Alteration in pancreatic islet function in human immunodeficiency virus.

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.

• Authors: Steen B Haugaard
• Journal: Endocrinology and metabolism clinics of North America (Endocrinol Metab Clin North Am) Vol. 43 Issue 3 Pg. 697-708 (Sep 2014) ISSN: 1558-4410 [Electronic] United States
• PMID: 25169562 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
• Copyright: Copyright © 2014 Elsevier Inc. All rights reserved.

Chemical References

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

Topics

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