Residual insulin production, glycaemic control and prevalence of microvascular lesions and polyneuropathy in long-term Type 1 (insulin-dependent) diabetes mellitus

Abstract

The aim of the present study was to evaluate the role of residual insulin production in long-term Type 1 (insulin-dependent) diabetes mellitus. Ninety-seven patients with a disease duration of 9-16 years and onset before the age of 30 years were studied. C-peptide excretion in 24-h urine samples was measured as an indicator of residual insulin production. Thirty-five patients (36%) excreted C-peptide (>-0.2 nmol); as many as possible of them were carefully matched with a non-excretor patient with regard to age at onset of diabetes and disease duration. Twenty-nine pairs were obtained, and 22 of them agreed to participate in further investigations of glycaemic control and microangiopathic lesions. The patients who excreted C-peptide had significantly lower HbA1c than the non-excretor group, 6.9±0.3% vs 7.9±0.3%, (p<0.025). Moderate-to-advanced background retinopathy was found in 2 patients in the excretor group and in 7 patients in the nonexcretor group. Microalbuminuria [ratio of albumin: creatinine (mg/l:mmol/l) >-5] was found in 1 and in 5 patients, respectively, while proteinuria [ratio of protein: creatinine (mg/l: mmol/l× 10) >-136] was found in 0 and in 4 patients, respectively. Microalbuminuria and/or proteinuria was found in 7 of the non-excretor group as compared to 1 in the excretor group (p=0.046). When all the variables were taken into account, microalbuminuria and/or proteinuria and/or moderate-to-advanced background retinopathy was found in 3 of the excretor group compared to 11 of the non-excretor group (p=0.022). Reduced sensory and motor nerve conduction velocities were common findings and occurred with the same frequency in the two groups. The data suggest that residual insulin production in long-term Type 1 diabetes is associated with a more satisfactory glycaemic control and a lower prevalence of early microangiopathic eye and kidney lesions. © 1987 Springer-Verlag.