Association Between Cortisol, Insulin Resistance and Zinc in Obesity: a Mini-Review

Biol Trace Elem Res. 2019 Oct;191(2):323-330. doi: 10.1007/s12011-018-1629-y. Epub 2019 Jan 7.

Abstract

Adipose tissue is considered an endocrine organ and its excess compromises the immune response and the metabolism of hormones and nutrients. Furthermore, visceral fat accumulation contributes to increased cortisol synthesis, which in turn induces metallothionein and Zip14 expression, which are proteins that contribute to reducing plasma zinc levels. Zinc plays a critical role in the secretion and signaling of insulin. Changes in the biochemical parameters of zinc, as observed in individuals who are obese, contribute to the manifestation of related disorders such as insulin resistance. Thus, the purpose of this review is to provide an update on the current information on the relationship between cortisol, zinc, and insulin resistance in obesity. The data in the literature provide evidence that cortisol affects zinc metabolism, and indicate possible repercussions on insulin signaling that might contribute to the development of resistance to the actions of insulin in obesity.

Keywords: Cortisol; Insulin resistance; Metabolism; Obesity; Zinc.

Publication types

  • Review

MeSH terms

  • Humans
  • Hydrocortisone / blood*
  • Insulin Resistance / physiology*
  • Obesity / blood*
  • Signal Transduction / physiology
  • Zinc / blood*

Substances

  • Zinc
  • Hydrocortisone