Document Detail


Regulation of splanchnic and renal substrate supply by insulin in humans.
MedLine Citation:
PMID:  10831183     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
To determine the effects of peripheral insulin infusion on total, hepatic, and renal glucose production and on the percent contribution to glucose production of gluconeogenesis versus glycogenolysis, 10 healthy subjects had arterialized hand and hepatic vein catheterization after an overnight fast and the results were compared with data from 12 age- and weight-matched subjects with renal vein catheterization during a 180-minute infusion of either insulin (0.25 mU/kg x min) with dextrose, or saline. Endogenous, hepatic, and renal glucose production was measured with [6,6(-2)H2]glucose, regional lactate, alanine, and glycerol balance by arteriovenous difference; hepatic blood flow by indocyanine green clearance; and renal blood flow by p-aminohippurate clearance, before and every 30 minutes during each infusion period. Insulin increased from about 42 to 98 pmol/L and blood glucose remained constant in all studies (3.8 +/- 0.2 v4.4 +/- 0.1 micromol/ml, hepatic vrenal vein). In response to insulin infusion, endogenous, hepatic, and renal glucose production decreased immediately (30 minutes) and reached a lower plateau value (10.8 +/- 0.8 v6.4 +/- 0.7, 10.4 +/- 1.1 v7.8 +/- 1.0, and 2.8 +/- 0.6 v 1.5 +/- 0.6 micromol/kg x min, respectively) between 120 and 180 minutes (all P < .05). Net renal uptake of lactate (2.4 +/- 0.4 v0.9 +/- 0.6) decreased earlier (30 minutes) and returned to baseline between 120 and 180 minutes (2.4 +/- 0.5 micromol/kg x min), whereas net splanchnic uptake of lactate (5.7 +/- 0.7 v 0.7 +/- 0.6) and alanine (1.8 +/- 0.1 v 1.0 +/- 0.5 micromol/kg x min) decreased later (120 to 180 minutes). Net renal (0.3 +/- 0.1 v 0.1 +/- 0.1) and splanchnic (0.7 +/- 0.3 v 0.4 +/- 0.2 micromol/kg x min) glycerol uptake decreased 90 to 180 minutes after insulin and increased (P < .05) with saline infusion (0.4 +/- 0.1 v0.6 +/- 0.3 and 1.0 +/- 0.5 v1.8 +/- 0.4 micromol/kg x min, respectively). These data indicate that the rapid suppression of endogenous glucose production by insulin reflects primarily a decrease in hepatic glucose release, most likely due to inhibition of net glycogenolysis, combined with suppression of renal gluconeogenesis. Inhibition of hepatic gluconeogenesis presumably occurs later during hyperinsulinemia. We conclude that peripheral insulin, in addition to its inhibition of glycogen degradation, regulates endogenous glucose production, in part, by modifying the splanchnic and renal substrate supply.
Authors:
E Cersosimo; P Garlick; J Ferretti
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Metabolism: clinical and experimental     Volume:  49     ISSN:  0026-0495     ISO Abbreviation:  Metab. Clin. Exp.     Publication Date:  2000 May 
Date Detail:
Created Date:  2000-06-08     Completed Date:  2000-06-08     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0375267     Medline TA:  Metabolism     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  676-83     Citation Subset:  IM    
Affiliation:
Department of Medicine, State University of New York at Stony Brook, USA.
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MeSH Terms
Descriptor/Qualifier:
Adult
Alanine / metabolism
Female
Gluconeogenesis
Glucose / metabolism*
Glycerol / metabolism
Humans
Insulin / blood,  pharmacology*
Kidney / metabolism*
Lactic Acid / metabolism
Liver / metabolism*
Liver Glycogen / metabolism
Male
Middle Aged
Grant Support
ID/Acronym/Agency:
DK49861/DK/NIDDK NIH HHS; M01-RR10710/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Liver Glycogen; 11061-68-0/Insulin; 50-21-5/Lactic Acid; 50-99-7/Glucose; 56-41-7/Alanine; 56-81-5/Glycerol

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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