Potential Health Benefits of Indian Spices in the Symptoms of the Metabolic Syndrome: A Review.

Spices used in Indian cooking have a long history of use as medicines to prevent and treat diseases. Many studies have confirmed that spices can be useful medicines, but the major challenge is now to provide scientific evidence and plausible mechanisms for their therapeutic responses. This review focuses on the therapeutic potential of Indian spices to treat multiple symptoms of the metabolic syndrome such as insulin resistance, diabetes, obesity, altered lipid profile and hypertension. The metabolic syndrome is prevalent and has become an important financial burden to the healthcare system in both developed and developing countries. Inflammation and oxidative stress have been proposed as initiators of the metabolic syndrome, especially of insulin resistance. Natural products with anti-inflammatory and anti-oxidant properties are found in spices. Adequate doses of these compounds may be effective in treating the metabolic syndrome. Testing these potential treatments requires adequate animal models, usually rodents, so the limitations of these models are important. Furthermore, this review highlights the need for adequate legislation and regulation to ensure the safety and success of evidence-based functional foods and nutraceuticals.

Is mycophenolate more than just an immunosuppressant?--An overview.

The development of immunosuppressant compounds, such as cyclosporine and tacrolimus was crucial to the success of transplant surgery and for treatment of autoimmune diseases. However, immunosuppressant therapy may increase the concentrations of reactive oxygen species (ROS), inducing oxidative damage such as an increased vascular damage. The major source of ROS in the vascular endothelial cells is NADPH oxidase. The subunit structure and function of this enzyme complex in vascular cells differs from that in phagocytic leucocytes. The enzyme subunits Nox1, Nox2 and Nox4 are only found in vascular cells. The GTP-dependent protein subunit Rac 1 needs to be activated for this enzyme to function. Inhibiting this protein subunit should reduce NADPH oxidase-induced oxidative stress. In the cardiovascular system, oxidative stress is observed as hypertension, hypertrophy, fibrosis, conduction abnormalities and endothelial dysfunction, as well as cardiac allograft vasculopathy in transplant patients. In contrast to cyclosporine and tacrolimus, the immunosuppressant mycophenolate inhibits the Rac 1 subunit thus inhibiting NADPH oxidase in the vasculature. This may reduce oxidative stress, prevent the development of cardiac allograft vasculopathy, decrease the deterioration of vascular function and improve cardiovascular function chronically in transplant patients. This overview discusses whether this antioxidant immunosuppressive property could translate into a more general protective role for mycophenolate in the prevention of cardiovascular disease.

Evaluation of the chronic complications of diabetes in a high fructose diet in rats.

The increasing prevalence of type 2 diabetes is associated with increasing health costs, especially for the treatment of cardiovascular disease. The development of new treatment modalities requires animal models that mimic the range of pathophysiological changes seen in diabetic humans. Dietary fructose intake has been linked to the increase in insulin resistance as part of the metabolic syndrome; fructose-fed rats develop type 2 diabetes. This study has characterized the cardiovascular changes in young adult male Wistar rats fed a 61% fructose diet for 16 weeks. Our results extend the reported changes of hypertension, lipid abnormalities, impaired glucose tolerance and impaired oxidative defense to include ventricular dilatation with hypertrophy and decreased contractile function, together with increased inflammatory cell infiltration into the ventricular myocardium, resulting in excessive collagen deposition and an increased stiffness of the left ventricle. However, endothelial dysfunction, tactile allodynia as a symptom of peripheral neuropathy and retinopathy are not present in these rats, in contrast to the streptozotocin-induced model of type 1 diabetes. Thus, fructose feeding mimics many, but not all, of the symptoms of type 2 diabetes in humans.