Open AccessAdipocyte STAT5 deficiency does not affect blood glucose homeostasis in obese mice
Author(s) -
Marianna Beghini,
T.L. Wagner,
Andreea Corina Luca,
Matthäus Metz,
Doris Kaltenecker,
Katrin Spirk,
Martina Häckl,
Johannes Haybaeck,
Richard Moriggl,
Alexandra KautzkyWiller,
Thomas Scherer,
Clemens Fürnsinn
Publication year - 2021
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0260501
Subject(s) - endocrinology , medicine , stat5 , adipocyte , lipid metabolism , carbohydrate metabolism , glucose homeostasis , insulin resistance , biology , calorie restriction , chemistry , adipose tissue , obesity , receptor
The aim of this study was to investigate whether the lack of signal transducer and activator of transcription 5 (STAT5) in mature adipocytes of obese mice ( Stat5 Adipoq mice) improves glucose and lipid metabolism as previously observed in lean mice. Male Stat5 Adipoq mice and their wild type (WT) littermates were fed high-fat diet (HFD). Effects of adipocyte STAT5 deficiency on adiposity as well as on glucose and lipid metabolism were determined under ad libitum feeding and after weight loss induced by calorie restriction. Compared to WT mice, obese Stat5 Adipoq mice showed modestly accelerated weight gain and blunted depletion of fat stores under calorie restriction (reduction in % body fat after 3 weeks: WT, -9.3±1.1, vs Stat5 Adipoq , -5.9±0.8, p = 0.04). No differences were observed between S tat5 Adipoq and WT mice with regard to parameters of glucose and lipid metabolism including basal glycaemia, glucose tolerance, and plasma triglycerides. In conclusion, STAT5 deficiency in the adipocyte of HFD-fed obese mice was associated with increased fat accumulation. In contrast to previous findings in lean mice, however, lipid accumulation was not associated with any improvement in glucose and lipid metabolism. Our results do not support adipocyte STAT5 as a promising target for the treatment of obesity-associated metabolic derangements.