Open AccessThe portal‐drained viscera release fibroblast growth factor 19 in humans
Author(s) -
Koelfat Kiran V. K.,
Bloemen Johanne G.,
Jansen Peter L. M.,
Dejong Cornelis H. C.,
Schaap Frank G.,
Olde Damink Steven W. M.
Publication year - 2016
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.13037
Subject(s) - fgf19 , medicine , fibroblast growth factor , splanchnic , endocrinology , ileum , gastroenterology , blood flow , receptor
Fibroblast growth factor 19 ( FGF 19) is an ileum‐derived endrocrine factor that is produced in response to transepithelial bile salt flux. FGF 19 represses bile salt synthesis in the liver. Despite the general assumption that FGF 19 signals to the liver via portal blood, no human data are available to support this notion. The aim was to study portal FGF 19 levels, and determined bile salt and FGF 19 fluxes across visceral organs in humans. Bile salt and FGF 19 levels were assessed in arterial, portal, and hepatic venous blood collected from fasted patients who underwent partial liver resection for colorectal liver metastases ( n = 30). Fluxes across the portal‐drained viscera ( PDV ), liver, and splanchnic area were calculated. Portal bile salt levels (7.8 [5.0–12.4] μ mol/L) were higher than levels in arterial (2.7 [1.7–5.5] μ mol/L, P < 0.0001) and hepatic venous blood (3.4 [2.5–6.5] μ mol/L, P < 0.0001). Bile salts released by the PDV (+1.2 [+0.7–+2.0] mmol kg −1 h −1 , P < 0.0001) were largely taken up by the liver (−1.0 [−1.8 to −0.4] mmol kg −1 h −1 , P < 0.0001). Portal levels of FGF 19 (161 ± 78 pg/mL) were higher than arterial levels (135 ± 65 pg/mL, P = 0.046). A net release of FGF 19 by the PDV (+4.0 [+2.1 to +9.9] ng kg −1 h −1 , P < 0.0001) was calculated. There was no significant flux of FGF 19 across the liver (−0.2 [−3.7 to +7.4] ng kg −1 h −1 , P = 0.93). In conclusion, FGF 19 levels in human portal blood are higher than in arterial blood. FGF 19 is released by the portal‐drained viscera under fasted steady state conditions.