Researchers suggest targeting aldosterone receptor for effective hypertension treatment in women. High aldosterone levels are linked to increased blood pressure and cardiovascular risk.
Researchers at the University of Bristol have made a groundbreaking discovery that could lead to a new treatment for heart attacks. Pericytes, cells surrounding blood vessels, stimulate new blood vessel growth with the help of hormone leptin, which may help restore blood supply to damaged heart muscle after a heart attack.
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Despite being hailed as the key regulator of leanness, leptin's function in humans remains uncharacterized. Researchers call for experimental evidence to demonstrate its mechanism of action, highlighting a crucial gap in our understanding of metabolism and obesity.
Researchers at Hiroshima University have identified a molecule, NPGL, that increases appetite during fasting and decreases it during gorging. This discovery suggests that the body has an evolved mechanism to maintain weight at a constant level, regardless of diet or energy intake.
Researchers found metreleptin treatment improved liver function and reduced fatty liver disease progression in patients with partial lipodystrophy. Patients with lower baseline leptin levels showed higher response rates to the treatment.
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.
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Researchers at UT Southwestern Medical Center identified an ion channel, TrpC5, essential for the brain's response to leptin and lorcaserin, two hormones and medications used to suppress appetite and reduce body weight. In mice deficient in TrpC5, these hormones were ineffective, leading to increased body weight and disrupted metabolism.
Researchers have created a genetically induced obesity model in fruit flies, shedding light on the brain's 'fullness' signal. The model highlights a hormone called unpaired 1, which plays a crucial role in regulating eating behavior and weight gain.
Researchers at UT Southwestern Medical Center found that intermittent fasting inhibits the development and progression of acute lymphoblastic leukemia (ALL), a type of childhood leukemia. However, fasting was ineffective against another type of blood cancer commonly affecting adults, acute myeloid leukemia (AML).
Research suggests that maternal B12 deficiency during pregnancy may predispose children to metabolic problems such as type-2 diabetes. The study found that babies born to mothers with low B12 levels had higher leptin levels, which can lead to insulin resistance and an increased risk of type-2 diabetes.
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Scientists have discovered that the Rap1 gene plays a crucial role in energy balance and that its inhibition can restore sensitivity to leptin, a hormone that regulates appetite and body weight. The study suggests that targeting Rap1 may be a potential therapeutic approach for treating human obesity.
A study by King's College London has discovered a link between maternal obesity during pregnancy and increased blood pressure in children, with the 'fullness' hormone leptin playing a key role. Mice exposed to high levels of leptin in the womb developed high blood pressure and kidney damage later in life.
A study has discovered a new mechanism in the mouse brain that regulates obesity, finding that Rap1 gene inhibition can reduce body weight and improve leptin sensitivity, potentially leading to a new therapeutic target for treating human obesity.
Researchers at McGill University have discovered a crucial role of NG2-glia cells in the median eminence in regulating appetite and body weight. The cells support and shelter leptin receptor neurons, enabling them to instruct the body when to stop eating, leading to potential new targeted anti-obesity approaches.
Researchers found that a small dose of E. coli wall can significantly reduce the desire for sweets in mice, possibly by triggering higher levels of leptin hormone. This effect persists for seven days and may have implications for obesity prevention.
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A new study found that higher levels of cord-blood leptin and adiponectin at birth were associated with greater fat in the child at ages 9 and 17. This suggests that fetal overnutrition may program greater adiposity in the child, extending into childhood and adolescence.
A new study found that leptin inhibits the development of neuronal connections between the brain and pancreas during embryonic development. This breakdown in communication can lead to impaired glucose regulation and increase the risk of type 2 diabetes in children, particularly those born to obese mothers.
Researchers are investigating the unhealthy connection between excess fat and cardiovascular disease to identify new treatment avenues. They aim to understand why visceral fat exacerbates cardiovascular problems by stimulating the production of aldosterone, a hormone linked to high blood pressure and diabetes.
Researchers at Helmholtz Munich identified a new component regulating body weight and food intake, with histone deacetylase 5 (HDAC5) playing a significant influence on leptin's effect. The study found that HDAC5 is essential for the brain to recognize fat depot levels, enabling adaptation to food intake and reducing obesity.
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Researchers from Rockefeller University have identified a hormone called amylin as a critical component of the system responsible for regulating food intake. Amylin acts in the brain to help control consumption, working in concert with another hormone leptin to control body weight.
