Active clinical trials for "Insulin Resistance"

The discovery that the vitamin D receptor is expressed in more than 30 tissues indicates that the physiologic functions of vitamin D are much broader than its well-known role in the regulation of calcium absorption and bone metabolism. There is evidence that vitamin D is involved in the pathogenesis of cancer, cardiovascular disease, multiple sclerosis, and type I diabetes. Recent epidemiological evidence points to a strong association between vitamin D insufficiency and insulin resistance, the metabolic syndrome, and type II diabetes. The investigators would like to examine the role of vitamin D in the development of insulin resistance in overweight children and adolescents, which represent a high risk population for cardiovascular and metabolic complications. The investigators propose a prospective randomized clinical trial of vitamin D supplementation in overweight, insulin resistant, vitamin D deficient children. The investigators objective is to assess if changes in insulin resistance, fasting lipid profiles, blood pressure, and inflammatory markers occur in these patients post treatment with vitamin D. Additionally, concomitant changes in calcium and bone metabolism after vitamin D treatment will be evaluated. This is because, contrary to adults, the optimal vitamin D concentrations that regulate calcium and bone metabolism have not been established in pediatrics.

Insulin resistance and a defect in early insulin secretion are risk factors for the development of type 2 diabetes mellitus. A recent longitudinal analysis which tracked the development of diabetes demonstrated that both insulin action and early insulin secretion deteriorate as individuals progress from normal to impaired glucose tolerance and then to diabetes. These results suggest that both inherent (apparent in normal glucose tolerant subjects who progress to diabetes and likely to have a genetic basis) and acquired (evident as individuals progress from NGT to IGT to diabetes and possibly environmental in origin) defects in insulin action and secretion contribute to the pathogenesis of type 2 diabetes. To identify the genetic and environmental determinants of diabetes we are continuing to determine: (1) if there are genes that segregate with metabolic risk factors for diabetes which might therefore be genetic markers for type 2 diabetes and (2) the mechanisms mediating genetic and environmental determinants of insulin resistance and impaired insulin secretion. <TAB> Volunteers for this study will be admitted to the clinical research ward where they will undergo several tests to determine body composition, oral and intravenous glucose tolerance and in vivo insulin action. In addition, in selected subjects, adipose and/or skeletal muscle tissue will be obtained by percutaneous biopsy for in vitro studies of gene expression and insulin action in these tissues. A transformed lymphocyte cell line will be established for each subject as a permanent source of DNA for genetic studies. Genetic markers for type 2 diabetes and insulin resistance will be sought by typing each individual at positional and functional candidate loci in the hopes of finding an association between these loci and obesity, insulin secretion, insulin resistance and/or type 2 diabetes.

Obesity is a strong risk factor for developing type 2 diabetes (T2DM), but the reasons for this are not fully understood. In particular, it is not known why some obese people develop T2DM while other obese individuals do not. This study tests whether differences in fat cells (adipocytes) are to blame. Even in adults, fat cells are constantly being formed to replace old fat cells and to respond to the body's need to store excess energy. The ability to form new fat cells may be diminished in some individuals, leading to larger fat cells. These large fat cells secrete hormones that may increase risk for T2DM. This study tests whether fat cells from obese insulin resistant subjects (who are at risk for developing T2DM) form at a slower rate than those from insulin sensitive subjects (who are at lower risk for developing T2DM). To address this question we will recruit and study two groups of obese subjects, selected to be similar in age, gender and degree of obesity. One group of subjects will be obese and insulin resistant (the OIR group), while the other will be comparably obese, but insulin sensitive (OIS). Subjects will undergo a series of studies to characterize their metabolism including measurement of body fat by DEXA scanning, oral glucose tolerance (a test used to diagnose diabetes) and measurement of insulin sensitivity in response to an infusion of insulin (a research study used to classify patients into the OIR and OIS groups). Small samples of fat (from just under the skin of the belly and the buttocks) will obtained using a needle on two occasions over 12 weeks. During these 12 weeks, subjects will drink a small amount of water that contains a non-radioactive label. This labeled water will allow us to measure the rate of growth of new fat cells in the body. We will also look at the rate of growth of fat cells obtained from these biopsies in the laboratory. The results of this study may tell us more about why certain obese people develop diabetes and why others do not. This might lead to new ways to prevent or treat T2DM.

The purpose of this study is to identify risks that may contribute to increased insulin resistance which may help explain some of the increased incidence of type 2 diabetes in American Indian Youth, at the Rosebud reservation ages 5 to 18 years old. If specific positive indicators of insulin resistance are present, individuals are recruited back in one year for repeat of all measures.

Prolactin is suggested to influence insulin resistance, but scarce data is available on the metabolic profile of patients with prolactinoma. The purpose of the protocol was to evaluate cardiovascular disease risk factors in women with prolactinoma treated with dopamine agonists and to study the influence of disease control and anthropometry on their metabolic profile.

