Disaccharidases in the small intestine of the mouse: Normal development and influence of cortisone, actinomycin D, and cycloheximide

Moog, Florence; Denes, Alex E.; Powell, Patricia M.

doi:10.1016/0012-1606(73)90012-2

Cited by 80 publications

(47 citation statements)

References 56 publications

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“…Corticosteroid has been shown to be an inducer for disaccharidase before weaning in mice (18) and rats (9,12,19). The accompanying increase in serum cortisol levels in the early weaned pups suggests a possible involvement of this hormone during the dietary shift in causing precocious increases in sucrase and maltase.…”

Section: Duodenal Segment Jejunal Segmentmentioning

confidence: 99%

Early Weanling and Precocious Development of Small Intestine in Rats: Genetic, Dietary or Hormonal Control

Lee

Lebenthal

1983

Pediatr Res

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Summary14); however, its relationship to diet has been explored only to a Small intestinal development was followed in rats from 17 to 28 days of age in order to evaluate the interactions of diets, genetic preprogramming, and hormones in influencing developmental changes. Control pups, weaned naturally at 21-24 days, showed a gradual increase in body weight, intestinal length, and segmental mucosal weight, total DNA, and protein content. In contrast, pups weaned at 17 days showed an immediate increase in intestinal length, decrease in lactase, and precocious increase in sucrase and maltase. The changes in segmental mucosal weight, DNA and protein contents, however, paralleled that of controls. Pups nursed "p to 25 days had a smalle; body weight, shorter intestine, lighter mucosa, and lesser mucosal protein content. They showed no significant delay in the increase in sucrase and maltase together with a persistent higher level of lactase. Enterokinase and leucine aminopeptidase showed little change irrespective of the dietary modifications. Significant increases in segmental mucosal mass, DNA, and protein contents during the studied period were seen in all animals. At 19 days, early weaned pups had serum levels of corticosteroids about 3 times that of control or prolonged nursed pups. The results support the concept of an inherent biologic program as a basic control of intestinal ontogeny whereas dietary changes seem to have a modifying role and act directly, or in concert with, hormonal changes.Neonatal rats have no detectable sucrase, low maltase, and high levels of lactase activities in their small intestines. The activities of sucrase and maltase increase abruptly about the 15th day of age. These two enzymes continue to rise during the third and fourth week with a concomitant decrease in lactase. The third week of life in rats corresponds to the weaning time that is marked by a shift from a fat-rich diet supplied by the mother (4) to a carbohydrate-rich lab-chow diet. The carbohydrate is also changed from an almost exclusive lactose-containing milk to a predominant glucose-polymer-and sucrose-containing chow. A casual relationship exists therefore between dietary changes and the increase in sucrase and maltase with a corresponding decrease in lactase. The possibility of a "dietary influence" of enzymes is further strengthened by the observations that sucrase rises precociously by early feeding of sucrose (15,21). In addition, we have shown (16) that prolonged nursing leads to a slower decline in lactase activity. At 25 days of age, prolonged nursed rats show similar maltase and sucrase activities as control weaned rats. Similar studies by Henning and Guerin (20) also showed no depression in sucrase activities when pups were weaned onto a special diet with lactose as the sole source of carbohydrate. These results are in agreement with those studies using intestinal explants (8,11) or in vitro cultures ( 6 ) and together suggest that the postnatal increase in sucrase and maltase in the rat is preprogrammed. Othe...

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Section: Duodenal Segment Jejunal Segmentmentioning

confidence: 99%

Early Weanling and Precocious Development of Small Intestine in Rats: Genetic, Dietary or Hormonal Control

Lee

Lebenthal

1983

Pediatr Res

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“…Administration of glucocorticoids to suckling rats or mice causes precocious increases in the activities of sucrase (40, 56,57), maltase (56,58), trehalase (56), amino peptidase (43,56), and alkaline phosphatase (42), as well as precocious disappearance of various lysosomal hydrolases (59), and the capacities for pinocytosis (15,19,60) and for the absorption of intact immunoglobulins (19,61). Conversely, it has been shown that if animals are adrenalectomized during the second postnatal week, the usual decrease of pinocytosis (62) and increase ofalkaline phosphatase (42) and sucrase (63) activities are largely prevented.…”

