The relevance of persistent C-peptide secretion in type 1 (insulin-dependent) diabetes mellitus to glycaemic control and diabetic complications.
The effect of residual C-peptide secretion in longer standing IDDM on glycaemic control and the prevalence and evolution of complications over 2 years was evaluated. Thirty-one subjects with IDDM of 15.4 (1.5) years duration (mean SEM)) and residual C-peptide secretion, were matched for age, duration of diabetes and body mass index with 31 subjects without detectable C-peptide secretion. At trial entry and over 2 years, levels of HbA1, fructosamine and mean blood glucose were essentially similar in both groups. Levels of glycated albumin (GSA) were significantly higher in the C-peptide negative group after 3 and 9 months (P less than 0.05). An increased prevalence of proliferative retinopathy in the C-peptide negative group and of peripheral vascular disease in the C-peptide secretor group was apparent at entry to the study (both P less than 0.05), although no significant differences were observed after 1 or 2 years. There was no difference in the prevalence of peripheral or autonomic neuropathy, hypertension, nephropathy or ischaemic heart disease. Subjects with C-peptide concentrations greater than 0.100 pmol/ml at entry to this study had lower daily insulin requirements after 1 and 2 years, but behaved like the larger group with any detectable C-peptide secretion in all other respects. Residual C-peptide secretion was lost after 1 year in 7 patients, in whom glycaemic control during the year had been particularly poor. Insulin antibody titres were no different in the 2 groups at any time point. This study suggests that residual C-peptide secretion in longer standing IDDM confers the potential for limited improvements in glycaemic control. This effect appears to be insufficient to prevent the evolution of microvascular complications over a 2-year period. Residual C-peptide secretion and relative hyperinsulinaemia may be associated with an excess of peripheral vascular disease.
Winocour
P H
PH
Department of Medicine, University of Manchester, Hope Hospital, Salford, U.K.
Jeacock
J
J
Kalsi
P
P
Gordon
C
C
Anderson
D C
DC
D000328:Adult; D000419:Albuminuria; D015415:Biomarkers / Q000097:blood*; D001786:Blood Glucose / Q000378:metabolism*; D015190:Blood Glucose Self-Monitoring; D001794:Blood Pressure; D002096:C-Peptide / Q000097:blood* / Q000378:metabolism; D003327:Coronary Disease / Q000175:diagnosis; D003922:Diabetes Mellitus, Type 1 / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D003925:Diabetic Angiopathies / Q000175:diagnosis; D003928:Diabetic Nephropathies / Q000175:diagnosis; D003929:Diabetic Neuropathies / Q000175:diagnosis; D003930:Diabetic Retinopathy / Q000175:diagnosis; D005500:Follow-Up Studies; D019270:Fructosamine; D006442:Glycated Hemoglobin / Q000032:analysis; D006595:Hexosamines / Q000097:blood; D006801:Humans; D006973:Hypertension / Q000175:diagnosis; D008875:Middle Aged
D015415:Biomarkers; D001786:Blood Glucose; D002096:C-Peptide; D019270:Fructosamine; D006442:Glycated Hemoglobin; D006595:Hexosamines