Non-hematopoietic IL-4Rα expression contributes to fructose-driven obesity and metabolic sequelae.

ABSTRACT:

Objective

The risks of excess sugar intake in addition to high-fat diet consumption on immunopathogenesis of obesity-associated metabolic diseases are poorly defined. Interleukin-4 (IL-4) and IL-13 signaling via IL-4Rα regulates adipose tissue lipolysis, insulin sensitivity, and liver fibrosis in obesity. However, the contribution of IL-4Rα to sugar rich diet-driven obesity and metabolic sequelae remains unknown.

Methods

WT, IL-4Rα-deficient (IL-4Rα^-/-) and STAT6-deficient mice (STAT6^-/-) male mice were fed low-fat chow, high fat (HF) or HF plus high carbohydrate (HC/fructose) diet (HF + HC). Analysis included quantification of: (i) body weight, adiposity, energy expenditure, fructose metabolism, fatty acid oxidation/synthesis, glucose dysmetabolism and

SUBMITTER: Damen MSMA 

PROVIDER: S-EPMC8528699 | biostudies-literature | 2021 Nov

REPOSITORIES: biostudies-literature