Summary ― Insulin and glucagon levels, the mass of glucose presented to the liver and the portal signal are important regulators of the liver's response to glucose delivery. The portal signal not only serves to direct glucose into the liver but also appears to stimulate its deposition in glycogen. Moreover, the portal signal impacts on tissues other than the liver: intraportal glucose delivery is associated with changes in glucose uptake by nonhepatic tissues and neurally-mediated enhancement of pancreatic insulin secretion. Our current understanding of the neural control of hepatic glucose metabolism includes a tonic block to the entry of glucose into the liver, probably mediated both by sympathetic neural activity and by a low insulin:glucagon ratio. An increase in the portal vein glucose level is detected by sensors in the portal region, which cause a decrease in the firing rate in the afferent fibers in the hepatic branch of the vagus nerve. The change in the afferent firing rate is processed in the hypothalamus and instigates a change in the efferent firing rate in the hepatic and pancreatic branches of the vagus (with corresponding increases in insulin secretion and net hepatic glucose uptake). The
The present study was undertaken to examine the influence of hyperglycemia in retarding the rise in circulating FFA noted after acute insulin withdrawal in man. The arterial FFA response to somatostatin administration was measured in the presence of (a) euglycemia and (b) hyperglycemia. In seven normal men who received somatostatin (0.9 mg/h) with euglycemia maintained by exogenous glucose infusion plasma insulin levels fell to levels 4 uU/ml and plasma FFA concentrations rose from 659 +/- 123 to 2057 +/- 268 uEq/l. When somatostatin was infused with hyperglycemia maintained at approximately 230 mg/dl, plasma insulin levels were again maintained at levels 4 uU/ml. Despite similar insulinopenia plasma FFA concentrations rose from 510 +/- 56 to only 1125 +/- 180 uEq/l, significantly less than in the previous protocol (p less than 0.01). These data indicate that hyperglycemia per se significantly attenuates the rise in circulating FFA caused by acute insulin withdrawal in man.
Immunosuppressive therapy is responsible for most of the alterations in postprandial carbohydrate metabolism observed in this model; the lack of hepatic nerves has little additional impact.
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