!Background: The prevalence and socioeconomic burden of type 2 diabetes (T2DM) and associated co-morbidities are rising worldwide. Aims: This guideline provides evidence-based recommendations for preventing T2DM. Methods: A European multidisciplinary consortium systematically reviewed the evidence on the effectiveness of screening and interventions for T2DM prevention using SIGN criteria. Results: Obesity and sedentary lifestyle are the main modifiable risk factors. Age and ethnicity are non-modifiable risk factors. Case-finding should follow a step-wise procedure using risk questionnaires and oral glucose tolerance testing. Persons with impaired glucose tolerance and/or fasting glucose are at high-risk and should be prioritized for intensive intervention. Interventions supporting lifestyle changes delay the onset of T2DM in high-risk adults (numberneeded-to-treat: 6.4 over 1.8-4.6 years). These should be supported by inter-sectoral strategies that create health promoting environments. Sustained body weight reduction by ≥ 5% lowers risk. Currently metformin, acarbose and orlistat can be considered as second-line prevention options. The population approach should use organized measures to raise awareness and change lifestyle with specific approaches for adolescents, minorities and disadvantaged people. Interventions promoting lifestyle changes are more effective if they target both diet and physical activity, mobilize social support, involve the planned use of established behaviour change techniques, and provide frequent contacts. Cost-effectiveness analysis should take a societal perspective. Conclusions: Prevention using lifestyle modifications in highrisk individuals is cost-effective and should be embedded in evaluated models of care. Effective prevention plans are predicated upon sustained government initiatives comprising advocacy, community support, fiscal and legislative changes, private sector engagement and continuous media communication.

OBJECTIVE -Diabetes is characterized by marked postprandial endothelial dysfunction induced by hyperglycemia, hypertriglyceridemia, advanced glycation end products (AGEs), and dicarbonyls (e.g., methylglyoxal [MG]). In vitro hyperglycemia-induced MG formation and endothelial dysfunction could be blocked by benfotiamine, but in vivo effects of benfotiamine on postprandial endothelial dysfunction and MG synthesis have not been investigated in humans until now.RESEARCH DESIGN AND METHODS -Thirteen people with type 2 diabetes were given a heat-processed test meal with a high AGE content (HAGE; 15.100 AGE kU, 580 kcal, 54 g protein, 17 g lipids, and 48 g carbohydrates) before and after a 3-day therapy with benfotiamine (1,050 mg/day). Macrovascular flow-mediated dilatation (FMD) and microvascular reactive hyperemia, along with serum markers of endothelial disfunction (E-selectin, vascular cell adhesion molecule-1, and intracellular adhesion molecule-1), oxidative stress, AGE, and MG were measured during both test meal days after an overnight fast and then at 2, 4, and 6 h postprandially.RESULTS -The HAGE induced a maximum reactive hyperemia decrease of Ϫ60.0% after 2 h and a maximum FMD impairment of Ϫ35.1% after 4 h, without affecting endotheliumindependent vasodilatation. The effects of HAGE on both FMD and reactive hyperemia were completely prevented by benfotiamine. Serum markers of endothelial dysfunction and oxidative stress, as well as AGE, increased after HAGE. These effects were significantly reduced by benfotiamine.CONCLUSIONS -Our study confirms micro-and macrovascular endothelial dysfunction accompanied by increased oxidative stress following a real-life, heat-processed, AGE-rich meal in individuals with type 2 diabetes and suggests benfotiamine as a potential treatment. Diabetes Care 29:2064 -2071, 2006E ndothelial dysfunction is an early marker of atherosclerosis and accompanies states showing a high cardiovascular risk, such as smoking (1), dyslipidemia (2), arterial hypertension (3), obesity (4), coronary artery disease (5), congestive heart failure (6), and type 1 (7) and type 2 (8) diabetes. Postprandial endothelial dysfunction has been proposed as the link between postprandial dysmetabolism and atherosclerosis (9) and occurs not only in patients with cardiovascular disease (10) or diabetes (11) but even in healthy subjects (12). Distinctive and cumulative (11) effects of hyperglycemia (13) and hypertriglyceridemia (14) on postprandial endothelial dysfunction have been shown. Since the postprandial state covers most of our daytime, interventions aimed at reducing postprandial endothelial dysfunction might play a decisive role in prevention of atherosclerosis. Several therapeutic approaches have been suggested for the treatment of postprandial endothelial dysfunction, including insulin, folic acid, tetrahydrobiopterin, vitamins C and E, and statins (11). These approaches aim at reducing postprandial oxidative stress (vitamins C and E, statins, and partly folic acid), postprandial hyperglycemia (insul...

In patients with T2DM, a HAGE meal induces a more pronounced acute impairment of vascular function than does an otherwise identical LAGE meal. Therefore, chemical modifications of food by means of cooking play a major role in influencing the extent of postprandial vascular dysfunction.

