Literature DB >> 30933374

Gallbladder Dyskinesia Is Associated With an Impaired Postprandial Fibroblast Growth Factor 19 Response in Critically Ill Patients.

Kiran V K Koelfat1, Mark P Plummer2, Frank G Schaap1,3, Martin Lenicek4, Peter L M Jansen1, Adam M Deane2, Steven W M Olde Damink1,3.   

Abstract

Critical illness is associated with a disturbed regulation of gastrointestinal hormones resulting in functional and metabolic anomalies. Fibroblast growth factor 19 (FGF19) is an ileum-derived metabolic hormone induced by bile salts upon gallbladder emptying after enteral nutrient stimulation. Our aim was to study the nutrient-stimulated FGF19 response in 24 patients admitted to the intensive care unit (ICU) compared with 12 healthy controls. All subjects received intraduodenal high-lipid nutrient infusion for 120 minutes. Blood was collected every 30 minutes until 1 hour after infusion, and gallbladder emptying was studied by ultrasound. Serum levels of bile salts and FGF19 were assessed. ICU patients had significantly higher fasting bile salt serum levels compared with controls, whereas FGF19 serum levels were similar. In both groups, nutrient infusion elicited substantial bile salt elevations (P < 0.001), peaking at 90 minutes, albeit with a significantly lower peak in the ICU patients (P = 0.029). In controls, FGF19 was significantly elevated relative to baseline from 120 minutes onward (P < 0.001). In ICU patients, the FGF19 response was blunted, as reflected by significantly lower FGF19 elevations at 120, 150, and 180 minutes (P < 0.05) and significantly lower area under the curve (AUC) values compared with controls (P < 0.001). Gallbladder dysmotility was associated with the impaired FGF19 response in critical illness. The gallbladder ejection fraction correlated positively with FGF19 AUC values (ρ = +0.34, P = 0.045). In 10 of 24 ICU patients, gallbladder emptying was disturbed. These patients had significantly lower FGF19 AUC values (P < 0.001). Gallbladder emptying and the FGF19 response were respectively disturbed or absent in patients receiving norepinephrine.
Conclusion: The nutrient-stimulated FGF19 response is impaired in ICU patients, which is mechanistically linked to gallbladder dysmotility in critical illness. This may contribute to disturbed liver metabolism in these patients and has potential as a nutritional biomarker.
© 2019 by the American Association for the Study of Liver Diseases.

Entities:  

Year:  2019        PMID: 30933374     DOI: 10.1002/hep.30629

Source DB:  PubMed          Journal:  Hepatology        ISSN: 0270-9139            Impact factor:   17.425


  4 in total

1.  Intestinal FGF15/19 physiologically repress hepatic lipogenesis in the late fed-state by activating SHP and DNMT3A.

Authors:  Young-Chae Kim; Sunmi Seok; Yang Zhang; Jian Ma; Bo Kong; Grace Guo; Byron Kemper; Jongsook Kim Kemper
Journal:  Nat Commun       Date:  2020-11-24       Impact factor: 14.919

Review 2.  Metabolic aspects of muscle wasting during critical illness.

Authors:  Robert J J van Gassel; Michelle R Baggerman; Marcel C G van de Poll
Journal:  Curr Opin Clin Nutr Metab Care       Date:  2020-03       Impact factor: 3.620

3.  Postprandial rise of essential amino acids is impaired during critical illness and unrelated to small-intestinal function.

Authors:  Rob J J van Gassel; Marcel C G van de Poll; Frank G Schaap; Mark Plummer; Adam Deane; Steven W M Olde Damink
Journal:  JPEN J Parenter Enteral Nutr       Date:  2021-05-06       Impact factor: 3.896

4.  Chyme Reinfusion Restores the Regulatory Bile Salt-FGF19 Axis in Patients With Intestinal Failure.

Authors:  Kiran V K Koelfat; Denis Picot; Xinwei Chang; Ronan Thibault; Frank G Schaap; Steven W M Olde Damink; Mireille Desille-Dugast; Hans M van Eijk; Sander M J van Kuijk; Martin Lenicek; Sabrina Layec; Marie Carsin; Laurence Dussaulx; Eloi Seynhaeve; Florence Trivin; Laurence Lacaze
Journal:  Hepatology       Date:  2021-08-26       Impact factor: 17.425

  4 in total

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