Effects of physiologic and supraphysiologic hyperglycemia on early and late-phase insulin secretion in chronically dialyzed uremic patients

Publisher Website
Google Scholar
Abstract
To test secretory capacity of the beta-cell to a glucose stimulus in uremeic patients on chronic dialysis, three hyperglycemic clamps (plasma glucose increments: 1, 4.5 and 11 mmol/l) were performed in 8 uremic and 8 healthy subjects. Early-phase insulin and C-peptide responses (.DELTA.I and .DELTA.C) during the initial 6 min were consistently exaggerated at all three steps in uremic patients compared with controls (.DELTA.I. 16 .+-. 4 vs 4 .+-. 2, 41 .+-. 11 vs 15 .+-. 4 and 60 .+-. 12 vs 24 .+-. 5 mU/l; .DELTA.C. 0.39 .+-. 0.13 vs 0.07 .+-. 0.02, 0.40 .+-. 0.13 vs 0.16 .+-. 0.02 and 0.73 .+-. 0.15 vs 0.29 .+-. 0.04 nmol/l, p < 0.05 in all cases). Similarly late-phase insulin secretion defined as the insulin increment between 90 and 120 min after initiation of the glucose challenge was enhanced in uremic patients at the two highest glycemic step (44 .+-. 10 vs 16 .+-. 2 and 123 .+-. 29 vs 44 .+-. 5 mU/l, both p < 0.01). The raised late-phase insulin response allowed comparable glucose disposal in the two groups (uremic patients: 9.2 .+-. 1.0 and 15.5 .+-. 1.6 mg .cntdot. kg-1 .cntdot. min-1. Controls: 0.9 .+-. 1.3 and 19.9 .+-. 2.4 mg .cntdot. kg-1 .cntdot. min-1). The slopes of potentiation, i.e. the slopes of te regression lines expressing the relationship between changes in insulin increments and changes in glucose, were markedly steeper in uremic patients (0.45 .+-. 0.09 and 0.66 .+-. 0.20, early and late-phase respectively) than in controls (0.20 .+-. 0.06 and 0.25 .+-. 0.03). No relationship between serum insulin responses and electrolytes or PTH was demonstrated. In conclusion, despite several factors which may inhibit the ability of the beta-cell to respond to a glucose stimulus, acute hyperglycemia elicits in insulin-resistant uremic subjects and exaggerated early and late-phase insulin secretion which is able to compensate for insulin resistance, thereby maintaninig normal glucose disposal.

This publication has 3 references indexed in Scilit: