Document Detail

Hyperinsulinemia inhibits myocardial protein degradation in patients with cardiovascular disease and insulin resistance.
MedLine Citation:
PMID:  7554195     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Insulin resistance, hyperinsulinemia, and myocardial hypertrophy frequently coexist in patients. Whether hyperinsulinemia directly affects myocardial protein metabolism in humans has not been examined, however. To test the hypothesis that hyperinsulinemia is anabolic for human heart protein, we examined the effects of insulin infusion on myocardial protein synthesis, degradation, and net balance in patients with ischemic heart disease. METHODS AND RESULTS: Eleven men (aged 57 +/- 3 years) with coronary artery disease who had fasted for 12 to 16 hours received a constant infusion of insulin (50 mU.m-2.min-1) while plasma concentrations of glucose and amino acids were kept constant. Rates of myocardial protein synthesis, degradation, and net balance were estimated from steady state extraction and isotopic dilution of L-[ring-2,6-3H]phenylalanine across the heart basally and 90 minutes into infusion. Subjects had elevated fasting plasma insulin concentrations (173 +/- 21 pmol/L) and used little exogenous glucose during insulin infusion, suggesting resistance to the effects of insulin on whole-body carbohydrate metabolism. Basally, myocardial protein degradation, as estimated by phenylalanine release (133 +/- 28 nmol/min), exceeded protein synthesis, estimated by phenylalanine uptake (31 +/- 15 nmol/min), resulting in net negative phenylalanine balance (-102 +/- 17 nmol/min). Insulin infusion reduced myocardial protein degradation by 80% but did not affect protein synthesis, returning net phenylalanine balance to neutral. CONCLUSIONS: Acute hyperinsulinemia markedly suppresses myocardial protein degradation in patients with cardiovascular disease who are resistant to its effects on whole-body glucose metabolism. This antiproteolytic action represents a potential mechanism by which hyperinsulinemia could contribute to the development of myocardial hypertrophy in patients with cardiovascular disease.
P H McNulty; R J Louard; L I Deckelbaum; B L Zaret; L H Young
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  Circulation     Volume:  92     ISSN:  0009-7322     ISO Abbreviation:  Circulation     Publication Date:  1995 Oct 
Date Detail:
Created Date:  1995-11-14     Completed Date:  1995-11-14     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  2151-6     Citation Subset:  AIM; IM    
Department of Internal Medicine, Veterans Affairs Medical Center, West Haven, Conn 06516, USA.
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MeSH Terms
Amino Acids / metabolism
Blood Glucose / metabolism
Coronary Disease / metabolism*
Fatty Acids, Nonesterified / metabolism
Glucose / metabolism
Hyperinsulinism / metabolism*
Insulin / administration & dosage,  blood*
Insulin Resistance*
Middle Aged
Muscle Proteins / metabolism*
Myocardium / metabolism*
Phenylalanine / metabolism*
Reg. No./Substance:
0/Amino Acids; 0/Blood Glucose; 0/Fatty Acids, Nonesterified; 0/Muscle Proteins; 11061-68-0/Insulin; 50-99-7/Glucose; 63-91-2/Phenylalanine

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