Glucose Ra Research Articles

GALACTOSE ALIMENTATION IN THE PUP OF A DIABETIC MOTHER

Galactose(GAL) may regulate neonatal carbohydrate assimilation and may not stimulate insulin(INS) secretion. GAL may therefore stabilize glucose(GLU) metabolism in the IDM. Pups born to INS dependent diabetic dogs or controls were fed 0.6g/kg of GAL or GLU (N=5). During fasting IDM pups had equivalent blood GLU levels and systemic GLU appearance rates(Ra), but had elevated INS (7.4±0.3 vs 2.5±0.3 uU/ml, p=0.01) compared to control pups. After GAL feeding to IDM pups, blood GAL increased and peaked to 1 mM at 30 min. The glycemic response in IDM pups was similar after GLU or GAL feeding. Plasma INS increased minimally in the IDM pup after GAL feedings. In contrast, INS increased 2.5 fold after GLU. Ra of GLU in IDM pups after GAL feeding peaked at 30 min. and was lower than after enteric GLU at 30 min. (81.9±6.2 vs 106.2±8.6 μmol/kg/min, p=0.01). Ra after enteric GLU peaked at 60 min. and again was higher (118.2±10.5 vs 67.7±6.7, p=0.01). Hepatic glycogen content increased in the IDM fed GAL compared to fasted controls (634±27 vs 485±27 μmol/g, p=0.01) while GLU feeding had little effect. GAL and GLU feeding had no effect on glycogen synthase activity but the active component of phosphorylase decreased in both IDM groups compared to fasted controls. In summary, enteric GAL alimentation in IDM dogs results in lower INS levels with comparable glycemic responses compared to GLU feeding, attenuates Ra and enhances net glycogen content. In the presence of fasting hyperinsulinemia, GAL alimentation may stabilize GLU metabolism without excessive INS secretion.

Effects of glucose infusion on hepatic and muscle glycogenolysis in exercising dogs.

Hepatic glucose production (Ra) and the rate of utilization of nonglucose sources (essentially muscle glycogen) were measured in dogs running on a treadmill (15%, 133 m/min) with indwelling catheters in the jugular vein and carotid artery. A mixture of [3-3H]glucose and [U-14C]glucose was used as tracer according to the principles of the primed constant-rate infusion techniques. Glucose was infused intravenously at a rate (12 mg.kg-1.min-1) about 20% higher than the endogenous glucose Ra in exercising dogs. Glucose infusion started either at the beginning of the run or midexercise. Plasma insulin (IRI), glucagon (IRG), and cAMP levels were measured. Exogenous glucose prevented the usual decline of both plasma glucose and IRI without causing hyperglycemia. Exercise increased the molar ratio of IRG/IRI from 0.7 to 1.4, and glucose infusion lowered it to the resting value. The rise of plasma cAMP was slowed significantly. Both the hepatic glucose Ra and intramuscular glycogenolysis were strongly inhibited and the metabolic clearance rate of glucose was increased by 60-100%. The ratio of the specific activities of [14C]lactate to [14C]glucose indicated that 75-95% of the lactate turnover arose from plasma glucose. The corresponding value in the control group was 40-50%. It is concluded that in prolonged exercise the decline of both plasma glucose and insulin play a major role in preserving glucose homeostasis, by limiting the glucose uptake of the working muscle and by helping to achieve an approximately equal contribution of the liver and the muscle glycogen for the elevated glycolysis.

Extrapancreatic glucagon in control of glucose turnover in depancreatized dogs.

Depancreatized dogs have plasma immunoreactive glucagon (IRG), which is of gastric origin and is immunologically indistinguishable from pancreatic glucagon. The effects of extrapancreatic IRG on the tracer-determined rate of glucose production were examined to establish whether this hormone contributes to the hyperglycemia observed in six conscious, depancreatized dogs after insulin withdrawal. The dogs were initially maintained normoglycemic with an intraportal insulin infusion. Insulin withdrawal resulted in a 53 and 70% decrease of serum immunoreactive insulin (IRI) at 60 and 210 min, respectively. At 60 min, plasma glucose rose and Ra increased by 50%. A somatostatin-induced decrease in IRG prevented a further increase in Ra and glucose; after somatostatin withdrawal, IRG, Ra, and plasma glucose increased. Arginine given 1 or 3 h after insulin withdrawal increased IRG by 100 pg/ml, and mean Ra rose by 8.9 mg/kg-min. Thus, in depancreatized dogs with low but detectable serum IRI, IRG suppression is associated with inhibition of Ra and further rise in plasma glucose is prevented. Stimulation of IRG release increases Ra and results in marked hyperglycemia. It is concluded that extrapancreatic glucagon has a diabetogenic effect during acute insulin defiency.

Glucose and lactate kinetics in burn shock.

We studied the glucose and lactate kinetics during burn shock by means of the primed constant infusion of [6-3H]glucose and Na-L-(+)-[U-14C]lactate. We found an early postburn hyperglycemia that was due to an increased rate of appearance (Ra) of glucose. Later, the ability of the tissues to extract glucose became impaired, and the plasma glucose concentration increased even more in spite of the return of Ra of glucose to the control level. The Ra of lactate rose rapidly postburn, whereas the rate of disappearance (Rd) of lactate stayed at the control level for 30 min. Consequently, plasma lactate rose approximately 350%. After 30 min, Rd of lactate increased to the same level as Ra; and Ra, Rd, plasma lactate concentration, and the percent of glucose derived from lactate remained elevated for the duration of the experiment. These results indicate an important role of lactate in burn shock metabolism and substrate kinetics.