Adipocyte STAT5 deficiency does not affect blood glucose homeostasis in obese mice

PLoS One. 2021 Nov 24;16(11):e0260501. doi: 10.1371/journal.pone.0260501. eCollection 2021.


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 (Stat5Adipoq mice) improves glucose and lipid metabolism as previously observed in lean mice. Male Stat5Adipoq 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 Stat5Adipoq 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 Stat5Adipoq, -5.9±0.8, p = 0.04). No differences were observed between Stat5Adipoq 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipocytes / metabolism*
  • Adiposity
  • Animals
  • Blood Glucose / genetics
  • Blood Glucose / metabolism*
  • Gene Deletion
  • Lipid Metabolism
  • Male
  • Mice, Inbred C57BL
  • Mice, Obese
  • Obesity / genetics*
  • Obesity / metabolism
  • STAT5 Transcription Factor / genetics*
  • STAT5 Transcription Factor / metabolism


  • Blood Glucose
  • STAT5 Transcription Factor
  • Stat5a protein, mouse
  • Stat5b protein, mouse

Grants and funding

RM, KS and DK were supported by the by the Austrian Science Fund (FWF) under grant SFB-F6105; ACL and CF were supported by the by the Austrian Science Fund (FWF) under grant P30830-B28. The sponsors or funders had no role in the study design, data collection and analysis, decision to publish, or prepration of the manuscript.