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This Article Full Text Full Text (PDF) All Versions of this Article: 286/6/E932    most recent 00511.2002v1 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 ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Ogihara, N. Articles by Kikuchi, M. Search for Related Content PubMed PubMed Citation Articles by Ogihara, N. Articles by Kikuchi, M.

Characterization of the portal signal during 24-h glucose delivery in unrestrained, conscious rats

¹Department of Endocrinology and Metabolism, Institute for Adult Diseases, Asahi Life Foundation, 160-0023 Tokyo; and ²Third Department of Internal Medicine, Nihon University, 173-8610 Tokyo, Japan

Submitted 21 November 2002 ; accepted in final form 2 January 2004

To characterize the "portal signal" during physiological glucose delivery, liver glycogen was measured in unrestrained rats during portal (Po) and peripheral (Pe) constant-rate infusion, with minimal differences in hepatic glucose load (HGL) and portal insulin between the delivery routes. Hepatic blood flows were measured by Doppler flowmetry during open surgery. Changes in hepatic glucose, portal insulin, glucagon, lactate, and free fatty acid concentrations were generally similar in either delivery except for glucagon at 4 h. Hepatic glycogen, however, increased continuously in Po and was higher than Pe at 8 and 24 h, although it decreased to the level of Pe upon the removal of Po at 8 h. There was a near-linear relationship between hepatic glycogen and HGL in either delivery, with the slope being twice as high in Po and the intercepts converging to basal HGL. The hepatic response to Po did not alter upon 80% replacement by Pe. These results suggest that negative arterial-portal glucose gradients increase the rate of hepatic glycogen synthesis against the incremental HGL in an all-or-nothing mode.

hepatic glycogen synthesis; hepatic glucose load; negative arterial-portal glucose gradients; nonsteady state

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