LNK deficiency decreases obesity-induced insulin resistance by regulating GLUT4 through the PI3K-Akt-AS160 pathway in adipose tissue.

ABSTRACT: In recent years, LNK, an adapter protein, has been found to be associated with metabolic diseases, including hypertension and diabetes. We found that the expression of LNK in human adipose tissue was positively correlated with serum glucose and insulin in obese people. We examined the role of LNK in insulin resistance and systemic energy metabolism using LNK-deficient mice (LNK^-/-). With consumption of a high-fat diet, wild type (WT) mice accumulated more intrahepatic triglyceride, higher serum triglyceride (TG), free fatty acid (FFA) and high sensitivity C-reactive protein (hsCRP) compared with LNK^-/- mice. However, there was no significant difference between LNK^-/- and WT mice under normal chow diet. Meanwhile, glucose transporter 4 (

SUBMITTER: Zhong X 

PROVIDER: S-EPMC7521507 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature