Active clinical trials for "Insulin Resistance"

A PRoBE design study will be used to obtain saliva from patients before undergoing blood study evaluation for screening at risk patients for the presence of undiagnosed pre-diabetes of type II diabetes. Pre-specified saliva biomarkers will be evaluated along with multi-marker models for their discriminatory value for distinguishing patients with normal glucose metabolism from those with disease. Appropriate housekeeping genes will also be incorporated to allow for the measurement of relative gene expression.

The study tests the hypothesis that correction of vitamin D deficiency among women with PCOS will improve insulin sensitivity and resistance and inflammatory response to PCOS.

The aim of this study is to explore whether and how high circulating levels of endothelin-1 (ET-1) in obese and overweight children may contribute to impair adiponectin (Ad) production, release and vascular activity

The prevalence of pediatric obesity is increasing at an unprecedented rate. Obese children are at risk for the development of insulin resistance, relative insulin deficiency and type 2 diabetes mellitus. However, the cause of insulin resistance remains an area of scientific interest. The study of type 2 diabetes in children is limited by the lack of a non-invasive method to evaluate insulin resistance. Recent studies have suggested that mitochondrial dysfunction is associated with, and perhaps predictive of insulin resistance in adult relatives of individuals with type 2 diabetes. Mitochondria generate energy in muscle tissue through the production of ATP, and are important in the metabolism of both glucose and fat. This study evaluates a novel, non invasive, safe method for predicting insulin resistance and diabetes in children using a magnetic resonance imaging (MRI) based technique to measure mitochondrial function. We propose to investigate mitochondrial function and glucose metabolism in obese and non-obese children in early, mid and late puberty. Analyses will be conducted to investigate the presence of mitochondrial dysfunction in obese children, to evaluate the contribution of mitochondrial dysfunction to insulin resistance, and to determine the contribution of pubertal status to mitochondrial dysfunction and insulin resistance. The successful completion of this study would provide evidence to support the hypothesis that mitochondrial dysfunction plays a role in insulin resistance and diabetes in children. In addition, it would provide a new technique for the prediction of disease states and perhaps lead to the development of preventative therapeutics for insulin resistance and type 2 diabetes in children. We hypothesize that mitochondrial dysfunction will mirror the progression of insulin resistance and precede and predict abnormal glucose metabolism in a population with pediatric obesity

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.

In the UK, 25% of the adults are affected by metabolic syndrome (NHS, 2016). Metabolic syndrome is a cluster of different conditions including: hyperglycaemia, insulin resistance hypertriglyceridemia, dyslipidaemia and hypertension. Such individuals also have increased risk of developing type 2 diabetes and cardiovascular disease. The factors contributing to the development of metabolic syndrome are potentially numerous and understudied in humans, with much of what we think we know coming from animal research. Recent animal studies have pointed towards gut health playing a role in metabolic health. More specifically it has been suggested that changes in the composition of the gut microbiota may drive insulin resistance and type 2 diabetes through a mechanism that is linked to increased gut permeability and the development of metabolic endotoxemia and inflammation. Yet, this link has not been confirmed in humans. This research will look at the relationship between diet, physical activity, sleeping patterns, obesity status and age etc. and measures of gut bacterial composition, gut barrier function and metabolic health. Findings will provide us with new insights on the effect of different physiological and behavioural/ lifestyle variables on gut health and metabolic function.

The hepatitis C virus is a major cause of chronic liver diseases, including cirrhosis and hepatocellular carcinoma, and infects approximately 3 % of the world population (150-170 million). It is estimated that approximately 80 % of patients with acute hepatitis C fail to eliminate the virus and become chronically infected Hepatitis C virus infection is strongly associated with the dysregulation of glucose homoeostasis such as insulin resistance and type 2 diabetes. Despite these findings of insulin resistance development via direct effects on insulin signalling pathway, the complex relationship between intrahepatic Hepatitis C virus infection and extrahepatic insulin resistance remains elusive. One of the countries most affected by Hepatitis C virus is Egypt. The Egyptian Demographic and Health Surveys measured antibody prevalence among the adult population aged 15-59 years at 10.0% in 2015-substantially higher than global levels. Several micro ribonucleic acids have been determined to play a key role in regulating viral replication and pathogenesis during infection. micro ribonucleic acid-122 expression is enriched in the liver, accounting for approximately 70 % of the total micro ribonucleic acid population in normal adult hepatocytes. Moreover, a particularly intriguing function of micro ribonucleic acid-122 involves its role in the Hepatitis C virus replication cycle. Antagonism of micro ribonucleic acid-122 not only reduces viral replication but also reduces Hepatitis C virus propagation by decreasing the expression of enzymes involved in lipid metabolism, which can enhance Hepatitis C virus replication in cell culture models.

Background Fetuin A, synthesized in hepatocyte, is a circulatory inhibitor of precipitation of calcium and phosphate and links to cardiovascular calcification and mortality in dialysis patients; besides, it is associated with insulin resistance in general population. Hepatic fat accumulation enhanced fetuin A secretion in animal model. Objects This study is designed to investigate the association of fetuin A level, insulin resistance and hepatic fat content in dialysis patients. Besides, we planed to observe the survival of dialysis patient with different hepatic fat content. Methods. This is a prospective observational study. Three hundred and fifty ESRD patients undergoing maintenance HD or PD will be recruited for this prospective investigation. All the participants will receive baseline abdominal ultrasound for estimation of hepatic fat content. Hepatic fat content will be estimated as minimal, mild, moderate or severe according to the Hepburn classification. Besides, all participants also check baseline fetuin A, HOMA-IR, hs-CRP, adiponectin, leptin and lipid profiles (T-CHO, TG, LDL-C, HDL-C), nutritional parameter and other biochemical parameters. All participants will be followed for 4 years for survival analysis. The outcomes are all-cause mortality and composite CV mortality. Expected results Dialysis patients with higher hepatic fat may have higher fetuin A levels which may lead to long-term survival benefits.

FPCOS is associated with an adverse cardiometabolic profile, consisting of increased total or central adiposity, increased insulin resistance and abnormal glucose metabolism. Low-grade chronic inflammation predicts cardiovascular outcomes and is observed in women with PCOS. However, obesity is also associated with increased inflammatory markers. Obesity is per se associated with increased adipose expression and plasma levels of leptin, lower expression of adiponectin, and elevated inflammatory markers. To study the insulin resistance、inflammatory markers and cardiovascular risk in women with PCOS, body weight status should be considered. Investigator therefore conduct this retrospective study to evaluate the insulin resistance、inflammatory and cardiovascular markers between PCOS and non-PCOS among obese and non-obese women.

This study includes 2 phases. During phase 1, pregnant women are followed over the course of pregnancy. The phase 2 is a follow-up of the mother-child dyad at 3 and 5 year after delivery. The purpose of this phase 1 is to : assess the contribution and interactions of adipokines in the development of insulin resistance during pregnancy and gestational diabetes; assess levels of maternal adipokines as determinants of development and fetal growth; determine the genetic variations that influence levels of adipokines and glucose regulation during pregnancy and in newborns. The purpose of this phase 2 is to: identify DNA methylation variations at birth that are predictive of childhood overweight/obesity. identify maternal characteristics associated with DNA methylation variations predictive of childhood overweight/obesity. establish whether the loci predictive of childhood overweight/obesity at birth are still differentially methylated at 5 years of age (samples collected at 5 years of age). identify DNA methylation variations at birth that are predictive of childhood neurodevelopment problems at 3 and 5 years of age.