Diversion of the gastroduodenal vein: an in situ model of systemic insulin drainage

Miller, Alexander; Barr, Darlene; Marsh, Christopher L.; Kryshak, Edward J.; Butler, Peter C.; Rizza, Robert A.; Perkins, James D.

doi:10.1016/0168-8227(89)90100-9

Cited by 2 publications

(1 citation statement)

References 11 publications

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“…To study peripheral pancreatic venous delivery, the superior pancreaticoduodenal vein (SPDV) was mobilized and transected from the portal vein and anastomosed end to side to the inferior vena cava in eight dogs as previously described (28). Venous tributaries between the pancreas and duodenum or spleen were transected and/or ligated.…”

Section: Animals and Surgerymentioning

confidence: 99%

Pattern of Postprandial Carbohydrate Metabolism and Effects of Portal and Peripheral Insulin Delivery

et al. 1990

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The importance of portal insulin delivery in the regulation of postprandial carbohydrate metabolism is uncertain. To address this question, three groups of dogs were studied: one group in which pancreatic venous drainage was transected and reanastomosed (portal insulin delivery), one in which the pancreatic drainage was transected and anastomosed to the inferior vena cava (peripheral insulin delivery), and one that received only a sham operation. Plasma insulin was greater (P less than 0.05) during peripheral insulin delivery than in either the portal or sham groups, respectively, before and after meal ingestion. On the other hand, C-peptide concentrations did not differ between groups, resulting in a higher (P less than 0.001) insulin to C-peptide ratio in the peripheral group. This indicated that the hyperinsulinemia in the peripheral group was due to decreased insulin clearance rather than increased insulin secretion. Isotopically determined splanchnic uptake of ingested glucose, postprandial suppression of hepatic glucose release, incorporation of CO2 into glucose (a qualitative measure of gluconeogenesis), and total-body glucose uptake were virtually identical in all groups. Similarly, plasma lipid, beta-hydroxybutyrate, and lactate concentrations did not differ between groups. Our data indicate that, despite differences in systemic insulin concentration, portal and peripheral insulin delivery comparably regulate hepatic and extrahepatic carbohydrate metabolism after meal ingestion.

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Section: Animals and Surgerymentioning

confidence: 99%

Pattern of Postprandial Carbohydrate Metabolism and Effects of Portal and Peripheral Insulin Delivery

et al. 1990

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Mechanisms of insulin resistance in experimental hyperinsulinemic dogs.

Miles

Hart

et al. 1998

J. Clin. Invest.

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This study was undertaken to characterize the insulin resistance and the mechanism thereof caused by chronic hyperinsulinemia produced in dogs by surgically diverting the veins of the pancreas from the portal vein to the vena cava. Pancreatic venous diversion (PVD, n = 8) caused a sustained increase in arterial insulin and decrease in portal insulin concentration compared with the control group (n = 6). Hyperinsulinemic euglycemic clamps were conducted 4 wk after surgery. The increase in the glucose disposal rate (GDR) was significantly less in the PVD group (39.0+/-5.0 vs. 27.9+/-3.2 micromol/kg/min, P < 0.01) compared with the control group, but the suppression of hepatic glucose production by insulin was similar for both groups. Muscle insulin receptor tyrosine kinase activity (IR-TKA) increased from 6.2+/-0.4 to 20.3+/-2.7 in the control group, but from 5.8+/-0.5 to only 12.7+/-1.7 fmol P/fmol IR in the PVD group (P < 0.01). With respect to the periphery, the time to half-maximum response (t1/2a) for arterial insulin was the same for both groups, whereas the t1/2a for lymph insulin (30+/-3 vs. 40+/-4 min, P < 0.05) and GDR (29+/-3 vs. 66+/-10 min, P < 0.01) were greater for the PVD group. Chronic hyperinsulinemia led to marked peripheral insulin resistance characterized by decreased insulin-stimulated GDR, and impaired activation of GDR kinetics due, in part, to reduced IR-TKA. Transendothelial insulin transport was impeded and was responsible for one third of the kinetic defect in insulin-resistant animals, while slower intracellular mechanisms of GDR were responsible for the remaining two thirds.

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Diversion of the gastroduodenal vein: an in situ model of systemic insulin drainage

Cited by 2 publications

References 11 publications

Pattern of Postprandial Carbohydrate Metabolism and Effects of Portal and Peripheral Insulin Delivery

Pattern of Postprandial Carbohydrate Metabolism and Effects of Portal and Peripheral Insulin Delivery

Mechanisms of insulin resistance in experimental hyperinsulinemic dogs.

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