OBJECTIVE
To quantify the relationship of residual C-peptide secretion to glycemic outcomes and microvascular complications in type 1 diabetes.
RESEARCH DESIGN AND METHODS
C-peptide was measured in an untimed blood sample in the Scottish Diabetes Research Network Type 1 Bioresource (SDRNT1BIO) cohort of 6,076 people with type 1 diabetes monitored for an average of 5.2 years.
RESULTS
In regression models adjusted for age at onset and duration, effect sizes for C-peptide ≥200 vs. <5 pmol/L were as follows: insulin dose at baseline, 9% lower (P = 2 × 10−17); HbA1c during follow-up, 4.9 mmol/mol lower (P = 3 × 10−13); hazard ratio for hospital admission for diabetic ketoacidosis during follow-up, 0.44 (P = 0.0001); odds ratio for incident retinopathy, 0.51 (P = 0.0003). Effects on the risk of serious hypoglycemic episodes were detectable at lower levels of C-peptide, and the form of the relationship was continuous down to the limit of detection (3 pmol/L). In regression models contrasting C-peptide 30 to <200 pmol/L with <5 pmol/L, the odds ratio for self-report of at least one serious hypoglycemic episode in the last year was 0.56 (P = 6 × 10−8), and the hazard ratio for hospital admission for hypoglycemia during follow-up was 0.52 (P = 0.03).
CONCLUSIONS
These results in a large representative cohort suggest that even minimal residual C-peptide secretion could have clinical benefit in type 1 diabetes, in contrast to a follow-up study of the Diabetes Control and Complications Trial (DCCT) intensively treated cohort where an effect on hypoglycemia was seen only at C-peptide levels ≥130 pmol/L. This has obvious implications for the design and evaluation of trials of interventions to preserve or restore pancreatic islet function in type 1 diabetes.
This study confirmed that the risk of mortality in individuals with type 1 diabetes remains elevated. Further studies are required to understand how gender affects the disparity in mortality and why obesity appears to be protective.
Aims/IntroductionThe increased mortality risk associated with diabetes is well established. The aim of the present study was to determine the causes of death of people with type 2 diabetes in Ayrshire and Arran, Scotland, between 2009 and 2014, and compare them with the national mortality rates.Materials and MethodsThe primary causes of death were collated. The causes of death were clustered into nine categories: heart disease, stroke, infection, renal failure, respiratory disorders, cancer, mental health, decompensated diabetes and other. The total rates were compared with national rates using the standardized mortality ratio (SMR), and then individually with heart disease, cerebrovascular disease and cancer.ResultsThere were 2116 deaths with the SMR, and 145 of those were caused by type 2 diabetes (n = 16,643; 95% confidence interval 139–152; P < 0.01). The SMR was >100 in all age bands, particularly in the younger age bands (P < 0.01). The SMR was consistently higher for women (P < 0.01). The SMR for heart disease was significantly >100 for both sexes in all age bands <65 years (P < 0.05). There was no difference in mortality causes related to the duration of diabetes. The most common cause of death was cancer (27.8%), followed by heart disease (24.1%). The SMR for cancer deaths was significantly elevated in women (120, 95% CI 104–137; P < 0.05).ConclusionsThis study confirmed increased mortality risk in type 2 diabetes patients, and suggests that where cardiovascular risk factors are being treated aggressively, cancer takes on a greater importance in the cause of death. Should greater consideration now be given for cancer as a complication of diabetes?
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