| Effects of insulin-like growth factor (IGF)-I/IGF-binding protein-3 treatment on glucose metabolism and fat distribution in human immunodeficiency virus-infected patients with abdominal obesity and insulin resistance. | |
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MedLine Citation:
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PMID: 20610601 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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CONTEXT: HIV-infected patients on antiretroviral therapy are at increased risk for excess visceral adiposity and insulin resistance. Treatment with GH decreases visceral adiposity but worsens glucose metabolism. IGF-I, which mediates many of the effects of GH, improves insulin sensitivity in HIV-negative individuals. OBJECTIVE: Our objective was to determine whether IGF-I, complexed to its major binding protein, IGF-binding protein-3 (IGFBP-3), improves glucose metabolism and alters body fat distribution in HIV-infected patients with abdominal obesity and insulin resistance. METHODS: We conducted a pilot, open-label study in 13 HIV-infected men with excess abdominal adiposity and insulin resistance to assess the effect of 3 months of treatment with IGF-I/IGFBP-3 on glucose metabolism and fat distribution. Glucose metabolism was assessed by oral glucose tolerance test and hyperinsulinemic-euglycemic clamp. Endogenous glucose production (EGP), gluconeogenesis, whole-body lipolysis, and de novo lipogenesis (DNL) were measured with stable isotope infusions. Body composition was assessed by dual-energy x-ray absorptiometry and abdominal computed tomography scan. RESULTS: Glucose tolerance improved and insulin-mediated glucose uptake increased significantly during treatment. EGP increased under fasting conditions, and suppression of EGP by insulin was blunted. Fasting triglycerides decreased significantly in association with a decrease in hepatic DNL. Lean body mass increased and total body fat decreased, whereas visceral adipose tissue did not change. CONCLUSIONS: Treatment with IGF-I/IGFBP-3 improved whole-body glucose uptake and glucose tolerance, while increasing hepatic glucose production. Fasting triglycerides improved, reflecting decreased DNL, and visceral adiposity was unchanged. |
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Authors:
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Madhu N Rao; Kathleen Mulligan; Viva Tai; Michael J Wen; Artem Dyachenko; Melissa Weinberg; Xiaojuan Li; Thomas Lang; Carl Grunfeld; Jean-Marc Schwarz; Morris Schambelan |
Publication Detail:
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Type: Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2010-07-07 |
Journal Detail:
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Title: The Journal of clinical endocrinology and metabolism Volume: 95 ISSN: 1945-7197 ISO Abbreviation: J. Clin. Endocrinol. Metab. Publication Date: 2010 Sep |
Date Detail:
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Created Date: 2010-09-08 Completed Date: 2010-09-28 Revised Date: 2011-09-13 |
Medline Journal Info:
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Nlm Unique ID: 0375362 Medline TA: J Clin Endocrinol Metab Country: United States |
Other Details:
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Languages: eng Pagination: 4361-6 Citation Subset: AIM; IM |
Affiliation:
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Department of Medicine, University of California, San Francisco, San Francisco, California 94143, USA. madhu.rao@ucsf.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adipose Tissue
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drug effects,
metabolism Body Composition / drug effects Body Fat Distribution* Drug Combinations Glucose / metabolism* HIV Infections / blood, complications, drug therapy*, metabolism HIV-1 / physiology HIV-Associated Lipodystrophy Syndrome / blood, drug therapy, metabolism Humans Insulin Resistance* Insulin-Like Growth Factor Binding Protein 3 / administration & dosage*, adverse effects, pharmacology Insulin-Like Growth Factor I / administration & dosage*, adverse effects, pharmacology Lipid Metabolism / drug effects Male Middle Aged Obesity, Abdominal / blood, drug therapy*, etiology, metabolism Pilot Projects |
| Grant Support | |
ID/Acronym/Agency:
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DK54615/DK/NIDDK NIH HHS; DK66999/DK/NIDDK NIH HHS; DK69185/DK/NIDDK NIH HHS; RR00083/RR/NCRR NIH HHS; RR24131/RR/NCRR NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Drug Combinations; 0/Insulin-Like Growth Factor Binding Protein 3; 50-99-7/Glucose; 67763-96-6/Insulin-Like Growth Factor I |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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