Canagliflozin and Cardiovascular disease- results of the CANVAS trial.

Canagliflozin is a new novel oral antidiabetic agent belonging to the class of sodium-glucose co-transporter 2 (SGLT2) inhibitors, inhibiting glucose reabsorption in the proximal tubule, leading to increased urinary glucose excretion and subsequently to reduction in plasma glucose concentration, in individuals with hyperglycemia. Before the approval of canagliflozin by the Food and Drug Administration (FDA) in 2013, a pair-wise meta-analyses of trials involving canagliflozin did not differ from control in terms of all-cause mortality, cardiovascular death, myocardial infarction, and stroke. However, no large, randomized-controlled trials were available for comparison until the results of the CANVAS (Canagliflozin Cardiovascular Assessment Study) trial were published. The CANVAS Trial was designed to assess the cardiovascular safety and efficacy of canagliflozin. Recently, results of the completed CANVAS Trial were released which showed patients with type 2 diabetes and established cardiovascular disease or at high risk for cardiovascular events who were treated with canagliflozin had significantly lower rates of the primary cardiovascular outcome than patients assigned to placebo. All three components of the primary outcome - death from cardiovascular causes, nonfatal myocardial infarction, and nonfatal stroke - showed point estimates of effect that suggested benefit .These results may represent a significant additional therapeutic tool in the clinical prevention and management of cardiovascular mortality and morbidity. However, data on the long-term efficacy on the use of Canagliflozin is still incomplete and their use in patients with type 2 diabetes should be carefully considered.

Use of dark chocolate for diabetic patients: a review of the literature and current evidence.

Dietary changes are a major lifestyle factor that can influence the progression of chronic diseases such as diabetes. Recently, flavanols, a subgroup of plant-derived phytochemicals called flavonoids, have gained increasing attention, due to studies showing an inverse correlation between dietary intake of flavanols and incidence of diabetes. Flavanoids in the cocoa plant may ameliorate insulin resistance by improving endothelial function, altering glucose metabolism, and reducing oxidative stress. Oxidative stress has been proposed as the main culprit for insulin resistance. The well-established effects of cocoa on endothelial function also points to a possible effect on insulin sensitivity. The relationship between insulin resistance and endothelial function is a reciprocal one. Overall, the evidence from these studies suggests that cocoa may be useful in slowing the progression to type 2 diabetes and ameliorating insulin resistance in metabolic syndrome. Additionally, results from several small studies indicate that cocoa may also have therapeutic potential in preventing cardiovascular complications in diabetic patients. Studies highlighting the potential of cocoa-containing diets, in large-randomized controlled trials should be performed which might give us a better opportunity to analyze the potential health-care benefit for reducing the risk of complications in diabetic patients at molecular level.

Resveratrol exacerbates both autoimmune and viral models of multiple sclerosis.

The polyphenol compound resveratrol is reported to have multiple functions, including neuroprotection, and no major adverse effects have been reported. Although the neuroprotective effects have been associated with sirtuin 1 activation by resveratrol, the mechanisms by which resveratrol exerts such functions are a matter of controversy. We examined whether resveratrol can be neuroprotective in two models of multiple sclerosis: experimental autoimmune encephalomyelitis (EAE) and Theiler's murine encephalomyelitis virus-induced demyelinating disease (TMEV-IDD). EAE was induced in C57BL/6 mice, which were fed a control diet or a diet containing resveratrol during either the induction or effector phase or through the whole course of EAE. SJL/J mice were infected with TMEV and fed a control diet or a diet containing resveratrol during the chronic phase of TMEV-IDD. In EAE, all groups of mice treated with resveratrol had more severe clinical signs than the control group. In particular, resveratrol treatment during the induction phase resulted in the most severe EAE, both clinically and histologically. Similarly, in the viral model, the mice treated with resveratrol developed significantly more severe TMEV-IDD than the control group. Thus, surprisingly, the resveratrol treatment significantly exacerbated demyelination and inflammation without neuroprotection in the central nervous system in both models. Our findings indicate that caution should be exercised in potential therapeutic applications of resveratrol in human inflammatory demyelinating diseases, including multiple sclerosis.