Pathways for glucose disposal after meal ingestion in humans

Abstract

To characterize postprandial glucose disposal more completely, we used the tritiated water technique, a triple-isotope approach (intravenous [3-H3]glucose and [14C]bicarbonate and oral [6,6-2H2]glucose) and indirect calorimetry to assess splanchnic and peripheral glucose disposal, direct and indirect glucose storage, oxidative and nonoxidative glycolysis, and the glucose entering plasma via gluconeogenesis after ingestion of a meal in 11 normal volunteers. During a 6-h postprandial period, a total of ∼98 g of glucose were disposed of. This was more than the glucose contained in the meal (∼78 g) due to persistent endogenous glucose release (∼21 g): splanchnic tissues initially took up ∼23 g, and an additional ∼75 g were removed from the systemic circulation. Direct glucose storage accounted for ∼32 g and glycolysis for ∼66 g (oxidative ∼43 g and nonoxidative ∼23 g). About 11 g of glucose appeared in plasma as a result of gluconeogenesis. If these carbons were wholly from glucose undergoing glycolysis, only ∼12 g would be available for indirect pathway glycogen formation. Our results thus indicate that glycolysis is the main initial postprandial fate of glucose, accounting for ∼66% of overall disposal; oxidation and storage each account for ∼45%. The majority of glycogen is formed via the direct pathway (∼73%).

Disordered Lipid Metabolism and the Pathogenesis of Insulin Resistance

“…Direct 13 C MRS measurements of muscle glycogen have also been undertaken in healthy subjects following standard meals. In this situation, muscle glycogen synthesis accounts for ϳ30% of the ingested glucose (123). Muscle glycogen concentrations peak at ϳ100 mM around 5 h after a meal, declining thereafter (20,115).…”

The Central Role of Glucose in Metabolism and Nutrition of Critically Ill Patients

“…Další metabolický efekt je v inhibici lipolýzy v tukové tkání, což vede ke snížené plasmatické koncentraci mastných kyselin a jejich snížené oxidaci, tímto se také spolupodílí zpětně na snížení glukoneogeneze. Glukoneogeneze nicméně nemůže být ani postprandiálně zcela inhibována, je pouze redukována její kinetika (18). Utilizace glukózy v periferních tkáních postprandiálně je určována mnoha faktory, které ovlivňují inzulinovou rezistenci.…”

Hepatic glucose sensing is required to preserve β cell glucose competence

“…However, several studies in humans and dogs have attempted to assess splanchnic, i.e., mostly liver, glucose disposal after glucose or mixed-meal ingestion. Although quite variable, these studies proposed that approximately 10%-25% of the ingested glucose is taken up by the liver (25)(26)(27)(28). In the absence of hepatic glucose absorption, the amount of glucose that would normally be taken up by the liver appears to be redirected to skeletal muscles.…”