A Biological Atlas of Severe Obesity (Biological Tissue Collection)

University Hospital, Lille20,000 enrolled

Overview

Type 2 diabetes and obesity are both multifactorial diseases resulting from gene-environment interactions. However, this interaction, as well as the specific effect of each polymorphism, remains poorly understood. We now proposed a prospective cohort study to improve our understanding of the influence of phenotypic characteristics on gene expression in tissues involved in glucose and/or lipid metabolism by collecting different biological samples.

Type 2 diabetes (T2D) is a disease commonly associated with obesity, which is an important risk factor for this condition. More than 80% of the diabetic subjects are obese. By analogy with the metabolic syndrome, the close association between obesity and T2D justifies the recognition of a new disease entity named by the neologism "diabesity". This study will examine the contribution of different genetic variants on "diabesity" development, by integrating multiple genomics approaches (linkage analysis on whole genome, transcriptomics and bioinformatics) and analysis of biological pathways in relevant animals models and humans.

Study Type

OBSERVATIONAL

Enrollment

20,000

Conditions

Obesity Glucose Intolerance Diabetes

Eligibility

Sex: ALLMin age: 18 YearsMax age: 65 YearsHealthy volunteers:

Medical Language ↔ Plain English

Inclusion Criteria: * Age between 18 and 65 years * Indication of abdominal surgery requiring a laparotomy or laparoscopy for bariatric surgery, cholecystectomy, or parietal surgical * Phenotype corresponding to one of the following four cases : 1. Body Mass Index ≥ 35 kg/m2 and diabetes defined by a fasting blood glucose ≥ 7 mmol/l and/or ≥ to 11.1 mmol/l, 120 minutes after ingestion of glucose (hyperglycemia caused by oral route) 2. Body Mass Index ≥ 35 kg/m2 with intolerance glucose defined by a fasting blood glucose\> 6 mmol/L and \<7 mmol/l and/or\> 7.8 mmol/l and \<11.1 mmol/l , 120 minutes after ingestion of glucose (hyperglycemia caused by oral route) 3. Body Mass Index ≥ 35 kg/m2 without diabetes defined by a blood glucose ≤ 6 mmol/L and / or ≤ 7.8 mmol/l, 120 minutes after ingestion of glucose (hyperglycemia caused by oral route) 4. Body Mass Index \<27 kg/m2 without diabetes defined by a blood glucose ≤ 6 mmol/L and / or ≤ 7.8 mmol/l, 120 minutes after ingestion of glucose (hyperglycemia caused by oral route) 5)27 \<Body Mass Index \<35 kg/m2 without diabetes defined by a blood glucose ≤ 6 mmol/L and / or ≤ 7.8 mmol/l, 120 minutes after ingestion of glucose (hyperglycemia caused by oral route) Exclusion Criteria: * unable to receive clear information * refusal to sign the consent form * pathology associated judged by the surgeon, may increase the risk of adverse events related to sampling tissue

Outcomes

Primary Outcomes

Study the influence of phenotypic characteristics on gene expression of tissues involved in glucose metabolism

Study the correlation between the glycemic status (fasting glucose and / or after ingestion of glucose) adjusted to the presence or absence of obesity (Body Mass Index) and gene expression in tissues involved in glucose metabolism before bariatric surgery

Time frame: Baseline

Secondary Outcomes

Correlation between gene expression and tissue insulin resistance index (HOMA2) (The Homeostasis Model Assessment)

Insulin resistance is individually calculated by homeostasis model assessment(HOMA2) by determination of fasting glucose and insulin

Time frame: 1 year

Correlation between gene expression and tissue insulin resistance index (HOMA2) (The Homeostasis Model Assessment)

Insulin resistance is individually calculated by homeostasis model assessment(HOMA2) by determination of fasting glucose and insulin

Time frame: 2 years

Correlation between gene expression and tissue insulin resistance index (HOMA2) (The Homeostasis Model Assessment)

Insulin resistance is individually calculated by homeostasis model assessment(HOMA2) by determination of fasting glucose and insulin

Time frame: 5 years

Prospective assessment of clinical and biological features before and after bariatric surgery

Prospective assessment of clinical and biological features before and after bariatric surgery: weight, BMI, blood pressure, alanine aminotransferase (ALT), gamma-glutamyl transferase (GGT), prothrombin time, platelets, serum triglyceride, cholesterolemia, fasting blood glucose, fasting insulin, blood glucose and insulin 120 minutes after ingestion of glucose (oral glucose tolerance test)

Time frame: 1 year

Prospective assessment of clinical and biological features before and after bariatric surgery

Prospective assessment of clinical and biological features before and after bariatric surgery: weight, BMI, blood pressure, alanine aminotransferase (ALT), gamma-glutamyl transferase (GGT), prothrombin time, platelets, serum triglyceride, cholesterolemia, fasting blood glucose and fasting insulin, blood glucose and insulin 120 minutes after ingestion of glucose (oral glucose tolerance test)

Time frame: 2 years

Prospective assessment of clinical ans biological features before and after bariatric surgery

Prospective assessment of clinical and biological features before and after bariatric surgery: weight, BMI, blood pressure, alanine aminotransferase (ALT), gamma-glutamyl transferase (GGT), prothrombin time, platelets, serum triglyceride, cholesterolemia, fasting blood glucose and fasting insulin, blood glucose and insulin 120 minutes after ingestion of glucose (oral glucose tolerance test)

Time frame: 5 years

Genotype-Phenotype correlation

Genotype-Phenotype correlation based on medical and family history

Time frame: Baseline

A Biological Atlas of Severe Obesity (Biological Tissue Collection)

Overview

Conditions

Eligibility

Locations (1)

Outcomes

Primary Outcomes

Secondary Outcomes

Central Contacts