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Gallbladder dyskinesia is associated with an impaired postprandial FGF19 response in critically ill patients.

08:00 EDT 1st April 2019 | BioPortfolio

Summary of "Gallbladder dyskinesia is associated with an impaired postprandial FGF19 response in critically ill patients."

Critical illness is associated with a disturbed regulation of gastrointestinal hormones resulting in functional and metabolic anomalies. 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 120min. Blood was collected every 30min 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, while FGF19 serum levels were similar. In both groups, nutrient infusion elicited substantial bile salt elevations (P<0.001), peaking at 90min, albeit with a significantly lower peak in the ICU-patients (P=0.029). In controls, FGF19 was significantly elevated relative to baseline from 120min onwards (P<0.001). In ICU-patients, the FGF19 response was blunted, as reflected by significantly lower FGF19 elevations at 120, 150 and 180min (P<0.05) and significantly lower AUC values compared with controls (P<0.001). Gallbladder dysmotility was associated with the impaired FGF19 response in critical illness. The gallbladder ejection fraction (GBEF) correlated positively with FGF19 AUC values (ρ=+0,34, P=0.034). In 10 out 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.
CONCLUSIONS:
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. This article is protected by copyright. All rights reserved.

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This article was published in the following journal.

Name: Hepatology (Baltimore, Md.)
ISSN: 1527-3350
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