Adrenocortical dysregulation as a major player in insulin resistance and onset of obesity

  • Roberge C
  • Carpentier A
  • Langlois M
 et al. 
  • 43

    Readers

    Mendeley users who have this article in their library.
  • 66

    Citations

    Citations of this article.

Abstract

The aim of this review is to explore the dysregulation of adrenocortical secretions as a major contributor in the development of obesity and insulin resistance. Disturbance of adipose tissue physiology is one of the primary events in the development of pathologies associated with the metabolic syndrome, such as obesity and type 2 diabetes. Several studies indicate that alterations in metabolism of glucocorticoids (GC) and androgens, as well as aldosterone in excess, are involved in the emergence of metabolic syndrome. Cross talk among adipose tissue, the hypothalamo-pituitary complex, and adrenal gland activity plays a major role in the control of food intake, glucose metabolism, lipid storage, and energy balance. Perturbation of this cross talk induces alterations in the regulatory mechanisms of adrenocortical steroid synthesis, secretion, degradation, and/or recycling, at the level of the zonae glomerulosa (aldosterone), fasciculata (GC and GC metabolites), and reticularis (androgens and androgen precursors DHEA and DHEAS). As a whole, these adrenocortical perturbations contribute to the development of metabolic syndrome at both the paracrine and systemic level by favoring the physiological dysregulation of organs responsive to aldosterone, GC, and/or androgens, including adipose tissue.

Get free article suggestions today

Mendeley saves you time finding and organizing research

Sign up here
Already have an account ?Sign in

Find this document

Authors

  • C. Roberge

  • A. C. Carpentier

  • M.-F. Langlois

  • J.-P. Baillargeon

  • J.-L. Ardilouze

  • P. Maheux

Cite this document

Choose a citation style from the tabs below

Save time finding and organizing research with Mendeley

Sign up for free