View clinical trials related to Metabolic Syndrome X.
Filter by:A short term post-market monitoring of serum prolactin level change among patients with schizophrenia shifting from other antispychotics to different dosages of aripiprazole.
The metabolic risks associated with obesity are closely correlated with central (abdominal), rather than a peripheral (gluteofemoral) fat pattern It has been shown that weight loss after bariatric surgery is followed by metabolic improvements. The amount of fat lost from each site may be independently regulated. Very scant information is found in the literature regarding the relative changes in different fat body compartments, and their effect on the improvement of the metabolic profile. In this study we define the absolute and relative changes in the different adipose tissue compartment after weight loss surgery
An abdominal distribution of fat is associated with the greatest heart disease risk, because commonly, several risk factors of metabolic origin cluster in these individuals. When this occurs the condition is called the 'metabolic syndrome'. Increased activity of the sympathetic nervous system resulting in enhanced release of the stress hormone 'noradrenaline', may be one mechanism by which adverse cardiovascular and metabolic sequela of the metabolic syndrome might be mediated. Impaired insulin action may be one factor contributing to increased noradrenaline release. The aim of this Study is to determine whether treatment with a drug called pioglitazone which is known to improve insulin action, results in reduced sympathetic nervous system activity and stress hormone release when compared to treatment with a dummy drug (placebo).
The metabolic syndrome is a highly prevalent disorder, which causes atherosclerotic cardiovascular disease and is closely associated with insulin resistance. The alteration of the secretion of adipocytokines from accumulated visceral adipose tissue in the obese induces insulin resistance. The purpose of this study is to identify gene polymorphisms that confer susceptibility to the metabolic syndrome and to make up a new health guidance program based on genetic risk assessment. About 25% of male employees over 45 years old in a certain company are diagnosed with the metabolic syndrome in medical examination. We, the researchers at Nagoya University, will analyze gene polymorphism and various biomarkers of over 3500 company employees.
Non-alcoholic fatty liver disease (NAFLD) is now recognised as the hepatic complication of the metabolic syndrome of insulin resistance. In some patients, the disease can progress into steatohepatitis (NASH) which associates fatty liver, hepatocellular damage, chronic inflammation and variable and progressive fibrosis. The latter can evolve into cirrhosis and end-stage liver disease. Thus the presence of fibrosis sign the severity of the disease, and therefore its accurate detection is crucial for the identification of patients in need of treatment and appropriate follow-up. To date, histological examination of a biopsy of the liver is the gold standard in the diagnosis of fibrosis. the procedure is however associated with significant complication in 0.01 to 0.1% of cases and with sampling errors because it analyses only a minimal portion fo the liver. The aim of the study is to evaluate, in a population of patients with the metabolic syndrome, whether non-invasive tests may identify those with hepatic fibrosis. At inclusion, serum tests, fibroscan (elastography of the liver by ultra-sounds) and elastography by MRI will be performed. Those tests will be repeated within 2 months. A liver biopsy will be performed if 2 out of the 3 (serum test, fibroscan or elastography) tests are suggestive of hepatic fibrosis. This study will allow to determine - whether hepatic fibrosis may be detected by non-invasive means in patients with NAFLD/NASH. - whether there is a correlation between non-invase tests and liver biopsy for assessment of fibrosis and it severity - whether the presence of fatty liver interfere with the results of the fibroscan and the elastography. - whether there are metabolic factors associated with an increased risk of fibrosis in this population.
The secondary objective is to evaluate the agreement between these criteria and the prevalence of concordant and discordant according to different criteria.
