Intestinal mucosal adaptation

Drozdowski, Laurie; Thomson, A. B. R.

doi:10.3748/wjg.v12.i29.4614

Cited by 87 publications

(78 citation statements)

References 190 publications

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“…In light of these previous studies, the changes we observed in colonic SCFA concentrations and microbiota composition suggest that feeding RS may have important effects on host metabolic processes in the young. The microbiota-mediated effect on host metabolism is further supported by the increased colonic-crypt length seen in RS-fed rats, which is indicative of increased intestinal growth and absorptive capacity (7,26). The importance of the microbiota to host metabolism was also illustrated by the observation that germ-free rats ate more food but gained less weight than conventional rats fed the same diets.…”

Section: Discussionmentioning

confidence: 93%

Changes in Bowel Microbiota Induced by Feeding Weanlings Resistant Starch Stimulate Transcriptomic and Physiological Responses

Young

Roy

Lee

et al. 2012

Appl Environ Microbiol

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ABSTRACTThe ability to predictably engineer the composition of bowel microbial communities (microbiota) using dietary components is important because of the reported associations of altered microbiota composition with medical conditions. In a synecological study, weanling conventional Sprague-Dawley rats (21 days old) were fed a basal diet (BD) or a diet supplemented with resistant starch (RS) at 5%, 2.5%, or 1.25% for 28 days. Pyrosequencing of 16S rRNA genes and temporal temperature gradient electrophoresis (TTGE) profiles in the colonic digesta showed that rats fed RS had altered microbiota compositions due to blooms ofBacteroidetesandActinobacteria. The altered microbiota was associated with changes in colonic short-chain fatty acid (SCFA) concentrations, colonic-tissue gene expression (Gsta2andEla1), and host physiology (serum metabolite profiles and colonic goblet cell numbers). Comparisons between germ-free and conventional rats showed that transcriptional and serum metabolite differences were mediated by the microbiota and were not the direct result of diet composition. Altered transcriptomic and physiological responses may reflect the young host's attempts to maintain homeostasis as a consequence of exposure to a new collection of bacteria and their associated biochemistry.

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Section: Discussionmentioning

confidence: 93%

Changes in Bowel Microbiota Induced by Feeding Weanlings Resistant Starch Stimulate Transcriptomic and Physiological Responses

Young

Roy

Lee

et al. 2012

Appl Environ Microbiol

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“…One such condition is the adaptation response of the remnant bowel to massive intestinal loss (24). During adaptation, enterocyte proliferation is triggered for the generation of taller villi, thereby augmenting the intestinal surface area for digestion and absorption.…”

Section: Discussionmentioning

confidence: 99%

Retinoblastoma Protein (pRb), but Not p107 or p130, Is Required for Maintenance of Enterocyte Quiescence and Differentiation in Small Intestine

