Adipocyte-specific Nos2 deletion improves insulin resistance and dyslipidemia through brown fat activation in diet-induced obese mice.

ABSTRACT:

Objective

Inducible nitric oxide (NO) synthase (NOS2) is a well-documented inflammatory mediator of insulin resistance in obesity. NOS2 expression is induced in both adipocytes and macrophages within adipose tissue during high-fat (HF)-induced obesity.

Methods

Eight-week-old male mice with adipocyte selective deletion of the Nos2 gene (Nos2^AD-KO) and their wildtype littermates (Nos2^fl/fl) were subjected to chow or high-fat high-sucrose (HFHS) diet for 10 weeks followed by metabolic phenotyping and determination of brown adipose tissue (BAT) thermogenesis. The direct impact of NO on BAT mitochondrial respiration was also assessed in brown adipocytes.

Results

HFHS-fed Nos2^AD-KO mice had improved insulin sensitivity as compared to Nos2

SUBMITTER: Vilela VR 

PROVIDER: S-EPMC8802131 | biostudies-literature | 2022 Mar

REPOSITORIES: biostudies-literature