Regulation of net hepatic glucose uptake in vivo.

Abstract

Increases in the glucose level in the absence of the portal signal or changes in insulin elicits little if any glucose uptake by the liver. NHGU is augmented by a rise in insulin (or drop in glucagon) and is further stimulated by the presence of a portal signal. Under postprandial conditions, NHGU will depend on the dynamic interaction between the pancreatic hormones, glucose and the portal signal. Moreover, in a simulated postprandial environment, the quantitative impact of the portal signal is at least as important as that of insulin. The presence of the portal signal should be of physiologic benefit because it will allow adequate net removal of glucose by the liver without requiring excessive excursions of insulin and glucose. The metabolic fate of ingested glucose within the liver is still controversial. It appears that the liver will remove 30-40% of the glucose that enters the portal vein following an oral glucose load and will replete its glycogen stores by both direct and indirect pathways. Whether the three-carbon precursors utilized by the indirect route are of hepatic or peripheral origin remains a matter of debate. Studies are under way to elucidate whether the hepatic response to the portal signal involves the autonomic nervous system, the nature of the interaction of the portal signal and insulin, and the metabolic fate of glucose removed by the liver in response to this signal.