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Glycaemic control, disease duration and β‐cell function in patients with Type 2 diabetes in a Swedish community. Skaraborg Hypertension and Diabetes Project
Author(s) -
Östgren C. J.,
Lindblad U.,
Ranstam J.,
Melander A.,
Råstam L.
Publication year - 2002
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1046/j.1464-5491.2002.00661.x
Subject(s) - medicine , diabetes mellitus , type 2 diabetes , odds ratio , insulin resistance , confidence interval , endocrinology , triglyceride , body mass index , cholesterol
Aims To examine determinants for glycaemic control in primary care patients with Type 2 diabetes. Methods In a community‐based surveillance of primary care patients with Type 2 diabetes, 190 men and 186 women were consecutively identified and examined for cardiovascular risk factors. Insulin resistance and β‐cell function were estimated using homeostasis model assessment (HOMA). Good glycaemic control was defined as HbA 1c < 6.5%. Results Following adjustment for age and gender, HbA 1c ≥ 6.5% was associated with duration of diabetes (10.6 vs. 6.4 years, P < 0.001), lower levels of serum insulin (6.3 vs. 8.0 mU/l, P = 0.012), higher serum triglyceride levels (2.0 vs. 1.7 mmol/l, P = 0.002) and impairment of β‐cell function (HOMA index 19.5 vs. 45.8, P < 0.001). The association between HbA 1c levels and duration remained with adjustment for age, gender, waist–hip ratio (WHR) and serum triglycerides (odds ratio (OR) for HbA 1c ≥ 6.5% by 5 years diabetes duration = 1.7; 95% confidence interval (CI) 1.4–2.1) but was lost following additional adjustment for β‐cell function (OR for HbA 1c ≥ 6.5%= 1.3; 95% CI 0.96–1.7). In a separate linear regression with β‐cell function as the dependent variable there was a significant association with HbA 1c after adjustments for differences in age, gender, WHR, serum triglyceride levels and diabetes duration ( P < 0.001). Conclusions Increasing HbA 1c by time was associated with declining β‐cell function. Diabet. Med. 19, 125–129 (2002)