View clinical trials related to Insulin Resistance Syndrome X.
Filter by:Magnesium is an essential mineral found in many foods; rich sources include whole grains, green leafy vegetables, coffee, and legumes. Magnesium is a critical cofactor in >300 enzymatic reactions, including those related to energy metabolism. Reduced magnesium intake and serum concentrations have been detected, both cross-sectionally and prospectively,in type 2 diabetes and insulin resistance, hypertension, dyslipidemia, and cardiovascular diseases. Different studies have reported inadequate magnesium intake and low serum magnesium concentrations may correlated also with metabolic syndrome, defined as a cluster of metabolic disorders including obesity, hypertension, dyslipidemia and impaired glucose tolerance or diabetes mellitus. Previous studies on this subject, however, reported contradicting results. Some investigations reported inadequate magnesium intake and low serum magnesium concentrations while others did not. To our knowledge, the epidemiological evidence on the relation between dietary magnesium intake and risk of metabolic syndrome has not yet been summarized.Therefore, the investigators will perform a systematic review and dose-response meta-analysis to assess the association between dietary and circulating magnesium level and risk of metabolic syndrome.
A prolonged elevation of plasma free fatty acids (FFA) impairs glucose stimulated insulin secretion. The concept of fatty acid impairment of glucose stimulated insulin secretion (lipotoxicity) has now been well accepted. Increased free fatty acid flux from adipose tissue to non-adipose tissue, resulting from abnormalities of fat metabolism, participates in and amplifies many of the metabolic derangements that are characteristic of insulin resistance syndrome and type 2 diabetes. Lipotoxicity is also likely to play an important role in the progression from normal glucose tolerance to fasting hyperglycemia and conversion to frank type 2 diabetes in insulin resistant individuals. This area of research is now focused on determining the mechanisms whereby FFAs impair b-cell function. There is some evidence to suggest that lipotoxicity could be mediated through induction of reactive oxygen species (ROS). N-acetylcysteine (NAC) is a known potent antioxidant and has been used experimentally in a number of medical conditions in humans for its protective antioxidant effects. The investigators now plan to administer NAC orally to humans for 48 hours to examine the effects of antioxidant therapy in ameliorating the deleterious effects of FFAs on pancreatic beta cell function. NAC is currently approved for the treatment of acetaminophen overdose and is also used as a mucolytic agent. The investigators are now using NAC as an antioxidant to determine whether it protects the pancreatic beta cell against the toxic effects of FFAs, as outlined in the detailed study protocol. This is a proof-of-principle study and is not designed to develop n-acetylcysteine for therapeutic use.