Effect of lumenal contents on colonic cell replacement.

Stragand, James J.; Hagemann, Ronald F.

doi:10.1152/ajpendo.1977.233.3.e208

Cited by 27 publications

(17 citation statements)

References 10 publications

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“…First, dietary constituents independent of bacteria can alter colonic mucosal growth characteristics. Second, the presence of bacteria in and of themselves do not pro- (15,54,60). The findings in our study support this because the inclusion of 5% or more dietary fiber in the diet of germ-free animals resulted in a mild, but significant, increase in mucosal volume.…”

Section: Introductionsupporting

confidence: 68%

“…The growthpromoting effect of increased colonic content mass may be mediated through increased stretch or tension that occurs in the colonic wall as increased mass is moved through the colon. Other studies have shown that the stretching of mucosal tissue in the colon and other epithelial sites is capable of inducing proliferation in epithelial cells (7,10,40,54). The observation in this study that there were not consistent differences in the subjective assessment of mucosal thickness between diet groups (42).…”

Section: Introductioncontrasting

confidence: 50%

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The Interactions of Diet and Colonic Microflora in Regulating Colonic Mucosal Growth

et al. 1996

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The colonic mucosa can adapt its growth to alterations in diet. Metabolites from colonic microflora are frequently implicated as the primary factor in mediating the colonic mucosal response to diet; however, there is also evidence indicating that diet may have a direct effect in mediating this response. The aim of this study was to determine the role of diet, microflora, and microflora metabolites in altering the growth of the colonic mucosa. Two 28-day feeding studies were conducted using Sprague-Dawley rats. The first study compared the growth of the colonic mucosa in germ-free and conventional rats fed 6 different diets. The second study compared the growth of the colonic mucosa to the concentration of bacterial-derived short-chain fatty acids (SCFAs), bile acids, and ammonia. The diets that were fed consisted of (1) AIN-76a diet without dietary fiber; (2) standard AIN-76a diet, which contained 5% cellulose; (3) AIN-76a diet with 5% guar gum; (4) a "Western" human diet with 20% fat and 10% cellulose; (5) AIN-76a diet formulated to mimic Diet 4 in fat content but with 2.5% cellulose; and (6) Purina Rodent Chow. Quantitative volumetric and stereologic analysis was used to assess changes in total colonic mucosal volume as a measure of mucosal growth. In germ-free rats, Diets 2-4 and 6 induced a significant increase (18-38%) in mucosal volume compared to Diet 1. In conventional animals, only Diets 4 and 6 induced a significant increase (up to 63%) in mucosal volume compared to Diet 1. Relative to the germ-free animals, only conventional animals on Diets 4 and 6 had an increase in mucosal volume. The increases in mucosal volume in Diets 4 and 6 were not consistently associated with increased SCFAs, ammonia, or bile acids. There was a wide range in the colonic concentrations of SCFAs (2-fold), ammonia (6-fold), and bile acids (10-fold). The presence of colonic microflora in and of itself does not lead to enhanced colonic mucosal growth. Rather, there are unique interactions between specific types of diet and microflora that lead to a growth-promoting effect. This effect could not be explained by alterations in the concentration of SCFAs, ammonia, or bile acids in colonic contents.

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Section: Introductionsupporting

confidence: 68%

Section: Introductioncontrasting

confidence: 50%

The Interactions of Diet and Colonic Microflora in Regulating Colonic Mucosal Growth

et al. 1996

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“…The method is applicable to normal colon of animals at any age and its application to grafts of foetal mouse colon has allowed definition of the effects of several factors on cell kinetics. The experimental situations examined here-of normal post-natal growth, of antigen-free growth in isografts, and the effects of cell-mediated immunity-parallel those examined in a previous morphological study (Holden and Ferguson 1976 (Dowling et al, 1967;Stragand and Hagemann, 1977). Alternatively, immune reactions between mucosal lymphoid tissues and antigens present in food or bacteria in the bowel lumen may be the initiating factor causing the rise in cell turnover.…”

Section: Discussionmentioning

confidence: 80%

Effects of age, antigen deprivation, and allograft rejection on epithelial cell kinetics in mouse colon.

