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Am J Physiol Gastrointest Liver Physiol 281: G29-G36, 2001;
0193-1857/01 $5.00
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Vol. 281, Issue 1, G29-G36, July 2001

Hepatic parasympathetic (HISS) control of insulin sensitivity determined by feeding and fasting

W. W. Lautt1, M. P. Macedo2, P. Sadri1, S. Takayama3, F. Duarte Ramos2, and D. J. Legare1

1 Faculty of Medicine, Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Manitoba, Canada R3E OW3; 2 Institute of Health Sciences, Quinta da Granja-Trav. da Granja, Monte da Caparica 2825, Portugal; and 3 Diabetes Center, Tokyo Women's Medical College, 162-8666 Tokyo, Japan

In response to insulin, a hormone [hepatic insulin sensitizing substance (HISS)] is released from the liver to stimulate glucose uptake in skeletal muscle but not liver or gut. The aim was to characterize dynamic control of HISS action in response to insulin and regulation of release by hepatic parasympathetic nerves. Insulin action was assessed by the rapid insulin sensitivity test, where the index is the glucose required (mg/kg) to maintain euglycemia after a bolus of insulin. Blocking HISS release by interruption of the hepatic parasympathetic nerves by surgical denervation, atropine, or blockade of hepatic nitric oxide synthase produced similar degrees of insulin resistance and revealed a similar dynamic pattern of hormone action that began 3-4 min after, and continued for 9-10 min beyond, insulin action (50 mU/kg). HISS action accounted for 56.5 ± 3.5% of insulin action at insulin doses from 5 to 100 mU/kg (fed). We also tested the hypothesis that HISS release is controlled by the feed/fast status. Feeding resulted in maximal HISS action, which decreased progressively with the duration of fasting.

insulin resistance; hepatic insulin sensitizing substance; pharmacodynamics; nerves; postprandial


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