Ontogeny of cell proliferation and DNA synthesis in rat colon: role of glucocorticoids

Buts, Jean-Paul; Meyer, Richard D.; Kolanowski, Jaroslaw

doi:10.1152/ajpgi.1983.244.5.g469

Cited by 18 publications

(20 citation statements)

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“…Previous observations also documented analogous changes in the stomach and colon [1, 2, 4, 5, 6, 7, 9, 10, 12, 14, 15, 28, 29]. It should be noted that a decrease in the values of all parameters is observed.…”

Section: Discussionsupporting

confidence: 69%

Two-Month Glucocorticoid Treatment Increases Proliferation in the Stomach and Large Intestine of Rats

Гунин

Nikolaev²

2000

Digestion

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Background/Aims: It has been shown that acute or short-term treatments with glucocorticoids lead to a marked decrease in proliferation in the stomach and large intestine. The effects of more prolonged glucocorticoid treatment on cell renewal in these organs are not known. The present work was therefore undertaken to examine the proliferative activity in the stomach and colon during 2 months of glucocorticoid treatment in comparison with shorter treatments. Methods: Rats were treated with either the glucocorticoid triamcinolone acetonide or vehicle for 63, 33 or 3 days. Proliferation was assessed in the glandular epithelium of the fundal part of the stomach and in the epithelium of the colonic crypts using three criteria: the mitotic index; the bromodeoxyuridinelabelling index, and the proliferating cell nuclear antigen-labelling index (percentage of mitotic or labelled cells). Results: Treatment with glucocorticoid for 63 days resulted in a very significant increase in all proliferative parameters tested in the gastric mucosa and the colonic crypts. On the contrary, treatments with glucocorticoid for 3 or 33 days had a marked inhibitory influence on proliferation in these tissues. Conclusion: As opposed to treatments for 3 or 33 days, glucocorticoid treatment for 2 months leads to an increase in the number of cycling cells in the gastric and colonic mucosae.

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Section: Discussionsupporting

confidence: 69%

Two-Month Glucocorticoid Treatment Increases Proliferation in the Stomach and Large Intestine of Rats

Гунин

Nikolaev²

2000

Digestion

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“…This observation may indicate that immature colonic tissue has an enhanced sensitivity to the inductive effect of aldosterone. Enhanced sensitivity to the inductive effect of glucocorticoid hormones has previously been observed in the immature small intestine (20) as well as in the immature renal proximal tubule (21). In the renal proximal tubule, the enhanced sensitivity to glucocorticoid hormones could be attributed to increased concentration of available hormone receptors (22).…”

Section: It Has Been Suggested That This Increase In Intracellular Somentioning

confidence: 82%

Role of Aldosterone for Control of Colonic NaKATPase Activity in Weanling Rats

Finkel

Aperia

1986

Pediatr Res

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ABSTRACT. Ex~eriments were ~erforrned to examine MATERIALS AND METHODShow aldosterone ;noddates coloniE NaKATPase activity during the weaning period. NaKATPase activity was determined in proximal and distal colon in control rats aged 16, 20, and 40 days, in rats aged 20 and 40 days fed low sodium diet for 4 days and in 20-day-old rats adrenalectomized on day 16. In some protocols net sodium and water transport was determined with in vivo perfusion technique. In control rats colonic NaKATPase activity increased significantly between day 16 and 20. This increase was abolished by adrenalectomy but restored by aldosterone substitution, 5 pg/lOO g body weight112 h. No significant increase in NaKATPase activity occurred between day 20 and 40. Serum levels of both aldosterone and of corticosterone were low until day 14 and increased to peak level at day 18-20. In 20-and 40-day-old rats fed a low sodium diet, NaKATPase activity increased significantly in proximal and distal colon in both age groups but the increases were significantly greater in the 20-than the 40-day-old animals. A low sodium diet increased serum aldosterone, but not serum corticosterone levels in both age groups: also the low sodium diet significantly increased net sodium and water transport in 20-but not in 40-day-old rats. Aldosterone is of physiological importance for the regulation of Pi, inorganic phosphorousAt the time of weaning there is an accelerated maturation of gastrointestinal enzymes and this maturation is attenuated by adrenalectomy (1). It is generally assumed that it is the glucocorticoid hormone which triggers the maturation. The serum levels of glucocorticoid hormones increase rapidly at the time of weaning (2) and treatment with large doses of glucocorticoid in suckling rats results in precocious development of enzymes in the gastrointestinal tract (3-6).There are few developmental studies of the large intestine. The adult large intestine has a high concentration of mineralocorticoid receptors (7,8), and the activity of NaKATPase enzyme in the adult colon can be modulated by mineralocorticoid (9). The present study was designed to explore the influence of mineralocorticoid hormone on colonic NaKATPase activity at the time of weaning. Animals. Sprague-Dawley rats from Anticimex, Sollentuna, Sweden were used. The animal quarters were air-conditioned (2 1 + lo C) with a 12-h light cycle (0700-1900 h) and a 12-h dark cycle. The litter sizes were maintained at four to six animals.Experimental Groups. Zn~act rats. The animals were kept with lactating dams. They had free access to ordinary rat food (Ewos R3) containing 0.13 mmol Na/g and tap water ad libitum until 20 days. Thereafter they were kept in litters without dams. Their body weight increased from a mean of 21.5 g at 10 days to a mean of 170 g at 40 days. Sodium depletion. These animals were fed a low sodium diet (Ewos) for 4 days. The diet was similar to the ordinary rat food but contained 0.009 mmol Na/g. Animals aged 16 days were separated from the dams and fed a low salt diet...

