Open AccessMechanisms of triglyceride metabolism in patients with bile acid diarrhea
Author(s) -
Nidhi Sagar,
Michael McFarlane,
Chuka U. Nwokolo,
Karna Dev Bardhan,
Ramesh P. Arasaradnam
Publication year - 2016
Publication title -
world journal of gastroenterology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.427
H-Index - 155
eISSN - 2219-2840
pISSN - 1007-9327
DOI - 10.3748/wjg.v22.i30.6757
Subject(s) - microsomal triglyceride transfer protein , farnesoid x receptor , very low density lipoprotein , medicine , endocrinology , apolipoprotein b , lipogenesis , triglyceride , lipid metabolism , chemistry , bile acid , hypertriglyceridemia , lipoprotein lipase , lipoprotein , biochemistry , biology , nuclear receptor , cholesterol , transcription factor , adipose tissue , gene
Bile acids (BAs) are essential for the absorption of lipids. BA synthesis is inhibited through intestinal farnesoid X receptor (FXR) activity. BA sequestration is known to influence BA metabolism and control serum lipid concentrations. Animal data has demonstrated a regulatory role for the FXR in triglyceride metabolism. FXR inhibits hepatic lipogenesis by inhibiting the expression of sterol regulatory element binding protein 1c via small heterodimer primer activity. Conversely, FXR promotes free fatty acids oxidation by inducing the expression of peroxisome proliferator-activated receptor α. FXR can reduce the expression of microsomal triglyceride transfer protein, which regulates the assembly of very low-density lipoproteins (VLDL). FXR activation in turn promotes the clearance of circulating triglycerides by inducing apolipoprotein C-II, very low-density lipoproteins receptor (VLDL-R) and the expression of Syndecan-1 together with the repression of apolipoprotein C-III, which increases lipoprotein lipase activity. There is currently minimal clinical data on triglyceride metabolism in patients with bile acid diarrhoea (BAD). Emerging data suggests that a third of patients with BAD have hypertriglyceridemia. Further research is required to establish the risk of hypertriglyceridaemia in patients with BAD and elicit the mechanisms behind this, allowing for targeted treatment.