Guo

Longshore

Nair

et al. 2009

Journal of Biological Chemistry

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The function of retinoblastoma protein (pRb) in the regulation of small intestine epithelial cell homeostasis has been challenged by several groups using various promoter-based Cre transgenic mouse lines. Interestingly, different pRb deletion systems yield dramatically disparate small intestinal phenotypes. These findings confound the function of pRb in this dynamic tissue. In this study, Villin-Cre transgenic mice were crossed with Rb (flox/flox) mice to conditionally delete pRb protein in small intestine enterocytes. We discovered a novel hyperplasia phenotype as well as ectopic cell cycle reentry within villus enterocytes in the small intestine. This phenotype was not seen in other pRb family member (p107 or p130) null mice. Using a newly developed crypt/villus isolation method, we uncovered that expression of pRb was undetectable, whereas proliferating cell nuclear antigen, p107, cyclin E, cyclin D3, Cdk2, and Cdc2 were dramatically increased in pRb-deficient villus cells. Cyclin A, cyclin D1, cyclin D2, and Cdk4/6 expression was not affected by absent pRb expression. pRb-deficient villus cells appeared capable of progressing to mitosis but with higher rates of apoptosis. However, the cycling villus enterocytes were not completely differentiated as gauged by significant reduction of intestinal fatty acid-binding protein expression. In summary, pRb, but not p107 or p130, is required for maintaining the postmitotic villus cell in quiescence, governing the expression of cell cycle regulatory proteins, and completing of absorptive enterocyte differentiation in the small intestine.The small intestine is a very dynamic tissue with proliferative epithelial cells invaginating into the mesenchyme to form flaskshaped crypts, whereas differentiated cells project into the lumen, covering finger-like villi. Fresh cells are generated from the stems cells that are either seated at the traditional ϩ4 position from the bottom of the crypts or scattered between Paneth cells (so-called crypt base columnar cells) (1-3). Newly produced cells either migrate upward onto the villus and differentiate into absorptive enterocytes, goblet cells, or enteroendocrine cells or migrate down to the crypt bottom and differentiate into Paneth cells. After the cells pass the cryptvillus junction, they have already exited the cell cycle and are terminally differentiated into functional absorptive or secretory cells. These functionally differentiated cells finally shed into the lumen roughly 3-5 days after original generation (4).Retinoblastoma protein (pRb) 2 belongs to a pocket protein family, which also includes p107 and p130 (5). The major function of the pocket protein family members is to regulate the G 1 /S checkpoint and cell cycle progression, mainly through interaction with the E2F family of transcription factors that, in turn, regulate many genes necessary for both the G 1 /S and G 2 /M transition (6). Because germ line Rb Ϫ/Ϫ is lethal, pRb function has recently been studied in a conditional tissue-specific ablation fashion (7,8). In ...

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“…Protein deficiency, however, changes the intestinal architecture without altering its absorption capacity. The absorption capacity is preserved with physiological adaptation and change in the turnover rate of the enterocytes (Drozdowski and Thomson, 2006). The data obtained from the intestinal measurements carried out in our study show that the administration of AKG acid affects the intestinal adaptation, but not the absorption capacity, in rats fed a PFD.…”

Section: Intestinal Tractmentioning

confidence: 47%

Anticatabolic activity of alpha-ketoglutaric acid in growing rats

Prandini

Morlacchini²,

Sigolo

et al. 2012

Italian Journal of Animal Science

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This study evaluated the anti-catabolic effect of a-ketoglutaric acid (AKG) in rats. Thirty Sprague Dowley male rats were divided into 3 groups of 10 animals each and fed ad libitum with protein-free diet (PFD) supplemented with 0, 3, and 6 g/kg feed of AKG for 14 consecutive days. The AKG administration had no effect on the growth performance of rats in the global trial period (0-14 d). After 7 d of excreta collection, the losses of endogenous nitrogen (N), both urinary and total, linearly reduced (P<0.05) following the administration of AKG, ranging from 35.00 mg/d to 28.00 mg/d, and from 45.28 mg/d to 36.36 mg/d, respectively. The villi and microvilli heights were lower when animals received 3 g/kg of AKG respecting to other tested AKG levels. Indeed, enterocytes length linearly increased (P<0.05) as the level of AKG increased in the diet by 25.0% (3 g/kg) and 49.0% (6 g/kg). The AKG levels quadratically influenced (P<0.05) the essential amino acids (EAA) concentrations in the blood, being EAA lower for animals treated with 6 g/kg of AKG (-21.6%) compared to the animals fed the control PFD and the PFD with 3 g/kg of AKG. In conclusion, AKG was effective in reducing catabolism and EAA depletion.

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Intestinal mucosal adaptation

Cited by 87 publications

References 190 publications

Changes in Bowel Microbiota Induced by Feeding Weanlings Resistant Starch Stimulate Transcriptomic and Physiological Responses

Changes in Bowel Microbiota Induced by Feeding Weanlings Resistant Starch Stimulate Transcriptomic and Physiological Responses

Retinoblastoma Protein (pRb), but Not p107 or p130, Is Required for Maintenance of Enterocyte Quiescence and Differentiation in Small Intestine

Anticatabolic activity of alpha-ketoglutaric acid in growing rats

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