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Diabetes 51:1663-1671, 2002
© 2002 by the American Diabetes Association, Inc.

Direct and Indirect Effects of Insulin on Glucose Uptake and Storage by the Liver

Shosuke Satake, Mary Courtney Moore, Kayano Igawa, Margaret Converse, Benjamin Farmer, Doss W. Neal, and Alan D. Cherrington

From the Department of Molecular Physiology and Biophysics, and Diabetes Research and Training Center, Vanderbilt University School of Medicine, Nashville, Tennessee

Studies were conducted in conscious 42-h–fasted dogs to determine how much of insulin’s effect on hepatic glucose uptake arises from its direct hepatic action versus its indirect (extrahepatic) action. Each experiment consisted of equilibration, basal, and experimental periods. During the latter, somatostatin, basal intraportal glucagon, portal glucose (21.3 µmol · kg-1 · min-1), and peripheral glucose (to double the hepatic glucose load) were infused. During the experimental period, insulin was infused intraportally at a basal rate (BI, n = 6), at a fourfold basal rate (PoI, n = 6), or via a peripheral vein to create a selective increase in the arterial insulin level similar to that in PoI (PeI, n = 6). Arterial and hepatic sinusoidal insulin levels (in picomoles per liter) during the experimental period were 31 ± 5 and 113 ± 15 in BI, 97 ± 11 and 394 ± 66 in PoI, and 111 ± 13 and 96 ± 9 in PeI, respectively. Net hepatic glucose uptake (NHGU) averaged 7.0 ± 1.1 µmol · kg-1 · min-1, 15.7 ± 2.7 µmol · kg-1 · min-1 (P < 0.05 vs. BI), and 12.0 ± 2.4 µmol · kg-1 · min-1 (P < 0.05 vs. BI) in BI, PoI, and PeI, respectively. Net hepatic carbon retention was 4.4 ± 1.2 µmol glucose equivalents · kg-1 · min-1, 12.3 ± 2.5 µmol glucose equivalents · kg-1 · min-1 (P < 0.05 vs. BI, P < 0.05 vs. PeI), and 7.1 ± 1.0 µmol glucose equivalents · kg-1 · min-1 (P < 0.05 vs. BI) in BI, PoI, and PeI, respectively. Both direct and indirect insulin actions increase NHGU, but the rise in hepatic sinusoidal insulin appears critical for efficient storage of glucose as hepatic glycogen.


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