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Svend G Hartling, Michael E Røder, Bo Dinesen and Christian Binder

Hartling SG, Røder ME, Dinesen B, Binder C. Proinsulin C-peptide, and insulin in normal subjects during an 8-h hyperglycemic clamp. Eur J Endocrinol 1996;134:197–200. ISSN 0804–4643

Increased concentrations of proinsulin immunoreactive material (PIM) absolutely or relative to insulin is a characteristic finding in patients with non-insulin-dependent diabetes mellitus (NIDDM). The aim of this study was to test if 8 h or mild hyperglycemia (7–9 nmol/l in healthy subjects could induce a preferential secretion of PIM from B cells. Serum concentrations of insulin, C-peptide and PIM were measured every 10 min during the 8 h of continuous glucose infusion in nine normal-weight healthy subjects without diabetes among their first-degree relatives. After a gradual rise in B-cell peptides, a steady state was reached. From 4 to 8 h no further difference in insulin, C-peptide or PIM concentration was found. Fasting PIM/C-peptide and PIM/insulin ratios of 0.5% and 2.3% increased during the glucose clamp to levels of 1.4% and 7.6%, respectively. Neither testing the regression slope nor comparing individual time points showed any significant difference for the PIM/C-peptide ratio from 2 to 8 h and for the PIM/insulin ratio from 3 to 8 h. These results do not support the hypothesis that an increased glucose drive per se results in an altered B-cell function with increasing PIM/Cpeptide ratio. At least 8 h of mild hyperglycemia in healthy subjects does not progressively alter B-cell function.

Svend Hartling, Department of Internal Medicine, Sundby Hospital, Italiensvej 1, DK-2300 Sundby, Denmark

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Benjamin Glaser, Gil Leibovich, Rafael Nesher, Svend Hartling, Christian Binder and Erol Cerasi

Abstract. In Type II, non-insulin-dependent diabetes, insulin secretion is often reduced to the point where oral hypoglycaemic agents fail to control the plasma glucose level. We studied 12 patients (age 41–66 years; 4 lean, 8 obese) with Type II diabetes mellitus for 1–25 years who were uncontrolled despite maximal dose glibenclamide and metformin. After withdrawal of medication, blood glucose control was determined by measuring glucose before and 2 h after each meal for 48 h, and beta-cell function by insulin or C-peptide response to glucagon and to iv glucose. Following these tests, intensive insulin treatment (CSII) was initiated, and near-euglycaemia (mean of 7 daily glucose determinations < 7.7 mmol/l) was maintained for 16.6 ± 1.5 days, at which time the tests were repeated. Mean daily insulin requirement was 61 ± 9 IU (0.81 ± 0.09 IU/kg). Glucose control was improved after cessation of CSII (mean glucose 12.7 ± 0.6 mmol/l after vs 20 ± 1.5 mmol/l before, P <0.005). Maximum incremental C-peptide response improved both to glucagon (214 ± 32 after vs 134 ± 48 pmol/l before, P = 0.05) and to glucose iv bolus injection (284 ± 53 vs 113 ± 32 pmol/l, P < 0.05). Peak insulin response, measured after iv glucose infusion, also tended to be higher in the post-CSII test (42 ± 18 vs 22 ± 5.6 mU/l). Basal and stimulated proinsulin concentrations were high relative to C-peptide levels during the pre-treatment period, but returned to normal after CSII. Thus: 1) adequate blood glucose control could be obtained in most of our patients using moderate doses of insulin even in those who were obese; 2) short-term euglycaemia resulted in improved insulin response to both glucagon and glucose, and reduction of the relative proinsulin secretion; 3) although beta-cell function improved in most patients, only 6 could be adequately controlled with oral agents after hospital discharge. In those patients who do not respond well to conventional treatment, CSII is an attractive alternative.