Alteration in pancreatic islet function in human immunodeficiency virus

Endocrinol Metab Clin North Am. 2014 Sep;43(3):697-708. doi: 10.1016/j.ecl.2014.06.004.

Abstract

Molecular mechanisms behind the defects in insulin production and secretion associated with antihuman immunodeficiency virus (anti-HIV) therapy and the development of HIV-associated lipodystrophy syndrome (HALS) are discussed in this article. Data suggesting insulin resistance on the beta cell and defects in first-phase insulin release of HALS patients are presented. Hepatic extraction of insulin, nonglucose insulin secretagogues and insulin-like growth factor release may exert influence on the demand of circulating insulin and on insulin secretion in HIV-infected patients. Finally, the paucity in understanding the incretin effects in HIV and HIV therapy in relation to insulin secretion is highlighted.

Keywords: Antiretroviral therapy; Incretins; Insulin secretion; Insulin-like growth factors; Lipodystrophy; Nonglucose insulin secretagogues; Prehepatic; Proinsulin.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Carbamates / adverse effects
  • Carbamates / therapeutic use
  • Furans
  • HIV Protease Inhibitors / adverse effects*
  • HIV Protease Inhibitors / therapeutic use
  • HIV-Associated Lipodystrophy Syndrome / chemically induced*
  • Humans
  • Indinavir / adverse effects
  • Indinavir / therapeutic use
  • Insulin / metabolism*
  • Insulin Resistance*
  • Insulin Secretion
  • Insulin-Secreting Cells / drug effects
  • Insulin-Secreting Cells / metabolism*
  • Nelfinavir / adverse effects
  • Nelfinavir / therapeutic use
  • Ritonavir / adverse effects
  • Ritonavir / therapeutic use
  • Sulfonamides / adverse effects
  • Sulfonamides / therapeutic use

Substances

  • Carbamates
  • Furans
  • HIV Protease Inhibitors
  • Insulin
  • Sulfonamides
  • amprenavir
  • Indinavir
  • Nelfinavir
  • Ritonavir