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This randomized clinical trial assesses the effect of application of cold atmospheric plasma in addition to standard care treatment compared with placebo on wound healing in terms of more rapid and clinical meaningful wound surface regression.

The transplantation of BMCs as well as TRCs proved to be safe and feasible. Improvements of microcirculation and complete wound healing were observed in the transplant groups.

OBJECTIVEMetformin is used as a first-line oral treatment for type 2 diabetes (T2D). However, the underlying mechanism is not fully understood. Here, we aimed to comprehensively investigate the pleiotropic effects of metformin. RESEARCH DESIGN AND METHODSWe analyzed both metabolomic and genomic data of the population-based KORA cohort. To evaluate the effect of metformin treatment on metabolite concentrations, we quantified 131 metabolites in fasting serum samples and used multivariable linear regression models in three independent cross-sectional studies (n = 151 patients with T2D treated with metformin [mt-T2D]). Additionally, we used linear mixed-effect models to study the longitudinal KORA samples (n = 912) and performed mediation analyses to investigate the effects of metformin intake on blood lipid profiles. We combined genotyping data with the identified metforminassociated metabolites in KORA individuals (n = 1,809) and explored the underlying pathways. RESULTSWe found significantly lower (P < 5.0E-06) concentrations of three metabolites (acyl-alkyl phosphatidylcholines [PCs]) when comparing mt-T2D with four control groups who were not using glucose-lowering oral medication. These findings were controlled for conventional risk factors of T2D and replicated in two independent studies. Furthermore, we observed that the levels of these metabolites decreased significantly in patients after they started metformin treatment during 7 years' follow-up. The reduction of these metabolites was also associated with a lowered blood level of LDL cholesterol (LDL-C). Variations of these three metabolites were significantly associated with 17 genes (including FADS1 and FADS2) and controlled by AMPK, a metformin target. CONCLUSIONSOur results indicate that metformin intake activates AMPK and consequently suppresses FADS, which leads to reduced levels of the three acyl-alkyl PCs and LDL-C. Our findings suggest potential beneficial effects of metformin in the prevention of cardiovascular disease.Type 2 diabetes (T2D) is a chronic disease with diminished response to insulin and relative insulin deficiency (1). Patients with T2D mostly take metformin as first-line oral treatment to lower their glucose levels and to improve insulin sensitivity (2). Despite metformin's use as an antihyperglycemic agent for more than 50 years, its

In therapy of the metabolic syndrome, the optimal dietary approach with regard to its macronutrient composition and metabolically favourable food components, such as the plant-derived n-3 fatty acid a-linolenic acid (ALA), is still a matter of debate. We investigated the effects of a hypoenergetic diet with low energy density (ED) enriched in rapeseed oil, resulting in high MUFA content and an ALA intake of 3·5 g/d on body weight and cardiovascular risk profile in eighty-one patients with the metabolic syndrome in comparison with an olive oil diet rich in MUFA, but with a low ALA content. After a 6-month dietary intervention, body weight was significantly reduced in the rapeseed oil and olive oil groups (27·8 v. 26·0 kg; P,0·05). There were significant decreases in systolic blood pressure, total cholesterol and LDL-cholesterol, and insulin levels in both groups (P,0·05). For all of these changes, no inter-group differences were observed. After the rapeseed oil diet, diastolic blood pressure declined more than after the olive oil diet (P, 0·05 for time £ group interaction). Furthermore, concentrations of serum TAG were significantly reduced after the high ALA intake, but not in the low ALA group (P,0·05 for time £ group interaction). In conclusion, our dietary food pattern with a low ED and high intakes of MUFA and ALA may be a practical approach for long-term dietary treatment in patients with the metabolic syndrome, leading to weight reduction and an improvement in the overall cardiovascular risk profile. The metabolic syndrome is a cluster of interrelated and modifiable risk factors for CVD including abdominal obesity, hypertension, dyslipidaemia and hyperglycaemia (1) . Diet is the cornerstone in the prevention and therapy of this metabolic disorder, with long-term weight reduction accompanied by an improvement in the metabolic risk profile as the primary therapeutic goal for obese patients. There is general agreement that a high intake of SFA and trans-fatty acids should be considerably reduced, because they increase LDL-cholesterol levels, impair insulin sensitivity and represent a dietary pattern with high energy density (ED), and therefore promote hyperenergetic diets (2 -5) . However, it is still a matter of debate whether saturated and hydrogenated fat should be replaced preferentially by carbohydrates or monounsaturated fat in these patients.For decades, low-fat, high-carbohydrate diets have been recommended as the most suitable approach for weight reduction with the focus on a high proportion of carbohydrates rather than on their physiological quality (6,7) . However, there is now evidence that the carbohydrate quality is more decisive than its quantity. A high intake of refined carbohydrates with a high glycaemic index has not only detrimental effects on the metabolic risk profile by raising serum glucose and TAG levels and decreasing , but is also positively associated with an elevated ED (4) , and therefore cannot be recommended for weight reduction. On the other hand, a high intake of fi...