محققین مسیر جدیدی برای کنترل شکل گیری چربی تشخیص دادند

☑️ محققین مسیر جدیدی برای کنترل شکل گیری چربی تشخیص دادند

محققین نشان دادند که افزایش بیان miR-26 از افزایش وزن موش با رژیم غذایی پرچربی جلوگیری می کند. miR-26 از بیان پروتئین FBXL19 که در تشکیل سلول های چربی نقش دارد جلوگیری می کند.

محققین با حذف خانواده ژنی این miRNAs با تکنیک کریسپر نشان دادند که وزن این موش ها با رژیم غذایی معمولی دو تا سه برابر بافت چربی آن ها افزایش پیدا می کند.

miR-26 suppresses adipocyte progenitor differentiation and fat production by targeting Fbxl19

Abstract

Fat storage in adult mammals is a highly regulated process that involves the mobilization of adipocyte progenitor cells (APCs) that differentiate to produce new adipocytes. Here we report a role for the broadly conserved miR-26 family of microRNAs (miR-26a-1, miR-26a-2, and miR-26b) as major regulators of APC differentiation and adipose tissue mass. Deletion of all miR-26-encoding loci in mice resulted in a dramatic expansion of adipose tissue in adult animals fed normal chow. Conversely, transgenic overexpression of miR-26a protected mice from high-fat diet-induced obesity. These effects were attributable to a cell-autonomous function of miR-26 as a potent inhibitor of APC differentiation. miR-26 blocks adipogenesis, at least in part, by repressing expression of Fbxl19, a conserved miR-26 target without a previously known role in adipocyte biology that encodes a component of SCF-type E3 ubiquitin ligase complexes. These findings have therefore revealed a novel pathway that plays a critical role in regulating adipose tissue formation in vivo and suggest new potential therapeutic targets for obesity and related disorders.