Overview
Bariatric surgery is currently the most efficient treatment for obesity. The sustained weight loss and metabolic improvement seen following Roux-en-Y gastric bypass (RYGB), is explained partly by modifications in hormones including bile acids (BA). After RYGB, an increased total BA pool and a reduction in hepatic cortisol exposure is observed. Hydroxysteroid 11-β dehydrogenase 1 (HSD11B1), steroid 5α-reductases (SRD5A), and steroid 5β-reductases, AKR1D1 (also a BA metabolizing enzyme), are three enzymes involved in the metabolism of cortisol in the liver and are known to participate in metabolic syndrome. Their activity has been shown to be decreased after RYGB. Interestingly, the mechanisms explaining the modification of hepatic cortisol exposure and the activity of theses enzymes after RYGB are unknown. In view of the few data suggesting a link between cortisol metabolism and bile acids, this work aim to study and characterize this link in a context of RYBP
Eligibility
Inclusion Criteria:
- Non-menopausal women
- BMI between 35 and 50 kg/m² included
- Social insured
- Ability to give consent
Exclusion Criteria:
- moderate and severe kidney insufficiency
- hepatic insufficiency
- known gallbladder lithiasis
- history of cholecystectomy or cholecystectomy planned during the gastric bypass
- history of bariatric surgery except gastric band and gastric balloon
- history of type 1
- treatment interfering with the cortisol metabolism: taking oral or inhaled glucocorticoids within the last 6 months
- treatment by BA as ursodeoxycholic acid, bile acids sequester, statin, fibrate stopped less than 4 weeks ago