Section: Role Of Hormonesmentioning

confidence: 99%

Biochemistry of Intestinal Development

Henning¹

1979

Environmental Health Perspectives

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In biochemical terms, the rat small intestine is relatively immature at birth and for the first two postnatal weeks. Then during the third week a dramatic array ofenzymic changes begins, and by the end ofthe fourth week the intestine has the digestive and absorptive properties of the adult. Selective examples of these changes are discussed with emphasis on their implications for toxicological studies. The review also includes a detailed consideration of the roles of the dietary change of weaning and of glucocorticoid and thyroid hormones in the regulation of intestinal development.My aim in this paper is to use the rat as a model system for a discussion of the postnatal development of small intestinal function. Factors which affect the developmental process will be reviewed in terms of their implications for toxicological studies. Morphologic Development of the IntestineBy the time of birth, the intestinal mucosa of the rat displays a high level of structural development characterized by villi lined with a single layer of columnar epithelial cells which have well-defined microvilli at their absorptive surface (1-3). After birth, continuous proliferation of epithelial cells occurs only in the lower regions of the crypts (4, 5), and cells migrate from there onto and along the villi, eventually being extruded from the tips into the lumen of the intestine. In adult rats and mice the generation time for the crypt cells is 10-14 hr (6), and the transit time along the length of the villus is approximately 48 hr (7). The characteristics of proliferation and migration of enterocytes in adult animals are dealt with in detail in the review by Lipkin (8). In neonatal rats, generation and migration of the cells is much slower than in adults. Despite the fact that the neonatal villi are shorter, the transit time is at least % hr (7, 9). During the third postnatal week there are significant changes in both cell kinetics and mor-

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“…Thus, a detailed understanding necessitates the use of a range of hormone doses at each age of interest. To date, most age-related studies of intestinal responsiveness to glucocorticoid have used a single dose of hormone (18,19,21). In addition, all of the prior rodent studies are confounded by the use of natural glucocorticoids whose circulating concentrations are profoundly influenced by corticosteroid-binding globulin.…”

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confidence: 99%

Development of Glucocorticoid-Responsiveness in Mouse Intestine

et al. 2001

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There are conflicting data from human studies regarding the ability of exogenous glucocorticoids to stimulate maturation of the small intestine. The discrepancies may relate to differences in hormone doses and age administered. To explore this general concept, we have used a mouse model to determine intestinal responsiveness to dexamethasone (DEX) at various times during development. We first showed that trehalase mRNA is a sensitive marker of intestinal maturation in the mouse; being undetectable (by Northern blotting) in the prenatal period, expressed at low levels during the first 2 postnatal weeks and then displaying a marked increase in the 3rd postnatal week. DEX was unable to elicit detectable trehalase mRNA in fetal mice, but caused significant increases in the postnatal period. The use of a range of DEX doses (0.0125-2.5 nmol/g BW per day) established that there is no change in sensitivity between the 1st and 2nd postnatal weeks, but there is a significant increase in maximal responsiveness of trehalase mRNA to the hormone. Similar results were obtained when sucrase-isomaltase mRNA was assayed in the same animals. Thus, in this rodent model, there appears to be at least three phases in the DEX responsiveness of the developing intestine: an early phase (prenatal) when DEX is unable to elicit intestinal maturation; then a phase (first postnatal week) of modest responsiveness; then a transition to increased responsiveness. These findings point to the need for careful attention to dose and age in analyses of glucocorticoid effects in human infants. Glucocorticoids have become an important component in the pharmacologic treatment of prematurity because of their maturational effects on certain tissues. In the lung, for example, corticosteroid therapy is central to the prevention of respiratory distress syndrome. Interestingly, several clinical trials using exogenous glucocorticoids in the treatment of prematurity also demonstrated a decreased incidence of necrotizing enterocolitis (NEC) in steroid-treated infants (1-3). In addition, Halac and coworkers conducted a prospective human study of the effect of DEX on the incidence of NEC and found a significant reduction in NEC among neonates receiving either prenatal or postnatal steroid (4). As NEC is typically associated with immaturity (5-7), these findings suggest that exogenous glucocorticoid may exert a maturational effect on the intestine. However, not all trials observed decreased NEC (2). Likewise, although investigators have found significant maturation of intestinal motility (8) and permeability (9) in premature infants whose mothers received prenatal glucocorticoid, another study reported no effect on lactase maturation (10). The latter in vivo observation is in contrast to several studies that have shown elevation of lactase activity in response to glucocorticoid treatment in explant cultures of human fetal intestine (11-13). We hypothesize that such seemingly disparate results may be explained by differences in dosages and timing of corticosteroid tr...

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Disaccharidases in the small intestine of the mouse: Normal development and influence of cortisone, actinomycin D, and cycloheximide

Cited by 80 publications

References 56 publications

Early Weanling and Precocious Development of Small Intestine in Rats: Genetic, Dietary or Hormonal Control

Early Weanling and Precocious Development of Small Intestine in Rats: Genetic, Dietary or Hormonal Control

Biochemistry of Intestinal Development

Development of Glucocorticoid-Responsiveness in Mouse Intestine

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