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This Article Full Text Full Text (PDF) All Versions of this Article: 297/2/E358    most recent 00043.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Winnick, J. J. Articles by Cherrington, A. D. Search for Related Content PubMed PubMed Citation Articles by Winnick, J. J. Articles by Cherrington, A. D.

A physiological increase in the hepatic glycogen level does not affect the response of net hepatic glucose uptake to insulin

Department of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, Tennessee

Submitted 21 January 2009 ; accepted in final form 18 May 2009

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·kg^–1·min^–1 and glycogen synthesis averaged 0.72 ± 0.24 and 3.98 ± 0.57 mg·kg^–1·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·kg^–1·min^–1 in the saline and fructose groups, respectively, a change of 1.6 mg·kg^–1·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.

liver glycogen; hyperglycemia; hyperinsulinemia; hepatic insulin signaling