A CD36-dependent pathway enhances macrophage and adipose tissue inflammation and impairs insulin signalling.

ABSTRACT:

Aims

Obesity and hyperlipidaemia are associated with insulin resistance (IR); however, the mechanisms responsible remain incompletely understood. Pro-atherogenic hyperlipidaemic states are characterized by inflammation, oxidant stress, and pathophysiologic oxidized lipids, including ligands for the scavenger receptor CD36. Here we tested the hypothesis that the absence of CD36 protects mice from IR associated with diet-induced obesity and hyperlipidaemia.

Methods and results

Adipose tissue from CD36(-/-) mice demonstrated a less inflammatory phenotype and improved insulin signalling in vivo and at the level of the adipocyte and macrophage. The pathophysiologic ligand oxidized low-density lipoprotein (oxLDL) activated c-Jun N-terminal kinase (JNK) and disrupted insulin signal

SUBMITTER: Kennedy DJ 

PROVIDER: S-EPMC3028977 | biostudies-literature | 2011 Feb

REPOSITORIES: biostudies-literature