scholarly journals Mechanism of Dyslipidemia in Obesity—Unique Regulation of Ileal Villus Cell Brush Border Membrane Sodium–Bile Acid Cotransport

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1197 ◽  
Author(s):  
Sundaram ◽  
Palaniappan ◽  
Nepal ◽  
Chaffins ◽  
Sundaram ◽  
...  
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Brush Border ◽  
Dietary Fat ◽  
Brush Border Membrane ◽  
Farnesoid X Receptor ◽  
Bile Acid Absorption ◽  
Associated Proteins ◽  
Villus Cell ◽  
Stimulation Of

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 OSTα) 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.

Intestinal transport of bile acids

1981 ◽  
Vol 241 (2) ◽  
pp. G83-G92 ◽  
Author(s):  
F. A. Wilson
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Active Transport ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Water Layer ◽  
Unstirred Layer ◽  
Jejunal Mucosa ◽  
Acid Uptake ◽  
Unstirred Water Layer

The intestinal absorption of bile acids is determined by two resistances: diffusion through an unstirred water layer and penetration of the cell membrane. Passive jejunal uptake of polar bile acids is limited by the mucosal membrane, whereas the unstirred layer exerts resistance on uptake of more nonpolar species. After correction for the diffusion layer, the membrane permeability coefficients were derived to calculate the delta delta Fw leads to 1 associated with uptake of the -OH (+874 cal.mol-1), glycine (+897), and taurine (+1,498) groups. The delta delta F1 (-6,126 cal.mol-1) for the -OH group suggested that the jejunal mucosa is a relatively polar membrane. The unstirred layer is even more rate limiting for bile acid uptake from micellar solutions. Once the micelle reaches the aqueous-membrane interface, it is not absorbed intact, but rather uptake is explained in terms of monomers in the aqueous phase that are in equilibrium with the micelle. The presence of the unstirred water layer introduces artifactually high Km values for active transport. Structure-activity studies suggest that the ileal recognition site consists of a component for the steroid moiety, a positive charge, and an adjacent anionic charge. The energy for active transport arises from the Na+ gradient across the brush-border membrane that, in turn, is dependent on the activity of Na+-K+-ATPase. The Na+ stimulation of bile acid transport across the ileal brush-border membrane is due to influx coupling via a cotransport system rather than electrical coupling to satisfy overall electrical neutrality.

Evidence for an anion exchange mechanism for uptake of conjugated bile acid from the rat jejunum

1999 ◽  
Vol 276 (3) ◽  
pp. G737-G742 ◽  
Author(s):  
Andree Amelsberg ◽  
Christina Jochims ◽  
Claus Peter Richter ◽  
Rolf Nitsche ◽  
Ulrich R. Fölsch
Keyword(s):  
Bile Acid ◽  
Epithelial Cells ◽  
Bile Acids ◽  
Anion Exchange ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Membrane Vesicles ◽  
Brush Border Membrane Vesicles ◽  
Intestinal Epithelial ◽  
Conjugated Bile Acids

Absorption of conjugated bile acids from the small intestine is very efficient. The mechanisms of jejunal absorption are not very well understood. The aim of this study was to clarify the mechanism of absorption of conjugated bile acid at the apical membrane of jejunal epithelial cells. Brush-border membrane vesicles from intestinal epithelial cells of the rat were prepared. Absorption of two taurine-conjugated bile acids that are representative of endogenous bile acids in many variate vertebrate species were studied. In ileal, but not jejunal brush-border membrane vesicles, transport of conjugated bile acids was cis-stimulated by sodium. Transport of conjugated bile acids was trans-stimulated by bicarbonate in the jejunum. Absorption of conjugated dihydroxy-bile acids was almost twice as fast as of trihydroxy-bile acids. Coincubation with other conjugated bile acids, bromosulfophthalein, and DIDS, as well as by incubation in the cold inhibited the transport rate effectively. Absorption of conjugated bile acids in the jejunum from the rat is driven by anion exchange and is most likely an antiport transport.

551 Regulation of Intestinal Villus Cell Brush Border Membrane Bile Acid Co-Transport in Obesity

2016 ◽  
Vol 150 (4) ◽  
pp. S116
Author(s):  
Subha Arthur ◽  
Ibrahim Mohammed ◽  
Balasubramanian Palaniappan ◽  
Soudamani Singh ◽  
Uma Sundaram
Keyword(s):  
Bile Acid ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Intestinal Villus ◽  
Villus Cell

Weanling, but not adult, rabbit colon absorbs bile acids: flux is linked to expression of putative bile acid transporters

2006 ◽  
Vol 290 (3) ◽  
pp. G439-G450 ◽  
Author(s):  
Dirk Weihrauch ◽  
Jainuch Kanchanapoo ◽  
Mei Ao ◽  
Roli Prasad ◽  
Pawinee Piyachaturawat ◽  
...  
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Short Circuit ◽  
Distal Colon ◽  
Lipid Binding ◽  
Farnesoid X Receptor ◽  
Acid Transport ◽  
Bile Acid Transport ◽  
Acid Absorption ◽  
Bile Acid Absorption

