A new study from the Icahn School of Medicine at Mount Sinai suggests that the sympathetic nervous system, not macrophages, is the main driver of thermogenesis. The research team found that catecholamines released by the sympathetic nervous system can convert white fat tissue into a tissue resembling brown fat.
High levels of protein Id1 suppresses brown fat's burning ability by binding to key regulators, leading to increased risk of diabetes and obesity. Conversely, lack of Id1 promotes conversion of white fat to healthier beige fat.
Researchers at Joslin Diabetes Center identified a lipid molecule that signals brown fat cells to activate in mice, improving metabolism. The molecule, 12,13-diHOME, may also be used as a biomarker for brown fat activation in humans.
Researchers at Technical University of Munich found a significant proportion of human bodies contain brown fat, which burns energy at an extraordinary rate. This discovery may lead to more effective obesity and diabetes medications that target brown adipose tissue.
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Scientists discovered an FDA-approved drug that increases 'good' fat mass and function, preventing weight gain and burning more calories. The drug, bexarotene, converts white fat cells into brown fat-like cells through cellular reprogramming.
Researchers found that epigenetic enzyme Lsd1 maintains brown fat tissue's metabolic properties. Inhibiting Lsd1 leads to whitening of brown adipose tissue, storing energy instead of expending it.
Researchers found that rutin extracted from mulberries activates brown adipose tissue to mimic cold-induced thermogenesis, enhancing energy metabolism and weight loss. This natural compound was tested on genetically obese mice and diet-induced obesity models, reducing adiposity and improving glucose homeostasis.
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Researchers discovered a chemical called Beta-LGND2 that converts white fat to brown fat, increasing metabolism and facilitating weight loss in mice. This breakthrough could lead to new treatments for obesity and metabolic diseases.
Researchers are working to enhance the heat-burning ability of brown fat to combat obesity. They discovered a gene, BSCL2, that regulates brown, white, and beige fat. Deleting this gene in mature brown fat surprisingly increased its efficiency at burning fat, while mice on high-fat diets still lost weight.
Researchers have discovered a new strategy to cultivate beneficial beige fat, which can help ward off obesity and diabetes. By preventing beige fat cells from digesting their own mitochondria, the intervention successfully protected against obesity and pre-diabetic symptoms in mice, raising hopes for future applications in human patients.
Researchers at McGill University have found a way to reprogram white fat cells into energy-burning beige or brown fat cells. This 'browning' process can help manage obesity and other metabolic disorders by burning excess energy instead of storing it.
A McMaster University research team is examining how environmental factors, such as agricultural practices and toxicants, affect brown adipose tissue activity in individuals with obesity or type-2 diabetes. The studies aim to develop new strategies to enhance BAT activity for treating and preventing these diseases.
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University of Bonn researchers have discovered a new method to measure the activity of energy-consuming brown fat cells in humans and mice. They found that microRNA-92a can be used as an indirect measure of brown fat cell activity, with a small blood sample sufficient for analysis.
Scientists have discovered a potential method for battling obesity by stimulating brown fat in genetically predisposed mice, which may help treat metabolic syndrome and its related health issues. The study found that increasing heat production in the fatty tissue improved weight management and glucose control.
Steroid medications like prednisolone suppress brown fat's activity, leading to weight gain and obesity. Researchers found that steroid use increases energy storage from food instead of burning it through brown fat.
Scientists at Sanford Burnham Prebys Medical Discovery Institute have identified a protein complex that converts
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The study reveals that TRPV2 is essential for thermogenesis in mouse brown adipose tissue. Without TRPV2, mice exhibit impaired thermogenesis and increased obesity on high-fat diet treatment.
Researchers found that individuals with more brown fat had smaller fluctuations in blood sugar levels. Brown fat may act as a 'glucose buffer', lessening the variation in blood glucose and potentially diminishing metabolic stresses that could increase the risk of diabetes.
Researchers discovered that human brown fat cells show circadian fluctuations in glucose consumption, which may act as a glucose buffer and lessen the stress on the pancreas. Individuals with high brown fat abundance showed less variability in glucose levels over time.
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A team of scientists at the University of Bonn discovered a switch that can convert unwanted white fat cells into energy-burning brown cells by blocking Gq proteins. This breakthrough has significant implications for obesity treatment, as it may lead to the development of pharmaceutical products that target this pathway.
