11β-Hydroxysteroid Dehydrogenase Type 1 in Obese Subjects With Type 2 Diabetes Mellitus

Am J Med Sci. 2017 Oct;354(4):408-414. doi: 10.1016/j.amjms.2017.03.023. Epub 2017 Mar 16.

Abstract

Obesity is one of the most significant contributors to the development of type 2 diabetes mellitus. Tissue-specific glucocorticoids regulated by 11β-hydroxysteroid dehydrogenase enzyme (11β-HSD) type 1 are involved in central obesity and obesity-related comorbidities. Moderate downregulation of 11β-HSD1 can attenuate insulin insensitivity and the impairment of glucose-stimulated insulin secretion. Some of the beneficial effects of 11β-HSD1 inhibition may be mediated, at least in part, through inactivation of tissue-specific glucocorticoid action related to insulin signaling mechanisms, alleviation of abnormal cytokine profile and the improvement of β-cell function. Thus, 11β-HSD1 is a promising target for the treatment and prevention of type 2 diabetes mellitus with obesity.

Keywords: 11β-Hydroxysteroid dehydrogenase type 1; Insulin resistance; Obesity; Type 2 diabetes mellitus.

Publication types

  • Review

MeSH terms

  • 11-beta-Hydroxysteroid Dehydrogenase Type 1 / antagonists & inhibitors
  • 11-beta-Hydroxysteroid Dehydrogenase Type 1 / metabolism*
  • Diabetes Mellitus, Type 2 / drug therapy
  • Diabetes Mellitus, Type 2 / enzymology*
  • Diabetes Mellitus, Type 2 / pathology
  • Enzyme Inhibitors / therapeutic use
  • Humans
  • Insulin / metabolism
  • Insulin Resistance*
  • Insulin Secretion
  • Insulin-Secreting Cells / enzymology*
  • Insulin-Secreting Cells / pathology
  • Obesity / drug therapy
  • Obesity / enzymology*
  • Obesity / pathology
  • Signal Transduction*

Substances

  • Enzyme Inhibitors
  • Insulin
  • 11-beta-Hydroxysteroid Dehydrogenase Type 1