View clinical trials related to Prediabetic State.
Filter by:Ezetimibe specifically blocks the absorption of dietary and biliary cholesterol and plant sterols. Synergism of ezetimibe-statin therapy on LDL-cholesterol has been demonstrated, but data concerning the pleiotropic effects of this combination are controversial. We tested the hypothesis that the combination of simvastatin and ezetimibe would induce improvement in inflammatory status, as reflected by leukocyte count and CRP, IL-6 and TNF-a levels. This open-label trial evaluated whether this combination results in a synergistic effect the pro-inflammatory status of pre-diabetic subjects. Fifty pre-diabetic subjects were randomly assigned to one of 2 groups, one receiving ezetimibe (10 mg/d), the other, simvastatin (20 mg/d) for 12 weeks, followed by an additional 12-week period of combined therapy.
The purpose of this study is to determine if, in a subset of patients treated with a beta-blocker and diuretic, prediabetes is detectable to a greater extent through a 2-hour oral glucose tolerance test (OGTT) compared to fasting glucose measurement.
The purpose of this study is to investigate the feasibility of using salivary biomarkers to screen for complications of metabolic syndrome including prediabetes.
To determine whether treatment with the diabetes medication, Januvia (sitagliptin), with or without another diabetes medicine, Actos (pioglitazone), will improve insulin secretion and insulin response individuals with Impaired Glucose Tolerance (IGT), a form of prediabetes.
The purpose of this study is to compare the effectiveness of a peer-led community-based lifestyle intervention, versus usual care, in achieving weight loss and prevention of diabetes among overweight adults with pre-diabetes in East Harlem.
This study will evaluate the effect of ACZ885 on vascular function in patients with documented atherosclerotic disease and T2DM or IGT.
The objective of this study is to determine the effect of 8 weeks of treatment with colesevelam HCl 3.75 g once daily with the evening meal on ß-cell function by evaluating the acute insulin response (AIRg) to an intravenous glucose load in subjects with prediabetes (impaired fasting glucose).
The primary objective of the study is to identify baseline and early predictors of favorable and unfavorable response to lifestyle intervention. As a secondary objective, the investigators would like to validate our questionnaire or other identified predictors as clinical tools to guide us in selection of the most suitable candidates for lifestyle intervention programs. Assuming the same capacity of our questionnaire to predict an absence of weight loss (≥5%) or a loss to follow-up (likelihood ratio for a positive test, LR+ = 9.9), 70 subjects need to be included in this study in order to find a lower limit of the 95% confidence interval above 2.0 for this LR+, which is the limit of an acceptable test. The investigators will enroll participants with pre-diabetes and BMI 27-40 in our program and administer to them at baseline and at 3 months the designed questionnaire, as well as other already well validated questionnaires assessing state of change and readiness to implement diet or exercise modifications.
Acute systemic hyperglycemia causes oxidative stress and a pro-inflammatory response. The pro-inflammatory cytokines induced by hyperglycemia are toxic to islet insulin producing cells, and thus worsen glucose intolerance. Patients with cystic fibrosis (CF) have a high prevalence of CF related diabetes (CFRD) and up to 40% of CF adults develop CFRD. During the prediabetic phase in CF, there is progression from normal glucose homeostasis to high risk prediabetes characterized by episodes of acute hyperglycemia after meals and during respiratory exacerbations. The mild hyperglycemia seen in CF patients with high risk prediabetes following a meal would be expected to induce a degree of systemic inflammation and oxidative stress. These repetitive episodes, if left unchecked, could lead to progression of glucose impairment, worsening severity of oxidative stress and inflammation, and ultimately the development of CFRD, all via hyperglycemia-induced toxicity to beta cells. Furthermore, this process may be accelerated in CF because lung disease and resultant respiratory exacerbations are associated with oxidative stress and inflammation and this will further contribute to beta cell damage. Sitagliptin is a recently approved agent for type 2 diabetes and markedly enhances insulin secretion in the presence of hyperglycemia and has been shown to be effective in preventing postprandial hyperglycemia. The hypothesis to be tested in this project is that sitagliptin will prevent the development of CFRD in CF subjects with high risk prediabetes by blocking postprandial hyperglycemia. The investigators propose a randomized, double-blind, placebo-controlled, multicenter, 15-month longitudinal study in 118 CF subjects with high risk prediabetes to test this hypothesis. Specifically, the investigators aim to show that chronic treatment with sitagliptin: prevents the conversion to diabetes; results in preservation of beta cell function; reduces systemic measures of oxidative stress and inflammation; and slows the rate of progression of lung disease. Funding Source - FDA Office of Orphan Products Development
The purpose of this study is to test whether vitamin K supplementation has an effect on glucose metabolism in terms of acute beta cell response.