Uncovering the pathogenesis of type 2 diabetes is the scourge of deestifyed free fatty acids!

A central question in diabetes research is why beta cells initially secrete too much insulinThe popular saying is that the body may not be aware of the presence of insulin at this time, so beta cells secrete more insulin to draw the body's "attention." But confusingly, even beta cells isolated in laboratory dishes over-secrete insulina new study published in the American journal Diabetes proposes a mechanism specifically for regulating insulin secretion (NGSIS) that regulates glucose stimulation on the islet, which is activated by deestitized free fatty acids ,the main fuel used by beta cells during fastinghttps://doi.org/10.2337/db19-0379In the course of the experiment, scientists studied the mechanism of the body's insulin secretion without glucose, using ordinary mice and prediabetes miceIt was found that in beta cells in prediabetes mice, mitochondrial permeable conversion hole-adjusting progenitor cyclophiline D (CypD) promoted insulin secretion without elevated glucoseCompared to lean mice, the islets of prediabetes obese mice showed significantly higher cypD-dependent proton leakage and NGSISIts mechanisms depend on fatty acids, which usually do not stimulate insulin secretion in healthy animals, obese mice lacking the CypD gene do not secrete too much insulinDuring the experiment, the researchers observed that NGSIS also occurred in isolated human pancreatic cells: when fatty acid levels reached typical levels in obese populations, the cells were able to secrete insulin without elevated glucose, this study reveals a selectively driven alternative free fatty acid stimulation pathway for islet NGSIS, and also provides us with new ways to prevent insulin resistance and treat diabetes, including by preventing beta cell proton leakagereferences:s1 s researchersdiscover process that may explain how type 2 diabetes develops2 smittenalProton Open Regulated by Cyclophilin D elevates InIslets at Non-Instagram