Open AccessChenodeoxycholic acid stimulates glucagon‐like peptide‐1 secretion in patients after Roux‐en‐Y gastric bypass
Author(s) -
Nielsen Signe,
Svane Maria S.,
Kuhre Rune E.,
Clausen Trine R.,
Kristiansen Viggo B.,
Rehfeld Jens F.,
Holst Jens J.,
Madsbad Sten,
BojsenMoller Kirstine N.
Publication year - 2017
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.13140
Subject(s) - chenodeoxycholic acid , medicine , ursodeoxycholic acid , endocrinology , glucagon like peptide 1 , bile acid , peptide yy , cholecystokinin , postprandial , gastric inhibitory polypeptide , hormone , chemistry , glucagon , receptor , insulin , type 2 diabetes , diabetes mellitus , neuropeptide , neuropeptide y receptor
Postprandial secretion of glucagon‐like peptide‐1 ( GLP ‐1) is enhanced after Roux‐en‐Y gastric bypass ( RYGB ), but the precise molecular mechanisms explaining this remain poorly understood. Plasma concentrations of bile acids ( BA s) increase after RYGB , and BA s may act as molecular enhancers of GLP ‐1 secretion through activation of TGR 5‐receptors. We aimed to evaluate GLP ‐1 secretion after oral administration of the primary bile acid chenodeoxycholic acid ( CDCA ) and the secondary bile acid ursodeoxycholic acid ( UDCA ) (which are available for oral use) in RYGB ‐operated participants. Eleven participants ( BMI 29.1 ± 1.2, age 37.0 ± 3.2 years, time from RYGB 32.3 ± 1.1 months, weight loss after RYGB 37.0 ± 3.1 kg) were studied in a placebo‐controlled, crossover‐study. On three different days, participants ingested (1) placebo (water), (2) UDCA 750 mg, (3) CDCA 1250 mg (highest recommended doses). Oral intake of CDCA increased plasma concentrations of GLP ‐1, C‐peptide, glucagon, peptide YY , neurotensin, total bile acids, and fibroblast growth factor 19 significantly compared with placebo (all P < 0.05 for peak and positive incremental area‐under‐the‐curve (pi AUC )). All plasma hormone concentrations were unaffected by UDCA . Neither UDCA nor CDCA changed glucose, cholecystokinin or glucose‐dependent insulinotropic polypeptide ( GIP ) concentrations. In conclusion, our findings demonstrate that the primary bile acid chenodeoxycholic acid is able to enhance secretion of gut hormones when administered orally in RYGB ‐operated patients—even in the absence of nutrients.