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“…Thus, bombesin [1,2] and epidermal growth factor [3][4][5] have been reported to stimulate the oxyntic mucosal growth in un weaned rats, and bombesin to stimulate that of the antral mucosa [2], Glucocorticoids also seem to play a major role before the weaning period. Indeed, in the very young rat, from the perinatal period until weaning (around the 20th day of life), high doses (up to 250 mg/kg) of hydrocortisone or cortico sterone, the natural corticosteroid hormone of the rat, induce a precocious differentia tion of gastric chief cells [6], increase basal acid output [7], and stimulate certain intesti nal enzyme activities [8], They also induce a premature appearance of gastrin receptors [9] and noticeably augment antral gastrin levels [8,9], However, using biochemical methods, it has been reported that glucocor ticoid treatment during development does not affect the gastric mucosal DNA content in the rat [7] nor the gastric DNA synthesis in the mouse [4] while it induces a decrease in mucosal cell proliferation in the colon of rat pups [10], On the whole, it appears that the main effect of glucocorticoids is maturation of the gastrointestinal functional activities rather than stimulation of cell growth, although few works have dealt with the latter point. So, the current study examines the influence of a 6-day administration of hydrocortisone on the development of the gastric mucosa and some gastric cell populations in suckling rats using histological quantitative and morpho metric methods.…”

mentioning

confidence: 99%

Influence of Hydrocortisone on the Development of the Gastric Mucosa in Suckling Rats

Puccio¹,

Lehy²

1988

Digestion

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The effect of a 6-day hydrocortisone administration on the development of gastric mucosa was investigated in suckling rats. Three doses of hydrocortisone (40, 20 and 5 mg/kg/day) were given during the 2nd week of life. Gastric morphometric parameters, and exocrine parietal cell and endocrine gastrin cell numbers were examined and gastrin content in antral tissue was determined. At the end of hydrocortisone treatment, parietal and chief cells were well differentiated. Their larger size was marked in comparison with controls, which likely explains in itself the significant increase in gastric mucosal height. Only the highest dose significantly increased antral gastrin content over control values. However, hydrocortisone, whatever the dose, reduced the apparent antral gastrin cell population by about 60% (p < 0.001), without noticeably modifying the numerical density of parietal cells per unit of fundic surface. It is nevertheless likely that the highest dose diminished total parietal cell number since the gastric surface decreased. These results suggest that glucocorticoids affect the development of the gastrin cell population while greatly accelerating the maturation of these cells during the suckling period.

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Ontogeny of cell proliferation and DNA synthesis in rat colon: role of glucocorticoids

Cited by 18 publications

References 0 publications

Two-Month Glucocorticoid Treatment Increases Proliferation in the Stomach and Large Intestine of Rats

Two-Month Glucocorticoid Treatment Increases Proliferation in the Stomach and Large Intestine of Rats

Role of Aldosterone for Control of Colonic NaKATPase Activity in Weanling Rats

Influence of Hydrocortisone on the Development of the Gastric Mucosa in Suckling Rats

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