Hepatic adaptations to sucrose and fructose.

The liver is an important site of postprandial glucose disposal, accounting for the removal of up to 30% of an oral glucose load. The liver is also centrally involved in dietary lipid and amino acid uptake, and the presence of either or both of these nutrients can influence hepatic glucose uptake. The composition of ingested carbohydrate also influences hepatic glucose metabolism.

An acute increase in fructose concentration increases hepatic glucose-6-phosphatase mRNA via mechanisms that are independent of glycogen synthase kinase-3 in rats.

It appears that low amounts of fructose improve, whereas increased concentrations impair glucose tolerance and hepatic glucose metabolism. In this study, we compared directly the effects of low vs. high portal vein fructose concentrations on hepatic glucose metabolism in rats, using glucose-6-phosphatase gene expression as an endpoint.

Skeletal muscle sterol regulatory element binding protein-1c decreases with food deprivation and increases with feeding in rats.

Sterol regulatory element binding protein-1c (SREBP-1c) is a transcription factor that responds to nutritional status and regulates metabolic gene expression in liver and adipose tissue. Although SREBP-1c RNA is expressed in skeletal muscle, little is known about its regulation in this tissue. To determine whether SREBP-1c is regulated by nutritional status in muscle, rats were food deprived for 48 h and then given access to a semipurified high cornstarch diet for 0, 6, 12 or 24 h.

Glucose-6-phosphatase activity is not suppressed but the mRNA level is increased by a sucrose-enriched meal in rats.

The expression of glucose-6-phosphatase (G6Pase) mRNA is repressed by insulin and stimulated by cAMP and dexamethasone, with the insulin effect dominant. Both lipids and glucose increase the expression of G6Pase mRNA under conditions in which insulin is either absent or at basal levels. The aim of the present study was to investigate dietary nutrient regulation of G6Pase mRNA and protein under postprandial conditions.

Diets enriched in sucrose or fat increase gluconeogenesis and G-6-Pase but not basal glucose production in rats.

High-fat (HFD) and high-sucrose diets (HSD) reduce insulin suppression of glucose production in vivo, increase the capacity for gluconeogenesis in vitro, and increase glucose-6-phosphatase (G-6-Pase) activity in whole cell homogenates. The present study examined the effects of HSD and HFD on in vivo gluconeogenesis, the catalytic and glucose-6-phosphate translocase subunits of G-6-Pase, glucokinase (GK) translocation, and glucose cycling. Rats were fed a high-starch control diet (STD; 68% cornstarch), HSD (68% sucrose), or HFD (45% fat) for 7-13 days.

Elevated basal PI 3-kinase activity and reduced insulin signaling in sucrose-induced hepatic insulin resistance.

Sucrose feeding reduces the ability of insulin to suppress glucose production and hepatic gluconeogenesis. The present study examined the effect of a high-sucrose diet on early insulin-signaling steps in the liver. Rats were provided a high-starch (STD, control diet) or high-sucrose diet (HSD) for 3 wk.