Researchers from the University of Cologne have successfully inhibited a protein that hampers activation of brown fat in mice, leading to improved glucose metabolism. By feeding Bace1 inhibitors to these animals, scientists were able to activate their brown fat and alleviate metabolic problems.
A Georgia State University biologist has received a four-year, $1.37 million grant from the National Institute of Health (NIH) to study epigenetic mechanisms and their link to obesity. The researcher aims to induce brown adipocytes in white fat tissues to prevent and treat obesity.
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A recent study by Hiroshima University has identified a key protein responsible for burning excess energy in the body, UCP1, found in brown fat cells. Increasing UCP1 levels can lead to a higher metabolism and less weight gain.
Researchers found that mild stress increases brown fat activity, linked to higher cortisol levels and potential heat production. This discovery has implications for preventing obesity and diabetes through sustainable interventions.
A study by Finnish researchers found that removing a gene from mice protected them against arterial disease and obesity, due to increased activity of brown adipose tissue. The discovery suggests that inhibiting the USF1 gene might be a good strategy for treating cardiovascular disease and diabetes.
Researchers discover a protein called Casein Kinase 2 that prevents white fat from burning energy in cold conditions. Inhibiting this molecule boosts metabolism and reduces weight gain in mice fed high-fat diets.
Researchers at UC Berkeley created an implant containing stem cells that form functional brown-fat-like tissue, reducing weight gain and lowering blood glucose levels in mice. The study's results suggest the technique could lead to new therapeutic approaches for metabolic disorders.
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Researchers have discovered that white fat can be transformed into a form resembling brown fat, increasing metabolic rate and lowering blood glucose levels. This finding has significant implications for the treatment of complications associated with obesity and sedentary lifestyle.
Researchers created human cell lines to study gene expression in precursor cells, enabling the prediction of UCP1 expression and potential transformation of white fat cells into brown fat cells. This breakthrough offers a promising tool for developing personalized obesity treatments.
Researchers at Duke-NUS Medical School have discovered a long non-coding RNA that regulates brown fat development in mice. This finding holds promise for developing new therapeutic strategies to prevent and treat obesity.
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A research team has isolated energy-burning beige fat from adult humans, which can convert unhealthy white fat into healthy brown fat. This discovery holds promise for developing new medications to fight obesity by recruiting and activating human brown fat.
Brown fat tissue communicates with the brain through sensory nerves, possibly sharing information that is important for fighting human obesity. The study found that when brown fat tissue was activated with a drug, it talked back to the brain by activating sensory nerves.
A new experimental drug, GC-1, has been found to convert 'bad' white fat into 'good' brown-like fat, leading to weight loss and improved insulin sensitivity in mice. Researchers believe this conversion may help treat obesity and metabolic disease.
Researchers found that exposure to cold temperatures increases levels of the protein Zfp516, which activates UCP1 in brown fat. Mice with boosted Zfp516 protein gained 30% less weight on a high-fat diet, suggesting a potential target for obesity and diabetes treatment.
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A FDA-approved drug may help combat obesity by stimulating brown fat's metabolic activity, increasing resting metabolic rate, and promoting weight loss in rodents. Researchers discovered that mirabegron activates the beta-3 adrenergic receptor, a promising target for obesity treatment.
Research in the FASEB Journal found that cold temperatures can induce cells to change from white to brown fat, which may help treat type 2 diabetes. About 30% of cells that appear white before cold stress rapidly turn into brown adipocytes.
Researchers from McMaster University have identified a key hormone responsible for reduced brown fat activity in obese individuals, leading to increased risk of obesity and diabetes. Blocking the production of peripheral serotonin enhances brown fat activity, providing a potential new treatment approach.
Researchers have discovered that brown fat, which burns calories and absorbs excess sugar, could be used to control blood glucose levels in people with type 2 diabetes. The study found that activating brown fat cells could lead to a new way of managing the disease without daily insulin injections.
Researchers at the University of Michigan discovered a new hormone called NRG4 that serves as a messenger from fat cells to the liver, regulating sugar conversion into fat. Mice with elevated NRG4 levels were protected from metabolic disorders, suggesting its potential as a treatment for obesity and related diseases.
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A newly discovered signaling pathway in brown fat cells stimulates glucose uptake, potentially treating type 2 diabetes. The mTORC2 pathway, involving protein kinase mTOR, enhances GLUT1 transport to the surface of brown fat cells.
