Document Detail


A physiological increase in the hepatic glycogen level does not affect the response of net hepatic glucose uptake to insulin.
MedLine Citation:
PMID:  19470836     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
To determine the effect of an acute increase in hepatic glycogen on net hepatic glucose uptake (NHGU) and disposition in response to insulin in vivo, studies were performed on two groups of dogs fasted 18 h. During the first 4 h of the study, somatostatin was infused peripherally, while insulin and glucagon were replaced intraportally in basal amounts. Hyperglycemia was brought about by glucose infusion, and either saline (n = 7) or fructose (n = 7; to stimulate NHGU and glycogen deposition) was infused intraportally. A 2-h control period then followed, during which the portal fructose and saline infusions were stopped, allowing NHGU and glycogen deposition in the fructose-infused animals to return to rates similar to those of the animals that received the saline infusion. This was followed by a 2-h experimental period, during which hyperglycemia was continued but insulin infusion was increased fourfold in both groups. During the initial 4-h glycogen loading period, NHGU averaged 1.18 +/- 0.27 and 5.55 +/- 0.53 mg x kg(-1) x min(-1) and glycogen synthesis averaged 0.72 +/- 0.24 and 3.98 +/- 0.57 mg x kg(-1) x min(-1) in the saline and fructose groups, respectively (P < 0.05). During the 2-h hyperinsulinemic period, NHGU rose from 1.5 +/- 0.4 and 0.9 +/- 0.2 to 3.1 +/- 0.6 and 2.5 +/- 0.5 mg x kg(-1) x min(-1) in the saline and fructose groups, respectively, a change of 1.6 mg x kg(-1) x min(-1) in both groups despite a significantly greater liver glycogen level in the fructose-infused group. Likewise, the metabolic fate of the extracted glucose (glycogen, lactate, or carbon dioxide) was not different between groups. These data indicate that an acute physiological increase in the hepatic glycogen content does not alter liver glucose uptake and storage under hyperglycemic/hyperinsulinemic conditions in the dog.
Authors:
Jason J Winnick; Zhibo An; Mary Courtney Moore; Christopher J Ramnanan; Ben Farmer; Masakazu Shiota; Alan D Cherrington
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2009-05-26
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  297     ISSN:  1522-1555     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2009 Aug 
Date Detail:
Created Date:  2009-07-23     Completed Date:  2009-08-18     Revised Date:  2010-09-24    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E358-66     Citation Subset:  IM    
Affiliation:
Department of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, Tennessee 37232-6015, USA. jason.winnick@vanderbilt.edu
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MeSH Terms
Descriptor/Qualifier:
Adipose Tissue / metabolism
Animals
Biological Transport, Active / drug effects
Blood Glucose / analysis,  metabolism
Dogs
Fructose / pharmacology
Glucagon / blood,  metabolism,  pharmacology
Glucose / metabolism*
Insulin / pharmacology*
Lactic Acid / metabolism
Lipid Metabolism / drug effects
Liver / metabolism*
Liver Glycogen / metabolism*,  physiology
Somatostatin / pharmacology
Up-Regulation / drug effects,  physiology
Grant Support
ID/Acronym/Agency:
5T32-DK-07563/DK/NIDDK NIH HHS; DK-20593/DK/NIDDK NIH HHS; F32-DK-080606/DK/NIDDK NIH HHS; R01-DK-43706/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/Liver Glycogen; 11061-68-0/Insulin; 30237-26-4/Fructose; 50-21-5/Lactic Acid; 50-99-7/Glucose; 51110-01-1/Somatostatin; 9007-92-5/Glucagon
Comments/Corrections

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


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