A new study has identified four genes associated with leptin levels, providing insight into the complex relationship between body fat and hunger. The findings have important implications for understanding obesity and developing targeted treatments.
Researchers at Oregon State University have successfully used gene therapy to aid weight loss in rats without causing significant bone loss. The study, published in the Journal of Endocrinology, found that delivering leptin directly to the brain via gene therapy reduced abdominal fat and preserved bone density.
Researchers find that leptin directly activates aldosterone production in the adrenal glands, leading to increased blood pressure and cardiovascular problems. Targeting aldosterone with existing drugs like spironolactone may help prevent cardiovascular disease in obese individuals.
Researchers at Yale University have found that hunger neurons control not only hunger and appetite but also regulate bone mass. The study reveals that lower levels of hunger are associated with lower bone density, highlighting a new mechanism in the regulation of skeletal bone metabolism.
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A breakthrough study has identified a neural mechanism responsible for fat breakdown, allowing researchers to develop novel anti-obesity therapies. The study found that fat tissue is innervated and direct stimulation of neurons in fat can induce fat breakdown, providing new hopes for treating central leptin resistance.
A new study has found that the satiety hormone leptin plays a crucial role in the 'runner's high' feeling, with mice running longer distances on a wheel due to reduced leptin signaling. The research also suggests that people with lower fat-adjusted leptin levels may be more inclined to exercise.
A team of scientists at Scripps Research Institute has devised an improved method to engineer therapeutic proteins into antibodies, which can persist long enough to be useful. The technique mimics evolution and harnesses the power of large numbers to select rare junction segments that allow inserted proteins to fold and function normally.
A recent study found that the thunder god vine extract reduces food intake by up to 80% and causes a 45% decrease in body weight in obese mice. The compound Celastrol enhances leptin action, a hormone signaling fullness to the brain, improving ER function and sensitivity.
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Researchers at the University of Cincinnati found that leptin action is normal in obese individuals, not impaired as previously thought. The study suggests that restoring leptin action may not be effective in reducing obesity, requiring a new approach to understanding and treating the condition.
Researchers discovered the brain's role in regulating body fat by combining hormones leptin and insulin, which stimulate the conversion of white fat to brown fat through the nervous system. This process normally maintains body weight but goes awry in diet-induced obesity.
A study published in Cell found that leptin, the 'satiety hormone', is linked to obesity-induced high blood pressure. Researchers discovered that obese individuals lacking leptin or its receptor had lower blood pressure despite being heavy.
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A groundbreaking study by Australian researchers has discovered that leptin hormone secreted by fat cells elevates blood pressure in obesity. The hormone acts in the brain to increase blood pressure, making it a promising target for treating obesity-induced hypertension and cardiovascular diseases.
A team of researchers has drawn connections between known regulators of body mass, pointing to possible treatments for obesity and metabolic disorders. They also found intriguing clues that these same molecular pathways may play a role in learning and perhaps even in some forms of brain cancer.
A new study from Uppsala University found that elderly carriers of the FTO gene have higher ghrelin levels and lower leptin levels, making them more prone to weight gain. The study suggests that this genetic variant may facilitate weight gain by shifting the endocrine balance towards hunger hormone ghrelin.
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Researchers at Yale School of Medicine discovered that leptin affects not only brain cells called neurons but also other types of cells involved in appetite regulation. This finding could lead to the development of new treatments for metabolic disorders such as obesity and diabetes.
A new study reveals that leptin acts directly on neurons in the preoptic region of the hypothalamus to regulate peripheral levels of leutinizing hormone, essential for reproduction. The study demonstrates that leptin communicates the status of peripheral energy stores to GnRH-releasing neurons via the preoptic hypothalamus.
A team of researchers from the University of Akron has made a groundbreaking discovery by identifying the missing hormone leptin in birds. Leptin plays a crucial role in regulating body fat storage, metabolism, and appetite, but its presence was unknown in avian species until now.
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A new study published in the Endocrine Society's Journal of Clinical Endocrinology & Metabolism found that childhood abuse or neglect can lead to long-term hormone impairment, increasing the risk of developing excess belly fat and metabolic disorders later in life.
The US FDA has approved metreleptin as a treatment for generalized lipodystrophy, a condition characterized by near-complete absence of fat tissue. Leptin replacement therapy has been shown to control severe insulin resistance and lower triglyceride levels in patients with severe generalized lipodystrophy.
