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Presents a study that examined the effect of enteral delivery of glucose on splanchnic glucose metabolism. Assessment of concentrations of glucose, insulin and C-peptide; Measurement of the rates of intravenous and intraduodenal glucose infusion; Analysis of endogenous glucose production and glucose disappearance.

Studies the impact of the lack of suppression of glucagon on glucose tolerance in humans. Plasma insulin, glucagon, C-peptide, and growth hormone concentrations; Endogenous glucose production; Rates of endogenous glucose production during either diabetic and nondiabetic insulin profiles.

Presents a study which determined whether lack of glucagon suppression causes hyperglycemia when insulin secretion is impaired. Methods; Results and discussion.

Portal infusion of glucose at rates approximating endogenous glucose production (EGP) causes paradoxical hypoglycemia in wild-type but not GLUT2 null mice, implying activation of a specific portal glucose sensor. To determine whether this occurs in humans, glucose containing [3-³H]glucose was infused intraduodenally at rates of 3.1 mg·kg[sup -1] · min[sup -1] (n = 5), 1.55 mg·kg[sup -1]·min[sup -1] (n = 9), or 0/0.1 mg·kg[sup -1]·min[sup -1] (n = 9) for 7 h in healthy nondiabetic subjects. [6,6-²H[sub 2]]glucose was infused intravenously to enable simultaneous measurement of EGP, glucose disappearance, and the rate of appearance of the intraduodenally infused glucose. Plasma glucose concentrations fell (P < 0.01) from 90 ± 1 to 84 ± 2 mg/dl during the 0/0.1 mg·kg[sup -1]·min[sup -1] id infusions but increased (P < 0.001) to 104 ± 5 and 107 ± 3 mg/dl, respectively, during the 1.55 and 3.1 mg·kg[sup -1]·min[sup -1] id infusions. In contrast, insulin increased (P < 0.05) during the 1.55 and 3.0 mg·kg[sup -1]·min[sup -1] infusions, reaching a peak of 10 ± 2 and 18 ± 5 µU/ml, respectively, by 2 h. Insulin concentrations then fell back to concentrations that no longer differed by study end (7 ± 1 vs. 8 ± 1 µU/ml). This resulted in comparable suppression of EGP by study end (0.84 ± 0.2 and 0.63 ± 0.1 mg·kg[sup -1]. min[sup -1]). Glucose disappearance was higher (P < 0.01) during the final hour of the 3.1 than 1.55 mg·kg[sup -1]·min[sup -1] id infusion (4.47 ± 0.2 vs. 2.6 ± 0.1 mg·kg[sup -1]·min[sup -1]), likely because of the slightly, but not significantly, higher glucose and insulin concentrations. We conclude that, in contrast to mice, selective portal glucose delivery at rates approximating EGP does not cause hypoglycemia in humans. [ABSTRACT FROM AUTHOR]

Examines whether type 2 diabetes mellitus alters systemic and regional free fatty acid ([sup 3 H]palmitate) metabolism. Relative contributions of splanchnic, leg and nonsplanchnic upper body regions to plamitate release; Association of type 2 diabetes with a generalized impairment in insulin suppression of lipolysis compared with equally obese nondiabetic individuals.

Examines whether type 2 diabetes mellitus alters systemic and regional free fatty acid metabolism. Correlation between abdominal fat compartments and systemic palmitate release; Controversy regarding insulin's effect on antilipolysis in type 2 diabetes; Markers associated with abdominal visceral fat content.