Articles tagged with Leptin
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Scientists have discovered that leptin controls our fondness for food by activating brain regions responsible for rewarding emotions and desires. The study found that individuals deficient in leptin show strong responses to food pictures, even after eating, whereas treatment with leptin normalizes these responses.
Researchers found that leptin upregulates E-cadherin in breast tissue, promoting tumor growth and cell aggregation. This link between obesity, leptin, and breast cancer suggests new targets for drug intervention.
A baby formula supplemented with leptin, a hunger hormone, has been found to promote permanent weight loss and prevent diabetes in rats. The researchers believe that early introduction of leptin can 'hard-wire' the body's energy balance, leading to more efficient energy expenditure.
Researchers at Vanderbilt University found that treatment with TGF-beta inhibitors may help prevent cancer metastasis in patients. Additionally, a study from the University of Michigan discovered that a negative feedback pathway involving leptin receptor signaling may contribute to leptin resistance in obese individuals.
Researchers found that obese mice's brains don't detect critical fat hormone levels, but the rest of the metabolic pathway remains responsive. SOCS-3 may be responsible for this loss of sensitivity to leptin, a hormone regulating energy balance.
The study reveals that leptin resistance causes the breakdown of the brain's appetite regulation system. Researchers found that a key gene called SOCS-3 plays a critical role in this process and may be targeted to aid in weight loss. The research provides new insights into obesity and potential therapeutic strategies.
Peter Shizgal's team investigated the role of leptin in food reward, finding that restricting diet to one meal per day strengthened reward sensations. The study's findings have implications for understanding human motivation and behavior, with potential applications in computer programming and robot development.
Researchers at Michigan Medicine have discovered a single protein, SH2B1, that plays a crucial role in controlling body weight, responding to insulin and leptin signals, and energy balance. The study found that restoring SH2B1 in brain cells corrects metabolic disorders and improves the brain's ability to regulate eating.
Research at Yale University reveals estrogen regulates brain energy metabolism similarly to leptin, leading to a promising avenue for addressing obesity in those resistant to leptin. The study's findings suggest that estrogen may suppress appetite using independent pathways from leptin, making it a potential target for weight management.
A Yale University study reveals leptin's powerful effect on the brain's reward center, impacting appetite regulation. The hormone suppresses dopamine neurons in the ventral tegmental area, linked to behaviors like obesity, drug addiction, and impulsivity.
Researchers found that increasing leptin production in the hypothalamus helps regulate insulin secretion, keeping blood glucose levels normal. Gene therapy successfully reversed type 2 diabetes in diabetic mice, even after a high-fat diet.
The study suggests a novel approach for duplicating leptin's actions when the body no longer responds to the hormone. STAT3 production is essential for leptin's best-known action: acutely reducing food intake. Activating STAT3 may allow normalizing appetite and producing health benefits for obesity, diabetes and infertility.
Researchers found that leptin affects brain processes, improving learning and long-term memory in mice. Low levels of leptin may also be related to cognitive deficits in disorders like type two diabetes.
Researchers found that leptin suppresses appetite in tadpoles, but not as it does in other animals, allowing them to continue eating and developing limbs. The study reveals a new role for leptin in frog development and highlights its importance in regulating energy balance.
The study suggests that the binding of CRP to leptin may be responsible for the reduced effectiveness of leptin in obese individuals. Researchers found that CRP can inhibit leptin's signaling, leading to increased food intake and weight gain.
Research found a significant association between high leptin levels and asthma risk in women, but not men. The study suggests leptin may play an independent role in increasing asthma risk, rather than being linked to obesity.
Researchers at Johns Hopkins Medicine discovered that injecting ciliary neurotrophic factor (CNTF) into obese mice with leptin deficiency or resistance reduced their heart muscle walls by up to a third and the size of the left ventricle by 41%. This breakthrough suggests a novel brain-signaling pathway for obesity-related heart failure.
A study found that genetic variation in the leptin and leptin receptor genes is associated with an increased risk of developing breast cancer. Individuals with two copies of the polymorphism had a threefold higher risk of developing breast cancer than those without it.
Researchers have discovered a new key area in the brain that responds to the fat hormone leptin, which plays a crucial role in resisting high-fat-diet-induced obesity. The ventromedial hypothalamus (VMH) region, previously thought to only be involved in appetite regulation, was found to also respond to leptin and is essential for maint...
Researchers found that leptin blockade improved clinical symptoms of disease, slowed progression, reduced relapses, and reduced antigen-specific T cells in experimental autoimmune encephalomyelitis. Additionally, the study suggests that leptin neutralization may be a potential way to treat multiple sclerosis.
