T reg-specific insulin receptor deletion prevents diet-induced and age-associated metabolic syndrome

J Exp Med. 2020 Aug 3;217(8):e20191542. doi: 10.1084/jem.20191542.

Abstract

Adipose tissue (AT) regulatory T cells (T regs) control inflammation and metabolism. Diet-induced obesity causes hyperinsulinemia and diminishes visceral AT (VAT) T reg number and function, but whether these two phenomena were mechanistically linked was unknown. Using a T reg-specific insulin receptor (Insr) deletion model, we found that diet-induced T reg dysfunction is driven by T reg-intrinsic insulin signaling. Compared with Foxp3cre mice, after 13 wk of high-fat diet, Foxp3creInsrfl/fl mice exhibited improved glucose tolerance and insulin sensitivity, effects associated with lower AT inflammation and increased numbers of ST2+ T regs in brown AT, but not VAT. Similarly, Foxp3creInsrfl/fl mice were protected from the metabolic effects of aging, but surprisingly had reduced VAT T regs and increased VAT inflammation compared with Foxp3cre mice. Thus, in both diet- and aging-associated hyperinsulinemia, excessive Insr signaling in T regs leads to undesirable metabolic outcomes. Ablation of Insr signaling in T regs represents a novel approach to mitigate the detrimental effects of hyperinsulinemia on immunoregulation of metabolic syndrome.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aging / genetics
  • Aging / immunology*
  • Aging / pathology
  • Animals
  • Diet, High-Fat / adverse effects*
  • Gene Deletion
  • Intra-Abdominal Fat / immunology*
  • Intra-Abdominal Fat / pathology
  • Metabolic Syndrome / chemically induced
  • Metabolic Syndrome / genetics
  • Metabolic Syndrome / immunology*
  • Metabolic Syndrome / pathology
  • Mice
  • Mice, Transgenic
  • Receptor, Insulin / deficiency*
  • Receptor, Insulin / immunology
  • T-Lymphocytes, Regulatory / immunology*
  • T-Lymphocytes, Regulatory / pathology

Substances

  • Receptor, Insulin

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