To determine the role of insulin resistance in peripheral vascular dynamics, sodium sensitivity, and blood pressure regulation in a young representative Black population and in a group of young Blacks at high risk for hypertension.

Familial Partial Lipodystrophy type 2 (FPLD2) is a heterogeneous group of rare lipodystrophy due to autosomal dominant mutation in LMNA encoding Lamin A/C. Lamins A and C form with the B-type lamins the lamina network underlying the nuclear envelope. Lamins are major components that provide structural and mechanical stability for the nucleus ubiquitously. Lamins are also key epigenetic regulator. Mutations in LMNA are involved in different inherited pathologies as Emery-Dreifuss muscular Dystrophy, Limb Girdle muscular dystrophy, dilated cardiomyopathy and conduction system disease, Charcot Marie Tooth Disorder type 2, mandibuloacral dysplasia, Hutchinson Gilford progeria and Dunnigan-type-familial partial lipodystrophy (FPLD2). Inherited lipodystrophy prevalence is reported around 1.3 to 10 cases per million worldwide and FPLD2 is the most frequent of all. Nevertheless, recent reports with systematic screening in all non-obese patients with type 2 diabetes or metabolic syndrome found higher prevalence of lipodystrophy up to 1/7000 subjects. FPLD2 remain a rare group of disease and only relatively small and heterogeneous cohorts of patients are reported. For this reason it is difficult to fully decipher all aspects of this rare group of diseases. The "typical" FPLD2 is associated with missense mutation affecting the arginin residue in position 482 (p.R482Q,p.R482W,p.R482L). Patients harbouring mutation in other spot are considered to have "atypical" lipodystrophy. The "typical" FPLD2 start around puberty with progressive subcutaneous fat loss in upper limbs, gluteo-femoral adipose tissue and trunk and fat accumulation in the cervicofacial area, neck, upper trunk, labia majora and visceral fat. Resulting from the inability to store fat, patients affected by inherited lipodystrophy develop severe metabolic syndrome and its complications: type 2 diabetes (DT2), dyslipidaemia, nonalcoholic fatty liver disease (NAFLD) and premature cardiovascular disease (CVD). In 2006 a specific mutation of LMNA has been described in a patient originated from La Réunion living in France mainland. To date this mutation have only been reported in patient native from La Réunion and is called 'Reunionese' mutation and consist in a G insertion after nucleotide 5670 (codon 654) in the prelamin-A-specific exon 11 (g.5670_5671insG) p.T655fsX49 that lead to a longer and non farnelysated prelamin A lacking the C-terminal CSIM motif. As a result, nonfarnelysated mutated prelamin A accumulated in the cells leading to oxidative stress and premature cell senescence. The 'Reunionese' mutation is expressed in 2 forms either homozygous or heterozygous. Homozygous patients present with more severe phenotype and cardiac laminopathy. The aim of our study is to update the characterization of the patients diagnosed with the 'Reunionese' mutation. The investigators report here the largest cohort of patient with FPLD2 due to one single LMNA mutation either homozygous or heterozygous.

Recently, an index based on the oral insulin sensitivity index with glucose (OGIS) has been proposed in combination with anthropometric variables, called PREDIcted M (PREDIM), however, there is no evidence of the correlation of this with respect to the various indices (McAuley, Belfiore, Cederholm, Avignon, Matsuda, Gutt, Stumvoll, HOMA-IR (Homeostatic Model Assessment for Insulin Resistance), ISI (Insulin Sensitivity Index), Raynaud, QUICKI (The quantitative insulin sensitivity check index), FIRI (Fasting Insulin Resistance Index), Bennett, TyG (triglycerides and glucose index)) in healthy patients.

This study intends to assess the role of inflammation in insulin resistant conditions (i.e., obesity and pre-diabetes) and the subsequent development of disease, such as type 2 diabetes (T2D) and cardiovascular disease (CVD), in the adolescent population.

Patients with type 1 diabetes (T1D) and metabolic syndrome (MS) require high doses of insulin to achieve a glycemic control, due to insulin resistance (IR). The investigators identified the presence of metabolic syndrome and insulin resistance in patients with T1D in a population of southeast Mexico. The sampled population was recruited from the Diabetes Clinic of the Regional Hospital of High Specialty "Dr. Gustavo A. Rovirosa Pérez"; from August 2021 to February 2022, graduated physicians interviewed patients previously diagnosed with T1D. This study included patients older than 18 years and at least six months after being diagnosed with T1D. The interviewers excluded patients who did not attend regular consultations and those who did not agree to participate or to give a blood sample. A diabetologist evaluated and diagnosed all patients based on the World Health Organization (WHO) criteria. Fasting glucose, total cholesterol, HDL cholesterol, LDL cholesterol, and triacylglycerols were determined in blood serum using a Clinical Chemistry System from Random Access Diagnostics. The reasearch team determined glycated hemoglobin concentrations by an enzymatic immunoassay method.