Scientists at the University of Bonn have discovered a new signaling pathway that utilizes adenosine to stimulate brown fat cells. This 'browning' process may help convert white fat cells into energy-burning brown cells, potentially aiding in weight loss and reducing the risk of chronic diseases.
A new study reveals that cold exposure can convert white fat tissue into calorie-burning beige fat, which can help prevent obesity. However, obese individuals exhibit a reduced ability to produce beneficial beige fat due to inflammation.
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A Yale study reveals the brain's control over transforming white fat into brown fat, which burns energy and aids in weight loss. The researchers found that neurons controlling hunger and appetite regulate this process, suggesting a novel approach to combating obesity.
Researchers at The Scripps Research Institute have identified a signaling pathway that activates the powerful calorie-burning process in brown fat cells. The study found that a protein called GADD45γ works alongside PGC-1α to boost thermogenesis, offering new possibilities for treating obesity and diabetes.
Researchers at Helmholtz Munich have developed a new approach to treat obesity and type 2 diabetes, targeting the brown adipose tissue. By identifying specific surface proteins, they aim to selectively deliver substances to this tissue to reduce excess weight without side effects.
Researchers found that people with higher levels of brown fat have better blood sugar control, higher insulin sensitivity, and improved metabolism. Brown fat's ability to regulate blood sugar makes it an important anti-diabetic tissue.
Researchers have found that cachexia, associated with cancer, is triggered by the conversion of white fat to brown fat tissue, a process also studied for obesity and diabetes. Blocking inflammation-promoting cytokine IL-6 can reduce cachexia symptoms.
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A new study by Beth Israel Deaconess Medical Center identifies IRF4 as a key regulator of brown fat's thermogenic process, driving energy expenditure and cold tolerance. The findings provide a crucial clue to understanding how brown fat burns energy and may lead to the development of novel therapies for obesity and diabetes.
Researchers found that long-term mild cold exposure increased brown fat amount and activity in humans, while mild warmth suppressed it. This discovery may lead to new avenues in treating impaired glucose metabolism and obesity.
A new study finds that ambient temperatures can influence brown fat growth or loss in humans. Brown fat burns energy to generate heat and improves insulin sensitivity when stimulated by cool environments.
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A new study by UC San Francisco researchers found that two signaling molecules secreted by immune cells trigger the conversion of white fat cells to beige fat cells, leading to weight loss. The discovery provides a potential new strategy for weight loss focused on the immune system rather than the brain.
Researchers discovered a new hormone called Metrnl that activates brown and beige fat, leading to improved metabolic health in obese mice. Interleukin-4 signaling also played a crucial role in stimulating beige fat formation.
Researchers have made a groundbreaking discovery using MRI scans to identify brown adipose tissue in adults, a major step towards developing new weight loss treatments. The study's findings could lead to the creation of safe and effective therapies that activate brown fat to promote energy expenditure.
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Research identifies cellular signaling dysfunction causing brown fat cells to lose blood vessels and mitochondria, leading to energy production failure and increased risk of metabolic disorders.
A new study suggests that shivering and bouts of moderate exercise can convert energy-storing 'white fat' into energy-burning 'brown fat'. This process could protect against diabetes, obesity, and fatty liver. The conversion is triggered by the hormones irisin and FGF21, which are stimulated by cold exposure and muscle activity.
Research found that shivering releases irisin, a hormone that stimulates calorie-burning brown fat and improves metabolism. This mechanism is similar to exercise-stimulated secretion of irisin, suggesting potential benefits for treating or preventing obesity.
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A study led by Boston University School of Medicine found that a lack of liver protein SIRT1 is associated with lower levels of FGF21, leading to fatty liver disease and obesity. Elevated FGF21 levels, however, transformed white fat cells into brown fat cells, producing heat and burning calories.
Joslin researchers have discovered that the hormone FGF21 stimulates the browning of white fat, leading to improved glucose metabolism and calorie burning. This finding has implications for the development of new medications for type 2 diabetes and obesity.
Researchers found that platelet-activating factor receptor (PAFR) deficiency leads to increased adiposity and weight gain in mice, causing brown fat dysfunction. This study suggests that regulating PAFR could lead to treatments for metabolic diseases.
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A recent study published in Stem Cells has identified brown fat stem cells in adult humans, which may lead to new treatments for heart and endocrine disorders. The discovery could help increase the body's own ability to make brown fat or find novel ways to directly implant the cells into patients.