Splanchnic glucose and amino acid metabolism in obesity

Abstract

In obesity, despite basal hyperinsulinemia, splanchnic uptake of glucose precursors is increased, the relative contribution to total glucose release attributable to gluconeogenesis being 70% higher than in controls. Infusion of glucose at rates causing equivalent increases in arterial insulin induces a smaller inhibition in splanchnic glucose output than in controls. Infusion of glucose at rates causing comparable inhibition in splanchnic glucose output is accompanied by a disproportionately greater increase in endogenous insulin than in controls. These data are compatible with hepatic resistance to insulin in obesity.