Molecular analysis of the adaptive response of intestinal bile acid transport after ileal resection in the rat

Coppola, Christopher P.; Gosche, John R.; Arrese, Marco; Ancowitz, Bret; Madsen, Jill; Vanderhoof, Jon A.; Shneider, Benjamin L.

doi:10.1016/s0016-5085(98)70088-5

Cited by 42 publications

(37 citation statements)

References 27 publications

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“…In our previous studies limited intestinal resection was not associated with a specific change in bile acid transporter expression, although hyperplasia led to supraphysiologic transporter expression when the distal ileum was left intact (2). Interestingly, in these studies 70% resection was associated with a very different specific response of ASBT compared with that seen when 85% resection was performed (2). This suggests that there may be threshold levels of residual intestine for different types of adaptive response.…”

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confidence: 86%

“…The other protein is ILBP, which binds bile acids within the enterocyte. It has been shown from previous studies on rats that bile acid transporter gene expression occurs predominantly in the terminal 30 cm of small intestine (2). Therefore, distal but not proximal native ileum expresses ASBT.…”

mentioning

confidence: 91%

“…Limited ileal resection (proximal or distal) leads to hyperplasia, which nonspecifically increases ASBT and other brush border proteins irrespective of whether the transporter itself is resected (2). As a result, proximal ileal resection, in which ASBT is not resected, leads to a supraphysiologic expression of the distal ileal sodium-dependent bile acid transporter.…”

mentioning

confidence: 99%

“…The cellular and molecular responses are potentially more complex and have the capacity to induce specific physiologic changes in transport and digestive capacity. Only a limited number of molecular investigations of the short gut adaptation of specific transporters and digestive enzymes have been performed (2,(23)(24)(25)(26)(27). In most circumstances intestinal resection leads to a compensatory up-regulation in transporter or digestive enzyme expression (23)(24)(25)(26).…”

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confidence: 99%

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Analysis of the Effect of Intestinal Resection on Rat Ileal Bile Acid Transporter Expression and on Bile Acid and Cholesterol Homeostasis

Al-Ansari

2002

Pediatric Research

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Ileal reclamation of bile salts is mediated in large part by an apical sodium-dependent bile acid transporter (ASBT) located in the terminal ileum. The following studies were performed to elucidate the adaptive response of ASBT to intestinal resection. Two separate series of intestinal resections were performed: 1) limited (25%) ileal and 2) massive (70%) intestinal resection. The boundaries of the resections were varied to examine differences in compensation when variable amounts of endogenous transporter activity were resected. Previously demonstrated supraphysiologic expression of ASBT, which was seen after proximal ileal resection, led to a contraction in the bile acid pool size and a paradoxical reduction in bile acid (cholesterol 7␣-hydroxylase and sterol 27-hydroxylase) and cholesterol (hydroxymethylglutaryl coenzyme A reductase) biosynthetic enzyme activities. Massive intestinal resection resulted in ileal hypertrophy and an apparently maladaptive specific downregulation in ASBT protein expression. In this model bile acid pool size correlated with the amount of residual ASBTexpressing terminal ileum. Cholesterol and bile acid biosynthetic enzyme activities were inversely related to bile acid pool size. Intestinal bile acid absorption in the rat primarily takes place in the terminal ileum. At least two specific proteins appear to mediate this process; one of these is ASBT, which facilitates uptake of bile acid from the ileal lumen (1). The other protein is ILBP, which binds bile acids within the enterocyte. It has been shown from previous studies on rats that bile acid transporter gene expression occurs predominantly in the terminal 30 cm of small intestine (2). Therefore, distal but not proximal native ileum expresses ASBT. After limited (25% of total small bowel length) resection, transport and expression were found only in the remaining portions of terminal ileum.Certain conditions affecting the gastrointestinal tract may require extensive intestinal resection as a treatment, which may eventually result in short gut. Examples of these conditions include necrotizing enterocolitis, Crohn's disease, midgut volvulus, mesenteric vascular disease, intestinal atresia, and irradiation or cancer (3). Within 24 to 48 h after a bowel resection, the remaining small intestine begins to undergo an adaptive process characterized by epithelial hyperplasia. As this process progresses, villi lengthen and intestinal absorptive surface area increases as much as 4-fold. Enhancement of digestive and absorptive function may lag behind the increase in mucosal surface area. As the jejunum normally has more absorptive capacity, the ability of the ileum to adapt is greater than that of the jejunum (4).Many processes are deranged in short gut syndrome, one of which is the interruption in the normal enterohepatic circulation of bile acids caused by loss of bile acid transport capacity.

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confidence: 86%

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confidence: 91%

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confidence: 99%

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confidence: 99%

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Analysis of the Effect of Intestinal Resection on Rat Ileal Bile Acid Transporter Expression and on Bile Acid and Cholesterol Homeostasis

Al-Ansari

2002

Pediatric Research

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“…Cells were lysed by four cycles of freezing and thawing, followed by centrifugation at 16,000 g at 4°C for 15 min ( 36 ). Cellular membranes were obtained by centrifugation of whole-cell lysate at 3,000 g for 10 min at 4°C, followed by a second spin of the supernatant at 30,000 g for 20 min ( 37 ). Western blot analyses were performed as previously described ( 38 ).…”

Section: Protein Preparation Immunoprecipitation and Western Blottingmentioning

confidence: 99%

Phospholipase D2 mediates signaling by ATPase class I type 8B membrane 1

Chen

Ghosh

Shneider

2013

Journal of Lipid Research

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Nuclear Receptor Control of Enterohepatic Circulation

Gonzalez¹

2012

Comprehensive Physiology

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Enterohepatic circulation is responsible for the capture of bile acids and other steroids produced or metabolized in the liver and secreted to the intestine, for reabsorption back into the circulation and transport back to the liver. Bile acids are secreted from the liver in the form of mixed micelles that also contain phosphatidylcholines and cholesterol that facilitate the uptake of fats and vitamins from the diet due to the surfactant properties of bile acids and lipids. Bile acids are synthesized in the liver from cholesterol by a cascade of enzymes that carry out oxidation and conjugation reactions, and transported to the bile duct and gall bladder where they are stored before being released into the intestine. Bile flow from the gall bladder to the small intestine is triggered by food intake in accordance with its role in lipid and vitamin absorption from the diet. Bile acids are further metabolized by gut bacteria and are transported back to the circulation. Metabolites produced in the liver are termed primary bile acids or primary conjugated bile salts, while the metabolites generated by bacterial are called secondary bile acids. About 95% of bile acids are reabsorbed in the proximal and distal ileum into the hepatic portal vein and then into the liver sinusoids, where they are efficiently transported into the liver with little remaining in circulation. Each bile acid is reabsorbed about 20 times on average before being eliminated. Enterohepatic circulation is under tight regulation by nuclear receptor signaling, notably by the farnesoid X receptor (FXR).

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Molecular analysis of the adaptive response of intestinal bile acid transport after ileal resection in the rat

Cited by 42 publications

References 27 publications

Analysis of the Effect of Intestinal Resection on Rat Ileal Bile Acid Transporter Expression and on Bile Acid and Cholesterol Homeostasis

Analysis of the Effect of Intestinal Resection on Rat Ileal Bile Acid Transporter Expression and on Bile Acid and Cholesterol Homeostasis

Phospholipase D2 mediates signaling by ATPase class I type 8B membrane 1

Nuclear Receptor Control of Enterohepatic Circulation

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