The Diabetes Intervention Study (DIS) is a prospective population-based multicentre trial of newly detected cases of non-insulin-dependent diabetes mellitus (NIDDM). This report analyses the risk factors for subsequent coronary heart disease and all-cause death during the 11-year follow-up. The prognostic significance of the categories of the NIDDM Policy Group was validated with respect to the incidence of coronary heart disease and mortality. At baseline 1139 subjects, aged 30-55 years at the time of diabetes detection and classified as diet controlled after a 6-week screening phase, were included. Of the patients 112 (15.2%) suffered from myocardial infarction, 197 (19.82%) of 994 had died. The odds ratio for all-cause mortality compared to the general population for males at the age of 36-45 years was 5.1 and for females 7.0. In multivariate analysis age, blood pressure and smoking were independent risk factors for myocardial infarction and male sex, age, blood pressure, triglycerides, postprandial blood glucose and smoking for death, respectively. The categories of the NIDDM Policy Group target parameters for blood glucose, triglycerides and blood pressure were significant predictors of both CHD and death. Thus, it appears that in NIDDM good control of blood glucose, blood pressure and triglycerides is associated with a lower incidence of coronary heart disease and death rate respectively.

IHE was of substantial benefit for the control of glycemia, significantly diminished the need for antidiabetic drugs, and reduced a cluster of risk factors but had no effect on the control of blood lipids. This could be one major reason for the failure of IHE, effective lowering of blood pressure, and clofibric acid to prevent cardiovascular complications. Clofibric acid was only effective in reducing triglycerides.

Our data suggest that B19V but not HBoV demonstrates a lifelong persistence in the heart. The detection of B19V DNA in heart tissue showed no correlation with clinical symptoms. We strongly recommend that serological testing become a standardized procedure for future studies, to obtain representative data concerning the prevalence of B19V in the heart.

In obese people, an increase of plasma leptin levels is well-known and is seen as a consequence of the increased body fat mass. Moreover, a relationship between fasting concentrations of leptin and insulin has been described. Hyperinsulinemia is considered to be indicative of insulin resistance. We aimed at elucidating the interrelations between leptin, insulin and insulin resistance in type 2 diabetic patients. Under metabolic ward conditions, we investigated 21 moderately overweight men with type 2 diabetes. The patients had a mean age of 49.1 years, a mean body mass index (BMI) of 26.8 kg/m(2), and a mean diabetes duration of 82.5 months. All patients were treated with diet alone. We measured fasting leptin and insulin levels, body composition by determination of total body water, and insulin resistance by euglycemic hyperinsulinemic clamp technique. At univariate analysis, fasting leptin level significantly and positively correlated with BMI (r=0.49, p=0.02) and with fasting insulin (r=0.69, p=0.001), while it negatively correlated with the glucose disposal rate (r=-0.62, p=0.002). Furthermore, leptin was inversely correlated with HDL-cholesterol (r=-0.45, p=0.04). When excluding the influence of body fat mass or of BMI in partial correlation analysis, the correlations between leptin and insulin or insulin sensitivity remained significant. The relationship between insulin resistance (as measured directly in the clamp experiments) and leptin concentrations was also shown by subdividing the diabetic patients according to tertiles of insulin sensitivity. The highest fasting leptin levels were observed in those patients with the most expressed insulin resistance. Our data point to a functional relationship between insulin resistance and leptin concentrations in insulin-resistant type 2 diabetic men, independently of body composition. This relationship is believed to be mediated by insulin.

Objective: Peripheral arterial disease (PAD), as well as diabetic neuropathy, is a risk factor for the development of diabetic foot ulcers. The aim of this study was to evaluate differences and predictors of outcome parameters in patients with diabetic foot by stratifying these subjects according to the severity of PAD. Research design and methods: In a prospective study, patients with new diabetic foot ulcers have been treated and investigated by structured healthcare. Subjects were recruited between 1 January 2000 and 31 December 2007. All study participants underwent a 2-year follow-up observation period. The patients underwent a standardized examination and classification of their foot ulcers according to a modification of the University of Texas Wound Classification System. The severity of PAD was estimated by measurement of the ankle brachial index (ABI) and the continuous wave Doppler flow curve into undisturbed perfusion (0.9 < ABI < 1.3), compensated perfusion (0.5 < ABI < 0.9), decompensated perfusion (ABI < 0.5) and medial arterial calcification. Results: A total of 678 patients with diabetic foot were consecutively included into the study (69% male, mean age 66.3 ± 11.0 years, mean diabetes duration 15.8 ± 10.2 years). Major amputations (above the ankle) were performed in 4.7% of the patients. 22.1% of these subjects had decompensated PAD. These subjects had delayed ulcer healing, higher risk for major amputation [odds ratio (OR) 7.7, 95% confidence interval (CI) 2.8-21.2, p < 0.001] and mortality (OR 4.9, 95 % CI 1.1-22.1, p < 0.05).Conclusion: This prospective study shows that the severity of PAD significantly influences the outcome of diabetic foot ulcers regarding to wound healing, major amputation and mortality.

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Adiponectin, which is encoded by the ADIPOQ gene, has been shown to modulate insulin sensitivity and glucose homeostasis. Plasma adiponectin levels are decreased in type 2 diabetes and obesity. Genetic variations within the ADIPOQ gene are associated with decreased adiponectin hormone levels. To analyze specific single-nucleotide polymorphisms (SNPs) and their association with T2D, 365 German subjects with T2D and 323 control subjects were screened. Three common SNPs - +45T>G in exon 2, and 2 promoter variants SNPs -11391G>A and -11377C>G - were analyzed. We found that the variant allele of SNP -11391G>A was significantly more frequent in the diabetic patient group than in the control group (p=0.003). Carrying the haplotype of SNP -11391A and SNP -11377C was associated with a 1.50-fold (p=0.03) increase in diabetes risk. The combination of the A-C haplotype and the G-C haplotype was associated with significantly elevated diabetes risk (OR=2.82 (95% CI: 1.35-5.91), p=0.006) after correction for BMI and age. Our observations suggest that diploid combinations of haplotype in the adiponectin gene promoter region contribute to the genetic risk of T2D in individuals from a German Caucasian population.

In patients with PD with sleep disturbances, rasagiline showed beneficial effects on sleep quality as measured by polysomnography. These effects were probably not related to motor improvement or translated into improved overall sleep quality perception by patients.