View clinical trials related to Lipodystrophy.
Filter by:The objective of this work is to identify biomarkers of interest in patients with insulin resistance leading to early disorders of glycemic regulation. For this the investigators want to assay the insulin resistance marker Insulin Regulated Amino Peptidase serique (IRAPs), the plasma lipidome and inflammation markers in 2 populations of insulin-resistant subjects due to Dunnigan's inherited lipodystrophy or overweight/obesity and insulin-sensitive subjects with or without a glycemic regulation disorder objectified during an Oral induced hyperglycemia. The results of the IRAPs, lipidome and inflammation assays will be compared in insulin-resistant subjects, between normoglycemic, prediabetic and diabetic subjects. Correlations will be made between these markers and the deterioration of glycemic regulation as well as with known insulin resistance parameters (HOmeostasis Assessment Model (HOMA), Quantitative Insulin-sensitivity Check Index (QUICKI),Insulin Sensitivity Index (Isi) MATSUDA).
The aim of the study is to compare the hemodynamic parameters of fluid resuscitation using Rohrich formula to cardiometry guided stroke volume variation in patients undergoing large volume liposuction surgery .
The Visceral Adiposity Measurement and Observation Study
The Research Question of the present study is the following: in a population of men and women presenting facial and neck dermal tissue defects (scars, hypertrophic scars, depressed plaques, and lipodystrophy defects) will linear hyaluronic acid (Jalucomplex®) significantly decrease and / or improve their appearance, results observed after 4 and 8 weeks?
The Research Question of the present study is the following: in a population of men and women presenting facial dermal tissue defects (scars, depressed plaques, and lipodystrophy defects) will cross-linked hyaluronic acid (Janesse®) significantly decrease and / or improve the appearance of these defects, results observed after 4, 8 and 12 weeks?
Two cohorts are being studied based on leptin levels. Cohort A is composed of patients with baseline leptin <8.0 ng/mL and Cohort B is composed of patients with baseline leptin 8.0 to ≤20.0 ng/mL The primary objectives will be evaluated for patients in Cohort A only: - To evaluate the effect of REGN4461 on fasting triglycerides (TG) in patients with elevated baseline fasting TG - To evaluate the effect of REGN4461 on hyperglycemia in patients with elevated baseline Hemoglobin A1c (HbA1c) The following secondary objectives of the study will be evaluated for Cohort B and for the combined set of Cohorts A plus B: - To evaluate the effect of REGN4461 on fasting TG levels in patients with hypertriglyceridemia - To evaluate the effect of REGN4461 on glycemic control in patients with hyperglycemia The following secondary objectives of the study will be evaluated for Cohorts A and B separately, and for the combined set of Cohorts A plus B: - To evaluate the effect of REGN4461 on liver fat in patients with hepatic steatosis - To evaluate the effect of REGN4461 on hunger - To evaluate safety and tolerability of REGN4461 - To characterize the concentration profile of REGN4461 over time - To assess immunogenicity to REGN4461
To compare the safety and efficacy profiles of Revanesse Shape + with Lidocaine versus Juvederm Voluma with Lidocaine for subcutaneous and/or supraperiosteal injection to improve appearance through the correction of age-related mid-face volume deficit in patients 22 years of age through 65 years of age. Midface volume deficit / lipoatrophy (loss of subcutaneous adipose tissue that is most apparent in the face) may be associated with acquired conditions, the aging process, or based on genetic causes.
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.
The goal of the study is to combine a collaborative and translational approach to evaluate the effect antiretroviral regimen switch to a dolutegravir containing regimen compared to continued treatment with a non- dolutegravir based regimen on on lipid and metabolic profiles, renal function, body composition, vascular function and diet.
The purpose of the present study is to evaluate the effects of six sessions of aerobic exercise associated with shock waves therapy in the severity of gynoid lipodystrophy.