Research reveals that blocking the fat hormone leptin can slow disease progression and reduce symptoms in multiple sclerosis. Leptin blockade improves clinical symptoms, slows disease progression, reduces disease relapses, and decreases antigen-specific T cells.
A study published in Neuron found that the CB1 receptor is integrated with leptin signaling to control appetite, with implications for obesity treatment. Blocking CB1 receptors may offer a promising approach to treating obesity, and recent antiobesity drugs like rimonabant may also work by reducing endocannabinoid signaling.
A new study published in the Journal of Clinical Investigation found that low-dose leptin therapy can reverse skeletal muscle, autonomic, and neuroendocrine adaptations associated with maintaining reduced body weight. The researchers suggest this approach may assist in long-term weight management.
Researchers found that genetically modified rats with high levels of leptin receptors didn't become obese, even on high-fat diets. This suggests that preventing the disappearance of leptin receptors may be key to controlling obesity.
Researchers uncover a new mechanism for post-ischemic arrhythmias, exploring the therapeutic potential of mitochondria-targeting compounds. Leptin signaling is shown to reverse obesity, diabetes, and infertility in mice. FcRn is identified as a promising target for treating autoimmune skin blistering diseases.
Researchers found that SH2-B regulates leptin sensitivity, energy balance, and body weight in mice, leading to obesity and metabolic syndrome. The study identifies SH2-B as a critical component in maintaining leptin sensitivity, potentially serving as a therapeutic target for treating obesity and type 2 diabetes
Researchers discovered that SH2-B, a protein increasing leptin sensitivity, maintains normal energy metabolism and body weight in mice. The absence of SH2-B impairs leptin signal transduction, leading to severe obesity.
A study published in Cell Metabolism suggests that premature leptin surge in newborn mice of underfed mothers leads to remodeling of key brain circuits contributing to obesity later in life. The researchers found that the early leptin surge alone causes accelerated weight gain.
Researchers found that leptin replacement treatment altered brain structure and reduced cravings for people with an obesity gene. The study suggests new potential treatments for weight-related issues.
Researchers found that leptin regulates blood sugar through two brain-body pathways, one controlling appetite and fat storage, and another influencing liver glucose reserves. The study suggests that disrupting both pathways may be necessary for developing full-blown diabetes.
Researchers develop small interfering RNA technology to silence a gene involved in cancer progression, reducing cell proliferation and killing cancer cells. Additionally, inhibiting stearoyl-CoA desaturase-1 decreases body fat and prevents obesity, validating SCD1 as a potential target for pharmacological intervention.
Johns Hopkins researchers have found that modern implanted heart devices are safe for use in magnetic resonance imaging (MRI) machines. The team has also developed new guidelines for their use, making MRI scans more available to people who may benefit from early detection of cancer and other diseases.
Researchers found that chronic lymphocytic leukemia (CLL) cells are born at a fast rate but die, leading to a slow rise in cell count over time due to variable birth and death rates. This dynamic interplay between CLL cell division and cell death may enable physicians to predict disease progression.
A single brain region, the hypothalamic arcuate nucleus (ARH), is sufficient for normal control of blood sugar and activity level by the fat hormone leptin. Restoration of leptin signaling in mice improves glucose homeostasis and locomotor activity.
Research found that individuals who slept for shorter durations had reduced leptin and elevated ghrelin, leading to increased feelings of hunger. This may contribute to the rising obesity pandemic, emphasizing the importance of good sleep in fighting weight-related issues.
A recent Stanford University School of Medicine study found a significant link between sleep loss and hormonal changes that contribute to obesity. Ghrelin and leptin hormone levels were consistently increased and decreased with reduced sleep duration, respectively.
Research subjects who slept only four hours a night experienced an 18% decrease in leptin and a 28% increase in ghrelin, leading to a 24% increase in appetite. The study also found that sleep-deprived individuals tend to crave more sugary and salty foods.
Research found that eicosapentaenoic acid (EPA), an omega-3 polyunsaturated fatty acid from fish oils, stimulates the secretion of leptin in primary cell cultures of fat from rats. This effect may be beneficial for maintaining body weight during obesity treatment and improving associated pathologies.
Researchers discovered that Shp-2, a tyrosine phosphatase, plays a crucial role in regulating metabolism and increasing sensitivity to leptin. The study found that mice with early-onset obesity had increased levels of leptin, insulin, glucose, and triglycerides.
