View clinical trials related to Insulin Resistance.
Filter by:BACKGROUND The effects of ACE-inhibitors on fibrinolysis are well documented. Experimental and clinical studies have shown that ACE inhibitors induce a reduction in plasma PAI-1 levels in many cardiovascular diseases, like hypertension, coronary heart disease, and heart failure. Their effects on t-PA are more controversial, due to the fact that t-PA exists in several forms, including free and bound to PAI-1. Indeed an increase in t-PA activity has been observed in humans and it seems related to bradykinin increase which is known to stimulate endothelial t-PA synthesis. These favourable effects on fibrinolysis could be related not only to the Angiotensin II reduction and the bradykinin increase but also to the improvement in insulin sensitivity, as insulin has been suggested as one of the main regulators of fibrinolytic activity. To date conflicting results have been reported about the effects of ARBs on fibrinolysis. Some studies have reported small improvements, others no significant effect. These conflicting results may be due to possible methodological bias but a possible pathophysiological explanation might be that receptor subtypes other than AT1 mediate the effect of Angiotensin-II on endothelial PAI-1 expression, i.e. the AT4 receptors, and during AT1 receptor blockade there is an important increase not only of Angiotensin-II, but also of all its catabolites including Angiotensin IV. The dissimilar effects on of ACE Is and ARBs may also depend on their different action on the RAS and their different effect on insulin sensitivity: ACE-Is improve insulin sensitivity, while the majority of ARBs have been reported to have a neutral effect. Moreover, unlike ACE-Is, ARBs do not affect the metabolism of bradykinin, which is known to stimulate t-PA synthesis and release. AIM OF THE STUDY The aim of this study is to verify the effect of imidapril compared to candesartan on insulin sensitivity, evaluated through the euglycemic hyperinsulinemic clamp, and on fibrinolysis, evaluated through the plasma PAI-1 and t-PA activity, in mild to moderate hypertensive patients.
Metabolic syndrome (MS), comprised of central obesity, glucose intolerance, hyperinsulinemia, low HDL-cholesterol (HDL-C), high triglyceride (TG) and hypertension, results in markedly increased risk for cardiovascular disease in the general population. The National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) report recommended the use of five variables for the diagnosis of the MS including waist circumference (WC), serum TG concentration, serum HDL-C concentration, blood pressure and fasting glucose concentration. A waist circumference of 80 cm in women and 90 cm in men would better identify those with the MS in Asian populations. However, the studies of modified asian criteria of metabolic syndrome in hemodialysis (HD) patients are scarce. We will perform prevalence investigation, cross-sectional study, and prospective investigation for metabolic syndrome in our HD patients (around 360 at present). We will enroll all the patients who receive maintenance HD more than three months in our HD center. The patients who are hospitalizing, suffered from active malignancy, active infections, recent cardiovascular events and surgery will be excluded in the beginning of study. Biochemistry and anthropometric parameters including HDL-C, TG, insulin resistance index, high sensitivity C-reactive protein and WC will be collected and analyzed. We will also prospectively establish the mortality and hospitalization indices of these patients, to study the prognosis of HD patient with or without metabolic syndrome. This study will be helpful to understand whether the application of a modified criteria of metabolic syndrome in HD patients is capable to predict cardiovascular events, hospitalization and mortality rates.
Insulin-resistance in type 2 diabetes is associated with chronic inflammation. Anti-inflammatory actions might increase sensitivity to insulin. Since some probiotics have anti-inflammatory properties, ingestion of the probiotic bacteria Lactobacillus Acidophilus NCFM might increase insulin-sensitivity. The inflammatory response to endotoxin injection and the insulin-sensitivity is examined before and after four weeks ingestion of probiotics.
Chronic hepatitis C virus (HCV) infection is associated with an increased risk for the development of type 2 diabetes and HCV infection itself may promote insulin resistance, irrespective of the severity of liver disease. Insulin resistance seems to be genotype specific and may play a role in fibrogenesis in chronic hepatitis C. In an “in vitro” model, increased levels of insulin may promote increased HCV replication. RATIONALE Decreased insulin resistance and reduced hyperinsulinemia may facilitate the efficacy of anti-viral drugs on HCV replication.
The purpose of this study is to directly compare the body composition, body fat distribution, and morphological and functional features of adipose tissue and skeletal muscle between South Asians and European Caucasians.
