Journal
CELLS
Volume 8, Issue 10, Pages -Publisher
MDPI
DOI: 10.3390/cells8101197
Keywords
obesity; ASBT; Na-bile acid cotransport; Zucker rats; TALLYHO mice; Farnesoid X receptor; bile-acid-associated protein
Categories
Funding
- National Institutes of Health [DK-67420, DK-108054, P20GM121299-01A1]
- Veteran's Administration Merit Review grant [BX003443-01, P20GM121299-01A1-]
- National Institute of General Medical Sciences of the National Institutes of Health [P20GM121299]
Ask authors/readers for more resources
In obesity, increased absorption of dietary fat contributes to altered lipid homeostasis. In turn, dyslipidemia of obesity leads to many of the complications of obesity. Bile acids are necessary for the absorption of dietary fat. In the mammalian intestine, apical sodium-dependent bile acid cotransporter (ASBT; SLC10A2) is exclusively responsible for the reabsorption of bile acids in the terminal ileum. In rat and mice models of obesity and importantly in obese humans, ASBT was increased in ileal villus cells. The mechanism of stimulation of ASBT was secondary to an increase in ASBT expression in villus cell brush border membrane. The stimulation of ASBT was not secondary to the altered Na-extruding capacity of villus cells during obesity. Further, increased Farnesoid X receptor (FXR) expression in villus cells during obesity likely mediated the increase in ASBT. Moreover, enhanced FXR expression increased the expression of bile-acid-associated proteins (IBABP and OST alpha) that are responsible for handling bile acids absorbed via ASBT in villus cells during obesity. Thus, this study demonstrated that in an epidemic condition, obesity, the dyslipidemia that leads to many of the complications of the condition, may, at least in part, be due to deregulation of intestinal bile acid absorption.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available