All articles tagged with #adipocytes
Researchers found that hormone-sensitive lipase, long viewed solely as a fat-mobilizing enzyme, also enters the nucleus of fat cells to regulate adipose tissue health. This nuclear role helps explain why HSL deficiency leads to lipodystrophy and how fat-tissue dysfunction links obesity with metabolic disease, potentially opening new paths to treat obesity by targeting fat-cell health rather than weight alone.
Scientists have discovered a new role for the enzyme HSL inside fat cells, where it not only breaks down fat but also helps maintain healthy adipose tissue by functioning in the nucleus, challenging long-held beliefs about fat metabolism and providing insights into metabolic diseases like obesity and lipodystrophy.
Scientists have discovered a new role for hormone-sensitive lipase (HSL) in the nucleus of fat cells, where it helps maintain healthy adipose tissue, explaining the paradox of fat loss in HSL deficiency and opening new avenues for understanding metabolic diseases like obesity and lipodystrophy.
Obesity leads to mitochondrial dysfunction in white adipocytes due to increased RalA activity, contributing to metabolic abnormalities. Deletion of RalA in white adipocytes attenuates high-fat-diet-induced obesity, increases energy expenditure, and improves glucose homeostasis in mice. RalA deletion also reduces hepatic steatosis and damage, while increasing mitochondrial oxidative phosphorylation in white adipose tissue.
A non-coding genetic variant linked to metabolic obesity with normal weight has been found to affect actin remodelling in subcutaneous adipocytes. The study sheds light on the genetic basis of metabolic obesity and its link to metabolic syndrome and type 2 diabetes.