Loss of myeloid lipoprotein lipase exacerbates adipose tissue fibrosis with collagen VI deposition and hyperlipidemia in leptin-deficient obese mice.

ABSTRACT: During obesity, tissue macrophages increase in number and become proinflammatory, thereby contributing to metabolic dysfunction. Lipoprotein lipase (LPL), which hydrolyzes triglyceride in lipoproteins, is secreted by macrophages. However, the role of macrophage-derived LPL in adipose tissue remodeling and lipoprotein metabolism is largely unknown. To clarify these issues, we crossed leptin-deficient Lep^ob/ob mice with mice lacking the Lpl gene in myeloid cells (Lpl^m-/m-) to generate Lpl^m-/m-;Lep^ob/ob mice. We found the weight of perigonadal white adipose tissue (WAT) was increased in Lpl^m-/m-;Lep^ob/ob mice compared with Lep^ob/ob mice due to substantial accumulation of both adipose tissue macrophages and collagen t

SUBMITTER: Takahashi M 

PROVIDER: S-EPMC9440390 | biostudies-literature | 2022 Sep

REPOSITORIES: biostudies-literature