A new study reveals that leptin can restore reproductive function in women with extreme low body fat levels, such as those with infertility, eating disorders, or osteoporosis. Leptin therapy showed dramatic results in raising reproductive hormones and improving menstrual cycles.
Researchers found that administering CD34+ cells after a mouse stroke increased new blood vessel growth and neural regeneration. The study suggests that angiogenesis is essential for repairing stroke damage, providing new hope for treating this deadly condition. Additionally, a separate study on leptin regulation revealed an additional...
Researchers at Brown Medical School have discovered two key enzymes, PC1 and PC2, that play a crucial role in processing the precursor of thyrotropin-releasing hormone (TRH) and regulating calorie-burning. This finding will aid in the understanding and treatment of obesity, which affects nearly 68 million adults in the United States.
Research finds that leptin controls hypothalamic prohormone convertases 1 and 2, influencing thyrotopin-releasing hormone production. This regulation plays a key role in energy balance and may lead to novel treatments for obesity and thyroid axis disorders.
A new study published in the Proceedings of the National Academy of Sciences found that leptin triggers production of áMSH, a powerful peptide signal that boosts metabolism. This discovery could lead to the development of obesity treatments that increase energy production and promote weight loss.
Researchers found that leptin signaling is necessary for regulating body weight homeostasis in mice. The study revealed that leptin receptors on POMC neurons play a key role in this process, and their absence leads to increased fat mass.
Researchers at Cincinnati Children's Hospital Medical Center have detected high levels of adiponectin in human milk, a protein that may help regulate body fat and reduce the risk of obesity. The study suggests that early exposure to this protein through breast milk could influence metabolic health later in life.
New Saint Louis University research reveals that high triglycerides in the bloodstream prevent leptin from reaching the brain, leading to increased hunger and weight gain. The study suggests that lowering triglyceride levels may be a key factor in solving the obesity epidemic.
Researchers at the University of Pennsylvania School of Medicine have discovered a fat cell hormone, adiponectin, that can cause weight loss in mice by increasing their metabolic rate. This finding has far-reaching potential to help treat obesity-related diseases such as diabetes and heart disease.
Researchers at OHSU discovered a possible connection between infant hormone exposure and obesity risk. The study found that early-life leptin surge affects brain development, particularly in the arcuate nucleus of the hypothalamus.
Researchers found that leptin changes the wiring of the brain by controlling synapses, regulating feeding behavior. The hormone induces visible changes in synaptic connections and recordable changes in electrical activity of specific brain cells.
Research reveals leptin rewires neural feeding circuits by suppressing appetite-stimulating neurons and enhancing those that decrease hunger. The study suggests a cause-and-effect relationship between neuronal changes and behavioral changes, potentially contributing to obesity.
Mice with disrupted STAT3 proteins exhibit severe obesity and enlarged livers due to excessive fat deposits. The study also reveals a link between STAT3 and energy balance through its effect on leptin, which could lead to new therapeutics for treating obesity and infertility.
Leptin treatment transforms rat fat-storing cells into unique fat-burning cells with increased mitochondria. This conversion leads to substantial weight loss and improved health in rats.
Researchers investigate how excess fat contributes to hypertension by increasing blood volume, as opposed to constricting it. Studies show impaired sodium handling mechanisms lead to prolonged elevated pressures in obese individuals.
Researchers at Johns Hopkins Medicine discovered that altering leptin's signaling pathway can minimize or even reverse left ventricular hypertrophy, a condition causing the heart to expand and stiffen. Leptin infusions led to weight loss and improved heart function in mice with obesity, while caloric restriction had no effect.
A recent study found that leptin levels dropped significantly during fasting periods, leading to reduced testosterone levels and slowed metabolism. The study also showed that leptin plays a crucial role in regulating the reproductive axis and thyroid function in humans.
A Saint Louis University study found that fat mice get fatter as they age due to a blood-brain barrier defect, while skinny ones remain the same. The researchers propose identifying substances that impair leptin transport to develop new obesity treatments.
A broad-based research program is needed to understand obesity, which cannot be easily explained by personal failing. Genes and environment interact to determine body weight, with genetic factors accounting for individual differences in weight among present time.
Researchers found leptin significantly correlates with reduction in food intake and weight loss prior to developing EAE symptoms. Modulating leptin concentration through dietary approaches may have potential utility in treating MS and other autoimmune diseases.
A recent study published in the journal Nicotine & Tobacco Research has found no significant difference in leptin levels among nonsmokers, ex-smokers, and current smokers. Despite this, researchers observed a rise in leptin levels among women who quit smoking for three weeks, leading to weight gain.