- Aim 1: We will test our primary hypothesis that combining niacin extended release (niacin-ER), at a daily dosage of up to 2.0 g with pioglitazone, at a daily dosage of 45 mg will result in a 12% greater increase in HDL-C when compared to niacin-ER monotherapy over 12 weeks in non-diabetic patients with the metabolic syndrome (see Table 1). - Aim 2: In this secondary aim, we will test our hypothesis that the combination of niacin-ER and pioglitazone will significantly increase insulin sensitivity, when compared to niacin-ER alone, as measured by the frequently sampled intravenous glucose tolerance test (FSIGTT). - Aim 3: In this additional secondary aim, we will test our hypothesis that the combination of pioglitazone and niacin-ER will reduce markers of inflammation, including C-reactive protein (CRP), interleukin-6 (IL-6), soluble tumor necrosis factor alpha receptor type II (sTNF--R2), and resistin, and raise adiponectin when compared to niacin-ER alone. - Aim 4: In this exploratory aim, we will measure a broad spectrum of emerging cardiovascular risk factors in order to derive a richer sense of the effects of combination pioglitazone and niacin-ER in these individuals. We will collect adipose tissue level expression (mRNA & protein) relating to cholesterol transport (PPAR-, PPAR-, and PPAR-, ABCA1, ABCG1, and SR-B1), triglyceride transport/lipolysis (HM74a, HSL), adipocytokines (TNF-a, IL-6, adiponectin, leptin, acylation-stimulating protein), and glucose regulation (glut-4 and IRS-1). [assuming sufficient mRNA yield]. These findings will serve as hypothesis-generating data for future studies..
Diabetes is prevalent in schizophrenics and may be induced by antipsychotic treatments. Several retrospective studies have suggested that psychiatric patients exposed to atypical antipsychotics may be at a higher risk for developing diabetes and ketoacidosis. The association between these atypical antipsychotics and the onset of diabetes is further strengthened by observations of: 1. the time sequence between the initiation of antipsychotic treatment and the onset of diabetes; 2. remission after the discontinuation of medications; and 3. re-emergence of diabetes following the re-introduction of atypical antipsychotics. The treatment emergent diabetes, along with other metabolic disturbances, represents a serious issue in the use of atypical antipsychotics. Major current debates and unresolved research issues which are also the focus of this proposal, are: 1. schizophrenia per se, versus the use of antipsychotics, in triggering diabetes; 2. whether there are differences between "typicals" and "atypicals" in such an effect; 3. whether there are differences among different "atypicals"; 4. whether, and to what extent, treatment emergent diabetes may be associated with, or independent of, weight gain, which also often is associated with the use of antipsychotics; and 5. genetic and environmental risks in association with treatment emergent diabetes. The policy of some hospitals in Taiwan that discourages the use of atypical antipsychotics for new onset schizophrenia directs the investigators to a study design looking at the associated diabetes of both types of antipsychotics. Such a design may provide some hints to the unresolved research issues mentioned above. Meanwhile, a broader defined term, X-syndrome, or metabolic syndrome, is being used to describe the diabetic condition associated with antipsychotics. X-syndrome is a risky condition leading to cardiovascular diseases and diabetes, with insulin resistance as the major outcome, associated with two of the following conditions: truncal obesity (deposited in the thorax and abdomen, instead of the hips and thighs), high triglycerides, high low-density lipoprotein (LDL) cholesterol or hypertension. The proposed study will combine the phenotypes of diabetes and X-syndrome to explore the abnormal metabolism caused by antipsychotics, bridge important information gaps, and provide data contributing towards a better understanding of the risk and management of diabetes and X-syndrome associated with the use of antipsychotics. Three assessment tools, namely the Clinical Global Severity (Clinical Global Impressions - Severity) or the Positive and Negative Symptom Scale (PANNS), the Diabetes Risk Assessment (ADA) and the Life Style Survey, together with physical measurements, collect additional information for this study. Diabetes related biochemistry, including glucose, insulin, leptin, lipids and glycohemoglobin, will be measured to form a composite phenotype for further pharmacogenetic studies. Candidate genes involved in pancreatic beta cell insulin secretion will be examined in priority to see if they play a role in the development of the antipsychotics-induced diabetes.
The purpose of this study is to define the mechanism(s) through which Obstructive Sleep Apnea/Hypopnea (OSAH) promotes abnormal metabolic processes which characterize the metabolic syndrome. The investigators hypothesize that the sleep fragmentation and intermittent sleep hypoxia which occur in OSAH patients promote oxidative stress and inflammation which in turn lead to insulin resistance, dyslipidemia, abnormal vascular reactivity and other processes which are consistent with the metabolic syndrome.
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.