The literature suggests that there may be an association between hepatitis C and type 2 diabetes mellitus independent of the presence of cirrhosis, the likely mechanism for which is insulin resistance. The prevalence of insulin resistance in patients with hepatitis C is unknown. Furthermore, there are no studies that indicate an increased prevalence of insulin resistance in patients with hepatitis C compared to other etiologies of liver disease. The role that hepatitis C may have in the development of insulin resistance is unclear. The effect of antiviral therapy for hepatitis C virus on insulin resistance has not been addressed. The long-term consequence of insulin resistance is type 2 diabetes mellitus. There is significant morbidity and mortality from type 2 diabetes mellitus in the general population, and similar complications would be expected in patients with hepatitis C and insulin resistance particularly if they develop type 2 diabetes mellitus. Our hypothesis: The prevalence of insulin resistance is increased in patients with chronic hepatitis C compared to chronic hepatitis B. Secondarily, insulin resistance when present in patients with chronic hepatitis C improves with successful antiviral therapy. This study has two phases. The first phase of our study will be to estimate the prevalence of insulin resistance in individuals with chronic hepatitis C without cirrhosis compared to patients with chronic hepatitis B without cirrhosis. The second phase of the study will be restricted to those patients with hepatitis C found to be insulin resistant from phase 1, in the absence of known risk factors for insulin resistance (cirrhosis, diabetes). The effect on insulin resistance of anti-viral therapy to eradicate hepatitis C will be assessed.
Approximately 1/4 of the US population has insulin resistance and the associated risk factors such as elevated lipid levels -triglycerides (type of fat from what we eat and what the liver produces and low HDL cholesterol which is the good cholesterol helping to protect against heart disease. Currently one known treatment for this a medication called fenofibrate, another medication that can improve insulin resistance is rosiglitazone, a third treatment known to improve insulin resistance an decrease triglycerides is weight loss. In this study insulin resistant individuals with elevated triglycerides and or a ratio of triglycerides to HDL cholesterol of 3:1 or greater will be randomized (selected by chance) to receive one of these treatments and results of insulin sensitivity and cardiac risk profiles will be compared at the end of the study.
Primary aldosteronism (PA) is occasionally associated with impaired glucose tolerance. Glucose intolerance, in general metabolic syndrome is caused by suppression of insulin release from the pancreas and suppression of insulin sensitivity of the target tissues. Several studies have suggested that impaired glucose tolerance in primary aldosteronism is due to an inability of the beta cells to release insulin by potassium depletion. It was suggested glucose intolerance in PA is caused by the suppression of insulin release related to hypopotassemia and compensatory increase of insulin sensitivity is observed in PA. The increased insulin secretory capacity associated with correction of negative potassium balance may account for the increase in plasma leptin after curing primary aldosteronism. The conclusion with respect to the possible causal relationship between diabetes mellitus (DM) and PA, however, can be obtained after the evaluation of the effect of surgical /pharmacological treatment of PA.
Polycystic ovary syndrome (PCOS) phenotype can be structured into three components: anovulation, hyperandrogenism and the metabolic syndrome (of which hyperinsulinemia, secondary to insulin resistance, is the central abnormality)(1). It is the most common endocrinologic disease seen in Gynecologic clinic. The follicular excess in polycystic ovaries and the failure of selection of one dominant follicle contribute to the anovulation of PCOS. The infertile PCOS female usually suffered from difficult ovulation induction and high risk of ovarian hyperstimulation syndrome because of extensive stimulation. PCOS is the main androgen disorder in women and has been suggested to be associated with a high risk of developing cardiovascular disease and type-2 diabetes. In many PCOS patients, overweight or central obesity is generally associated with increases in fasting insulin levels, insulin resistance, and glucose intolerance, and has been identified as a target for new therapeutic strategy, including early change in lifestyle. Insulin resistance, defined as decreased insulin-mediated glucose utilization, is commonly (10-25%) found in the normal population. In women with PCOS, insulin resistance appears even more common (up to 50%), in both obese and non-obese women.Hyperinsulinemia appears to play a key pathogenic role in the ovarian androgen overproduction, because of the stimulatory effect of insulin on ovarian steroid production.
Insulin resistance and disturbances in energy homeostasis are associated with body weight changes, such as diabetes, hypertension, hyperlipidemia, obesity, cancer cachexia, aging, and acute or chronic infectious diseases. Cytokines secreted by adipose tissue and inflammatory cells play important roles in the pathological conditions. Several novel cytokines were disclosed recently, but their functions have not been well known. Further investigation of these cytokines, resulting in insulin resistance and energy homeostasis, is very important to elucidate the mechanisms and develop new therapeutic strategies.