Intestinal handling of bile acids is age dependent; adult, but not newborn, ileum absorbs bile acids, and adult, but not weanling or newborn, distal colon secretes Cl− in response to bile acids. Bile acid transport involving the apical Na+-dependent bile acid transporter (Asbt) and lipid-binding protein (LBP) is well characterized in the ileum, but little is known about colonic bile acid transport. We investigated colonic bile acid transport and the nature of the underlying transporters and receptors. Colon from adult, weanling, and newborn rabbits was screened by semiquantitative RT-PCR for Asbt, its truncated variant t-Asbt, LBP, multidrug resistance-associated protein 3, organic solute transporter-α, and farnesoid X receptor. Asbt and LBP showed maximal expression in weanling and significantly less expression in adult and newborn rabbits. The ileum, but not the colon, expressed t-Asbt. Asbt, LBP, and farnesoid X receptor mRNA expression in weanling colon parallel the profile in adult ileum, a tissue designed for high bile acid absorption. To examine their functional role, transepithelial [3H]taurocholate transport was measured in weanling and adult colon and ileum. Under short-circuit conditions, weanling colon and ileum and adult ileum showed net bile acid absorption: 1.23 ± 0.62, 5.53 ± 1.20, and 11.41 ± 3.45 nmol·cm−2·h−1, respectively. However, adult colon secreted bile acids (−1.39 ± 0.47 nmol·cm−2·h−1). We demonstrate for the first time that weanling, but not adult, distal colon shows net bile acid absorption. Thus increased expression of Asbt and LBP in weanling colon, which is associated with parallel increases in taurocholate absorption, has relevance in enterohepatic conservation of bile acids when ileal bile acid recycling is not fully developed.

scholarly journals Role of Bile Acids in the Regulation of Food Intake, and Their Dysregulation in Metabolic Disease

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1104
Author(s):  
Cong Xie ◽  
Weikun Huang ◽  
Richard L. Young ◽  
Karen L. Jones ◽  
Michael Horowitz ◽  
...  
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Peptide Yy ◽  
Glycogen Synthesis ◽  
Hormone Secretion ◽  
Gastrointestinal Hormones ◽  
Farnesoid X Receptor ◽  
Gastrointestinal Hormone ◽  
Bile Acid Sequestrants

Bile acids are cholesterol-derived metabolites with a well-established role in the digestion and absorption of dietary fat. More recently, the discovery of bile acids as natural ligands for the nuclear farnesoid X receptor (FXR) and membrane Takeda G-protein-coupled receptor 5 (TGR5), and the recognition of the effects of FXR and TGR5 signaling have led to a paradigm shift in knowledge regarding bile acid physiology and metabolic health. Bile acids are now recognized as signaling molecules that orchestrate blood glucose, lipid and energy metabolism. Changes in FXR and/or TGR5 signaling modulates the secretion of gastrointestinal hormones including glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), hepatic gluconeogenesis, glycogen synthesis, energy expenditure, and the composition of the gut microbiome. These effects may contribute to the metabolic benefits of bile acid sequestrants, metformin, and bariatric surgery. This review focuses on the role of bile acids in energy intake and body weight, particularly their effects on gastrointestinal hormone secretion, the changes in obesity and T2D, and their potential relevance to the management of metabolic disorders.

Effect of chronic inflammation on electrolyte transport in rabbit ileal villus and crypt cells

1997 ◽  
Vol 272 (4) ◽  
pp. G732-G741 ◽  
Author(s):  
U. Sundaram ◽  
A. B. West
Keyword(s):  
Chronic Inflammation ◽  
Inflammatory Mediators ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Basolateral Membrane ◽  
Rabbit Model ◽  
Electrolyte Transport ◽  
Acid Load ◽  
Crypt Cells ◽  
Stimulation Of

The effect of chronic inflammation on electrolyte transport in rabbit ileal villus and crypt cells was determined with the use of a rabbit model of chronic ileitis. In both cells, Na+/H+ exchange was monitored by following recovery from an acid load, and Cl-/HCO3- exchange was monitored by following recovery from an alkaline load. In villus cells, recovery from an acid load was not affected; however, recovery from an alkaline load was slowed. These data suggest that chronic inflammation inhibits Cl-/HCO3- exchange in villus cells. In contrast, in crypt cells, recovery from an alkaline load was unaffected, whereas recovery from an acid load was accelerated. These data suggest that chronic inflammation stimulates Na+/H+ exchange in crypt cells. Inhibition of Cl-/HCO3- exchange in villus cells would be expected to inhibit coupled NaCl absorption, which occurs by the coupling of brush-border membrane (BBM) Na+/H+ and Cl-/HCO3- exchange. Stimulation of Na+/H+ exchange in crypt cells, known to be present only on the basolateral membrane, alkalinizes the cell. This alkalinization may stimulate BBM Cl-/HCO3- exchange, resulting in HCO3- secretion. Thus these unique alterations in transporter activity suggest that different endogenous immune-inflammatory mediators may have differing effects on specific transporters in villus and crypt cells in the chronically inflamed ileum.

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