Holden¹,

Ferguson²

1979

Gut

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SUMMARY A technique of microdissection of colonic mucosa has allowed the study of mitotic activity, measured by metaphase accumulation following colchicine blockade, in individual crypts of mouse colon. The changes occurring during growth and development of normal colon have been studied and compared with changes found in antigen free colon (colonic isografts) and in cell-mediated immune damage of the bowel (allograft rejection). Metaphase accumulation was steady at two metaphases per hour in baby mouse colon until 18 days after birth. Between 18 and 24 days a rapid, and significant increase in mitotic activity occurred (p < 0 1), reached adult values, and changed no further. Metaphase accumulation in isografts was similar to normal colon for the first two weeks after transplantation but the rise in mitotic activity in the third week did not occur. Allografts of colon showed two-to three-fold increases in metaphase accumulation when compared with both normal colon and isografts (P < 001). When crypt mitotic activity was compared with the length of crypts measured in histological sections of normal colon, isografts, and allografts, no clear relationship was observed. Both changes in the luminal environment of the gut at the time of weaning and cell-mediated immune reactions in the colonic wall appeared to be associated with increased mitotic activity in colonic crypts.The epithelial cell kinetics of the gastrointestinal tract mucosae maintain a steady state with cell renewal balanced by cell loss. In the stomach the proliferative region is in the neck of the gastric glands and supplies cells which migrate upwards to mature as surface mucous cells and downwards to mature as chief and parietal cells. In the small intestine and colon, the proliferative region is in the lower part of the crypt and the cells migrate upwards towards the surface as they mature (Lipkin, 1973). In a previous report (Holden and Ferguson, 1976), we described the morphological development of normal mouse colon, and the effects of an antigenfree state (isografts of mouse colon) and local cellmediated immune damage (rejection of colonic allografts) on morphology. The effects of a local cell-mediated immune reaction on the colon were contrasted with those of similarly induced damage to the small intestine. In mouse small intestine, rejection produces crypt hyperplasia and shortening of the villi, so that the architecture of the mucosa resembles that of untreated coeliac disease or severe tAddress for correspondence: Dr R.

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“…It is well known that gut wall distention by the luminal contents stimulates epithelial cell proliferation in the gut [6,7], gallbladder [8], uterine [9] and skin [10]. We speculated that gut wall stimulation by a hard stomach curd, the formation of which occurs with milk formulas based on casein, might be one cause of gut hypertrophy, since the hardness of the stomach curd could depend on the casein-towhey protein ratio in the milk.…”

Section: Introductionmentioning

confidence: 99%

Gut Hypertrophy in Response to the Ratios of Casein and Whey Protein in Milk Formulas in Artificially Reared Rat Pups

Yajima

Kanno²,

Katoku³

et al. 1998

Neonatology

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To elucidate the mechanism of gut hypertrophy observed in rats artificially reared (AR) on milk formulas, the effects of four refined formulas with different ratios of casein (C) and whey protein (W), CW 2:8, CW 4:6, CW 6:4 and CW 8:2, on the gut growth of AR rats were examined. Four groups of pups were infused with each formula through an intragastric cannula from age 5 to 15 days. Each of the four milk formulas showed a different character in the stomach, such as no curd, very soft curd, soft curd and hard curd, in response to an increasing ratio of C:W. There were no significant differences in body weight gain among the AR groups and mother-reared (MR) controls. The stomach growth, in weight, of AR rats increased in response to the increasing ratios of C:W. In comparison with MR controls, hypertrophy of the stomach of AR rats appeared within the formulas with higher proportions of casein than whey protein (CW 6:4 and CW 8:2), but not those with lower proportions (CW 2:8 and CW 4:6). The growth of the small intestine was also related to the increasing ratio of C:W in the formulas. A similar pattern of hypertrophy in the hindgut was seen in AR rats. There was no association between hypertrophy of the gut in AR rats and plasma triiodothyronine. The present results clearly demonstrated that the gut growth of AR rat pups was directly influenced by the diet but not by AR per se, and that hard casein-curd in the stomach might be one cause of gut hypertrophy.

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Effect of lumenal contents on colonic cell replacement.

Cited by 27 publications

References 10 publications

The Interactions of Diet and Colonic Microflora in Regulating Colonic Mucosal Growth

The Interactions of Diet and Colonic Microflora in Regulating Colonic Mucosal Growth

Effects of age, antigen deprivation, and allograft rejection on epithelial cell kinetics in mouse colon.

Gut Hypertrophy in Response to the Ratios of Casein and Whey Protein in Milk Formulas in Artificially Reared Rat Pups

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