OBJECTIVE -Insulin detemir is a soluble basal insulin analog with a unique mechanism of protracted action designed to reduce the variability associated with conventional basal insulins. This trial compared the glycemic control, risk of hypoglycemia, and effect on body weight of insulin detemir and NPH insulin in patients with type 1 diabetes treated with rapid-acting insulin aspart at meals.
RESEARCH DESIGN AND METHODS-This study was a 6-month multinational open parallel-group comparison conducted at 46 centers in five countries and included 448 patients with type 1 diabetes randomized 2:1 to insulin detemir or NPH insulin, respectively. RESULTS -After 6 months, comparable HbA 1c levels were found between the two treatment groups. Fasting plasma glucose tended to be lower in patients treated with insulin detemir, but this difference was not statistically significant (Ϫ0.76 mmol/l, P ϭ 0.097). Within-subject variation in self-measured fasting blood glucose was lower with insulin detemir than with NPH insulin (SD 3.37 vs. 3.78 mmol/l, P Ͻ 0.001). Risk of hypoglycemia was 22% lower with insulin detemir than with NPH insulin (P Ͻ 0.05) and 34% lower for nocturnal (2300 -0600) hypoglycemia (P Ͻ 0.005). Nightly plasma glucose profiles were smoother and more stable with insulin detemir (P ϭ 0.05). Body weight was significantly lower with insulin detemir at the end of the trial (P Ͻ 0.001).CONCLUSIONS -Treatment with insulin detemir resulted in more predictable glycemic control, with smoother plasma glucose profiles than NPH insulin and a significant reduction in the risk of hypoglycemia. The reduction in body weight with insulin detemir is a potential additional advantage. Regimens optimized for insulin detemir may be able to improve glycemic control beyond that possible with NPH insulin.
In long-term basal-bolus therapy, insulin detemir with insulin aspart as mealtime insulin is well tolerated and reduces the risks of nocturnal hypoglycaemia and weight gain compared to NPH insulin.
Objective: To investigate the relationship between dietary intakes and in vivo oxidative stress (OS) status in diabetic patients. Design: Case-control study. Setting: Outpatient-Clinic and Laboratory Endocrinology, University Antwerp. Subjects and methods: A total of 30 patients (24 type 1 diabetes mellitus (T1DM)/6 type 2 diabetes mellitus (T2DM) were asked to complete a 2 weekdays+1weekend day food consumption questionnaire during the week preceding their yearly diabetes control consultation, when samples were collected for the assay of oxidative stress (OS) (blood levels of antioxidants, peroxides, malondialdehyde (MDA) and minerals). Blood samples were also collected from 25 age-and sex-matched healthy controls. Results: Diabetic patients had lower glutathione (5.8071.15 vs 6.7571.03 mmol/g Hb in the controls, P ¼ 0.002) and higher MDA (0.68770.212 vs 0.54570.101 mmol/l, P ¼ 0.002). Although the group average intakes were within the Belgian RDA, intakes of fat 435% energy, fibre o15 g/1000 kcal, fruit o2 portions and vitamin E o10 mg/day were seen in more than 20 patients. Blood antioxidants did not correlate with intakes of energy, fat, protein or fibres or of their respective antioxidant. Vitamins A and E correlated with serum lipids (r ¼ 0.58, P o0.0005 between serum a-tocopherol and cholesterol). Blood peroxide levels were only related to intakes of saturated fat and cholesterol (Po0.05). In diabetic subjects but not in controls (Po0.05) MDA was related to glutathione and uric acid. Conclusions: In diabetic patients, blood levels of antioxidants are not related to their dietary intakes but to serum lipids. Levels of oxidative damage products are only related to intakes of saturated fats and cholesterol and to levels of endogenous antioxidants.
Interactions between leptin and insulin have been shown previously, in vitro and in vivo. In this study, we evaluate the associations of leptin levels with insulin secretion and insulin sensitivity in type 2 diabetes. Fasting leptin levels, HbA 1c, glucose, insulin, C-peptide, intact and des-31,32-proinsulin were measured in 100 non-insulin-treated type 2 diabetic patients. Glucose, insulin and C-peptide were measured 2 hours after an oral glucose load. Insulin resistance and beta-cell function were calculated using HOMA. Leptin levels were found to be associated with all measures of beta-cell secretion: with fasting and 2 hours insulin and C-peptide, with intact and des-31,32-proinsulin concentrations, and with beta-cell secretion estimated with HOMA. This association was independent of age and body fat in women, but in men, associations with insulin and C-peptide weakened after controlling for fat mass, whereas those with intact and des-31,32-proinsulin disappeared. Fasting insulin and C-peptide levels were also significant in multiple regression analyses, besides gender and fat mass. Insulin resistance, as assessed by HOMA, was strongly correlated with leptin, also after correction for age and fat mass in both genders. We conclude that, besides fat mass and gender - the main determinants for leptin levels in type 2 diabetic subjects as in healthy subjects - insulin secretion and the degree of insulin resistance also seem to contribute significantly to leptin levels.
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