagoya University have uncovered a novel brain circuit for hunger responses during starvation, revealing the role of neuropeptide Y signals in controlling heat production by brown adipose tissue. The study found that inhibitory GABAergic inputs from medullary reticular neurons inhibit BAT thermogenesis.
Researchers found altered brain pathways in individuals with anorexia and bulimia nervosa, overriding the hypothalamus' drive to eat. This reversal allows their brains to fend off hunger signals, making it harder for them to consume food.
Scientists from Daegu Gyeongbuk Institute of Science and Technology have identified a key enzyme in regulating our appetite, revealing how low glucose levels activate AMPK to control food intake. This breakthrough provides new insights into the complex mechanisms governing our eating behavior.
A new study from Boston Children's Hospital reveals that specific neurons in the hypothalamus play a central role in triggering anxiety. Blocking these neurons selectively erased natural fears in mice, suggesting a potential more effective treatment for anxiety and other psychiatric disorders.
A recent study published in Cell Metabolism shows that neurons in the brain have a significant role in regulating metabolic responses to stressful situations. The CRFR1 receptor, typically associated with the sympathetic nervous system, is found to be expressed on cells involved in appetite regulation and energy expenditure.
A study in mice reveals a specific brain region, the ventrolateral part of the ventromedial hypothalamus, is responsible for aggressive motivations that lead to violence. The research suggests targeting this region could lead to better control of aggressive behaviors without sedation.
Researchers have identified novel populations of nerve cells that regulate appetite, thermogenesis, and physical activity. Deleting the BDNF gene impairs thermogenesis and causes hyperphagia and severe obesity. The study reveals two distinct types of BDNF neurons with different biological roles.
The study found that a key enzyme produced by fat tissue regulates brain function and energy levels, suggesting an optimal amount of body fat for maximizing health and longevity. Mice with low NAMPT in fat tissue had impaired energy levels and physical activity, while those with high NAMPT exhibited increased physical activity.
Researchers at UCSF discovered that immune cells in brain respond to fat in diet by causing mice to consume more food. The study found that a population explosion of microglia, a type of immune cell, in the hypothalamus region drives increased food intake.
A new study using PET/CT technology found that military veterans with post-traumatic stress disorder (PTSD) often have abnormal pituitary gland function. The research suggests that hormone imbalances in the pituitary gland may be a key factor in the development of PTSD in veterans who have also suffered from mild traumatic brain injury.
A new study finds that the brain of children with gender dysphoria reacts to androstadienone, a male musk-like steroid, in a way typical of their biological sex at puberty, but shifts to their experienced gender afterwards. This suggests a partial rewiring of the brain as children grow up.
Researchers at Imperial College London identified an anti-appetite molecule called acetate, naturally released when we digest fibre in the gut, which produces a signal to stop eating. The study found that acetate reduces appetite and could inform potential methods to prevent weight gain.
Researchers pinpointed the precise cellular connections responsible for triggering overeating behavior in mice, suggesting a neurological basis for obesity and eating disorders. The study highlights a potential target for drug treatments to correct malfunctioning brain circuits.
Researchers have identified a mechanism by which Sirt1 promotes neural activity in the brain, leading to significant delays in aging and increases in longevity. The study found that mice with increased Sirt1 expression in their brains exhibited dramatic physical changes, including improved muscle structure and vigor.
Researchers at Lund University have prevented early symptoms of Huntington's disease, depression, and anxiety in mice by deactivating the mutated huntingtin protein. This discovery is a major breakthrough and may lead to more accurate treatments for this debilitating disease.
Scientists at Albert Einstein College of Medicine have found that the hypothalamus controls aging throughout the body, opening up new avenues for treating age-related diseases. Activating specific pathways can accelerate or slow down aging, and blocking them may increase longevity by up to 20 percent.
Research at Baylor College of Medicine found that bone marrow cells producing BDNF travel to the hypothalamus, where they fine-tune appetite. A bone marrow transplant restoring the gene for BDNF can normalize appetite and reduce overeating in mice with insulin resistance.
Researchers at the University of Utah discovered that Wnt signaling is essential for the production and specialization of nerve cell precursors in the hypothalamus. The study found that Wnt signaling continues to be required for adult neurogenesis, suggesting a key role in brain plasticity.
A team of scientists at Beth Israel Deaconess Medical Center has identified the mechanism responsible for inhibition of AMPK activity in the hypothalamus, a crucial integration point where multiple signaling pathways converge. This discovery could lead to new treatments for metabolic diseases and cancer.
Exposure to environmental chemicals like PCBs in the womb causes long-term changes to the developing brain, leading to delayed puberty and disrupted reproductive cycles. The study identified five genes critical to normal hypothalamic control of reproduction, providing a potential target for interventions.
Researchers discovered that underweight babies are more likely to become obese due to a disrupted hypothalamus, which leads to an increased appetite for calories. This results in the child consuming more calories to catch up on lost nutrition in utero, potentially leading to childhood obesity.
Researchers at Lund University have discovered a causal relationship between mutated Huntington's protein and weight gain in mice. The study shows significant changes in the brain's hormone control centre, leading to insulin resistance and metabolic dysfunction.