A new peptide treatment has been shown to restore leptin responsiveness, improve body weight and glucose metabolism in obese mice fed a high-fat, high-sugar diet. The treatment overcomes leptin resistance, a major obstacle in treating obesity and type 2 diabetes.
New research suggests that childhood exercise can improve leptin sensitivity and reduce fat deposits, potentially staving off some bad effects of maternal obesity. Exercise as early as adolescence has been shown to have a persistent effect on the satiety centers of the brain, even years later.
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Scientists identified mechanisms necessary to live without insulin, a breakthrough that could lead to alternative treatments against diabetes. Researchers found leptin regulates glucose levels and reduces the risk of hypoglycemia, offering hope for patients.
Researchers found decreased neuropeptide Y neurons, upregulated leptin receptors, and disrupted feeding behavior pathways in rats with chronic immobilization stress. Chronic stress leads to increased leptin receptor expression and suppressed neuropeptide Y synthesis.
University of Texas Medical Branch researchers have identified a protein called Epac1 that blocks leptin's activity in the brain. Blocking this protein can increase leptin sensitivity and lead to lower body weight, body fat percentage, blood plasma leptin levels, and improved glucose tolerance.
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A study of 439 overweight postmenopausal women found that weight loss and physical activity lower the risk of breast, colorectal, and cervical cancers. Adiponectin levels increased with weight loss, while leptin levels decreased, suggesting a protective effect against tumor cell growth.
Obese individuals are more prone to asthma due to the regulation of airway diameter by leptin. Leptin therapy may provide a new treatment option for body weight-associated asthma, with existing drugs targeting parasympathetic signaling already available.
Research reveals that partial sleep deprivation affects ghrelin and leptin levels, leading to increased energy intake and potential weight gain. The study suggests a possible link between sleep patterns and body weight regulation.
Scientists at the University of Michigan have made a groundbreaking discovery in understanding how the hormone leptin regulates metabolism and body weight. By visualizing the interaction between leptin and its receptor, researchers may develop new drugs to overcome leptin resistance, a key factor in obesity.
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Scientists have identified a key metabolic hormone called leptin in fruit flies, which regulates energy intake and appetite. The discovery opens up new avenues for genetic research on the molecular mechanisms of fat sensing and could provide insights into obesity and diabetes.
A new study by researchers at The University of Akron found that leptin may play a role in hearing and vision loss in humans. Leptin also affects the development of eyes and ears in fish, suggesting a potential link to sensory loss.
A new compound, JD5037, targets cannabinoid receptors and increases sensitivity to leptin, reducing obesity and improving metabolic health. The findings have implications for the development of new treatments for obesity in humans.
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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.
Researchers at the University of Sheffield have defined the structure of the human obesity receptor, a key factor in regulating body fat. This breakthrough could lead to new treatments for complications of obesity and anorexia.
A study published in Nature Medicine reveals that a mutation in the Bdnf gene can lead to uncontrolled obesity due to the inability of neurons to pass along appetite-suppressing signals. The researchers found that stimulating expression of this gene may offer a novel strategy for treating obesity.
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Researchers found that sleep-deprived individuals consumed an average of 549 additional calories per day, while leptin levels increased and ghrelin decreased. This study suggests that sleep deprivation may be a preventable cause of weight gain and obesity.
Researchers have discovered a new way to enhance trastuzumab treatment in HER2-positive breast cancer patients by stimulating natural killer cells. Additionally, the activation of FoxO1 has been linked to the development of diabetic cardiomyopathy, offering a promising therapeutic target. Leptin's direct action on POMC neurons may also...
Research published in the FASEB Journal reveals that intestinal microbiota play a crucial role in determining the outcome of heart attacks in rats. The study found that probiotics can tilt the scales in favor of improved cardiovascular health, reducing heart attack risk and improving recovery from myocardial infarction.
Researchers successfully transplanted young neurons into diseased brain circuitry, repairing defective circuits and enabling mice to respond to leptin. This breakthrough suggests new therapeutic approaches for conditions like spinal cord injury, autism, and Parkinson's disease.
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Researchers at Monash University have discovered how leptin-resistance develops in overweight and obese individuals. The study reveals that targeting only one of the negative regulators won't be enough to increase leptin-sensitivity in obesity, suggesting that all three regulators might need to be switched off.
Leptin's antiobesity effects are attributed to modulation of inhibitory output via GABA neurons, which suppress appetite and energy expenditure.