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Signal Transduction

STAT1 Dissociates Adipose Tissue Inflammation From Insulin Sensitivity in Obesity

  1. Aaron R. Cox1,2,
  2. Natasha Chernis1,2,
  3. David A. Bader3,
  4. Pradip K. Saha1,2,
  5. Peter M. Masschelin1,2,3,
  6. Jessica B. Felix1,2,3,
  7. Robert Sharp1,2,
  8. Zeqin Lian2,
  9. Vasanta Putluri4,
  10. Kimal Rajapakshe3,4,
  11. Kang Ho Kim3,
  12. Dennis T. Villareal1,2,5,
  13. Reina Armamento-Villareal1,2,5,
  14. Huaizhu Wu2,
  15. Cristian Coarfa3,4,
  16. Nagireddy Putluri3,4 and
  17. Sean M. Hartig1,2,3⇑
  1. 1Division of Endocrinology, Diabetes and Metabolism, Baylor College of Medicine, Houston, TX
  2. 2Department of Medicine, Baylor College of Medicine, Houston, TX
  3. 3Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX
  4. 4Dan L. Duncan Comprehensive Cancer Center, Advanced Technology Cores, Baylor College of Medicine, Houston, TX
  5. 5Center for Translational Research on Inflammatory Diseases, Michael E. DeBakey VA Medical Center, Houston, TX
  1. Corresponding author: Sean M. Hartig, hartig{at}bcm.edu
Diabetes 2020 Dec; 69(12): 2630-2641. https://doi.org/10.2337/db20-0384
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Abstract

Obesity fosters low-grade inflammation in white adipose tissue (WAT) that may contribute to the insulin resistance that characterizes type 2 diabetes. However, the causal relationship of these events remains unclear. The established dominance of STAT1 function in the immune response suggests an obligate link between inflammation and the comorbidities of obesity. To this end, we sought to determine how STAT1 activity in white adipocytes affects insulin sensitivity. STAT1 expression in WAT inversely correlated with fasting plasma glucose in both obese mice and humans. Metabolomic and gene expression profiling established STAT1 deletion in adipocytes (STAT1a-KO) enhanced mitochondrial function and accelerated tricarboxylic acid cycle flux coupled with reduced fat cell size in subcutaneous WAT depots. STAT1a-KO reduced WAT inflammation, but insulin resistance persisted in obese mice. Rather, elimination of type I cytokine interferon-γ activity enhanced insulin sensitivity in diet-induced obesity. Our findings reveal a permissive mechanism that bridges WAT inflammation to whole-body insulin sensitivity.

Footnotes

  • This article contains supplementary material online at https://doi.org/10.2337/figshare.12985514.

  • Received April 17, 2020.
  • Accepted September 16, 2020.
  • © 2020 by the American Diabetes Association
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December 2020, 69(12)
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STAT1 Dissociates Adipose Tissue Inflammation From Insulin Sensitivity in Obesity
Aaron R. Cox, Natasha Chernis, David A. Bader, Pradip K. Saha, Peter M. Masschelin, Jessica B. Felix, Robert Sharp, Zeqin Lian, Vasanta Putluri, Kimal Rajapakshe, Kang Ho Kim, Dennis T. Villareal, Reina Armamento-Villareal, Huaizhu Wu, Cristian Coarfa, Nagireddy Putluri, Sean M. Hartig
Diabetes Dec 2020, 69 (12) 2630-2641; DOI: 10.2337/db20-0384

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STAT1 Dissociates Adipose Tissue Inflammation From Insulin Sensitivity in Obesity
Aaron R. Cox, Natasha Chernis, David A. Bader, Pradip K. Saha, Peter M. Masschelin, Jessica B. Felix, Robert Sharp, Zeqin Lian, Vasanta Putluri, Kimal Rajapakshe, Kang Ho Kim, Dennis T. Villareal, Reina Armamento-Villareal, Huaizhu Wu, Cristian Coarfa, Nagireddy Putluri, Sean M. Hartig
Diabetes Dec 2020, 69 (12) 2630-2641; DOI: 10.2337/db20-0384
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