Articles tagged with Adipocytes
Researchers at Duke University Medical Center have successfully reprogrammed human fat cells to become adult stem cells capable of forming bone, cartilage, and other cell types, providing a promising new approach for treating diseases such as osteoarthritis.
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.
Purdue University researchers discovered that fat cells in humans defend against biochemical processes involved in illnesses such as diabetes and cancer. The study found that fat cells produce hormone-like proteins called cytokines to regulate the immune response.
A study by Massachusetts General Hospital researchers found that blood vessel development is intricately linked with fat tissue formation. This interaction can be controlled to develop new treatments for cancer and obesity, as well as support the growth of new organs.
Scientists found certain fibroblasts can transform into myofibroblasts, leading to fibrosis, and lipofibroblasts, developing into fat cells that cause thyroid eye disease. This research may lead to new diagnostic tools and treatments for diseases like fibrosis and fatty tissue buildup.
Researchers found that 8 out of 20 commonly used NSAIDs can selectively lower Abeta42 levels in mice, with flurbiprofen showing the most promise. Additionally, studies revealed increased T cell reactivity to Abeta protein in older humans and patients with Alzheimer's disease, which could inform the design of future vaccines.
Researchers have identified a gene called Foxa-2 that is switched on only in the fat cells of obese mice. This gene acts as a brake to slow down further fat production and storage. In pre-adipocytes, Foxa-2 activates genes important for insulin sensitivity, providing an ideal combination for treating obesity and type 2 diabetes.
Researchers identify protein that bridges signaling and membrane movement, linking insulin's action to glucose uptake. This finding could provide clues for understanding type 2 diabetes, where muscle and fat tissues resist insulin.
Researchers found that RGS2-deficient mice developed strongly hypertensive conditions and persistent vessel constriction due to prolonged GPCR signaling. Genetic defects affecting RGS2 function may also contribute to hypertension in humans, according to findings published in the Journal of Clinical Investigation.
Cell division is necessary for fat cells to mature, according to a new study. The researchers found that primitive fat cells need to divide at least twice before they can store fat, and that interfering with this process could prevent the formation of new fat cells.
TZDs trigger a 'futile' cycle where glycerol kinase stores fatty acids faster than fat cells release them, leading to increased insulin sensitivity. Researchers also found that TZDs alter chemical signals produced by fat cells, potentially benefiting future anti-diabetes drug development.
Scientists have successfully implanted cartilage made from stem cells in mice, showing promise for repairing damaged tissues. The study uses fat cells to produce cartilage-like cells that can be used as implants to treat injuries and diseases.
Researchers used Sangamo's ZFP technology to repress a specific gene variant, preventing fat cells from developing. This breakthrough demonstrates the precision of ZFPs in regulating gene expression and may lead to new treatments for diseases related to fat cell development.
Researchers identify PPARgamma2 as critical player in fat cell differentiation process. The discovery provides a molecular target for rational drug design to combat obesity.
Researchers explore how hormones impact glucose production in fat cells, shedding light on metabolic health. Key findings reveal complex interactions between hormone receptors and glucose metabolism pathways.
A study by Michigan Medicine researchers found that high oxygen levels can be toxic to stem cells, converting muscle cells into fat cells. This discovery has important clinical implications for the treatment of obesity and diabetes, as it may be related to aging and oxidative stress conditions.
Researchers found that signals from fat cells can directly influence neurons outside of the brain, affecting the storage and burning of fat. The study suggests that nerve cells outside of the brain secrete a messenger called neuropeptide Y to prevent fat deposits from being burned for energy.
Duke researchers have identified caveolae, small pits on cell membranes, as a route of entry for various pathogens and toxins. This finding could lead to new avenues for treating infections and delivering drugs into cells.
The study demonstrates a fundamental role of caveolin-1 and caveolae in organizing multiple signalling pathways in the cell. The absence of caveolae impaired nitric oxide and calcium signaling, leading to severe physical limitations in caveolin-1-disrupted mice.
Researchers at Baylor College of Medicine have identified perilipin as a crucial protein that protects fat cells from breakdown. By eliminating this protein, mice lost weight despite consuming more food and gained increased muscle mass. The findings hold promise for developing new anti-perilipin drugs to combat obesity.
Researchers at the University of Michigan have identified a molecular switch, Wnt signaling, that inhibits fat cell development. By activating Wnt signaling, even muscle cells can turn into fat cells.
Scientists at National Jewish Health have identified a key protein that regulates fat cell development, which could lead to new strategies for treating obesity and related conditions. By inserting a negative version of CREB into fat cells, researchers can inhibit the growth of new fat cells.
Researchers at the University of Georgia have made a groundbreaking discovery that leptin causes the programmed death of fat cells. This finding could play a significant role in the development of new treatments for obesity, as rats injected with leptin stay thin even after treatment is stopped.