Prostaglandin-Mediated Effects on Growth and Markers of Biochemical Development in the Rat

Neu, Josef; Hoffmann, Raymond G.; Crim, Wendell

doi:10.1203/00006450-198307000-00004

Cited by 19 publications

(7 citation statements)

References 6 publications

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“…Data from previous investigations have suggested that similar effects may follow subcutaneous administration of PG12 or subcutaneous implantation of 16,16-DMPGE? minipumps (7). Similar effects also have been seen after enteral administration of 16,16-DMPGE* by gavage to suckling but not adult rats (8).…”

Section: Discussionsupporting

confidence: 61%

Comparative Effects of Glucocorticoids and Prostaglandins on Small Intestine of Infant Rats

1986

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ABSTRACT. Previous studies have suggested similarities between the effects of exogenously administered glucocorticoids and prostaglandins in the developing rat small intestine. In this study the effects of exogenously administered glucocorticoids and prostaglandins were compared. In addition, the effects of prostaglandins in adrenalectomized rats were evaluated. Members of both classes of compounds stimulate small intestinal disaccharidase activities, and increase RNA to DNA ratio and brush border membrane protein synthesis. Hydrocortisone accelerates enterocyte turnover, whereas prostacyclin does not. Enteral administration of 16,16-dimethyl prostaglandinEz stimulates disaccharidase activities in intact as well as shamoperated and adrenalectomized animals. The data suggest that certain prostaglandins may play a role in small intestinal metabolism which is similar to that of the glucocorticoids but is independent of the adrenal-intestinal axis. Glucocorticoids are known to play a significant role in the development of small intestinal biochemical function. These hormones appear to mediate a series of enzymatic changes in the small intestine of rats during the 3rd wk of postnatal life (I-3). Administration of hydrocortisone or ACTH during the 2nd postnatal wk causes precocious appearance of sucrase activity (4), whereas adrenalectomy at this time markedly slows the usual increase of sucrase activity (5). In adult rats, sucrase activity is independent of glucocorticoids (6).In a previous study by our group (7), prostaglandins were administered to suckling rats to determine their effects on growth and development. Analysis of small intestinal hydrolase activities demonstrated effects similar to those of the glucocorticoids. Other than this, little information is available regarding the physiological role of prostaglandins in the gastrointestinal tract of the developing fetus and neonate. More recent studies by Koelz (q a/. (8) have demonstrated that an enterally administered prostaglandin analog, 16,l 6-DMPGE2, will stimulate disaccharidase activity in the small intestine of suckling but not adult rats.Since the stimulation of the enzyme activities by the glucocorticoids and prostaglandins are similar in many respects, we decided to investigate further the comparative effects of these two classes of compounds. The purpose of these studies was

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Section: Discussionsupporting

confidence: 61%

Comparative Effects of Glucocorticoids and Prostaglandins on Small Intestine of Infant Rats

1986

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“…Prosta glandins have been studied extensively as potential therapeutic agents in the treatment of peptic ulcer disease [24], 16,16-dimethyl-PGE2 has previously been shown to induce increases in mucosal mass in both the stomach and duodenum of normal weanling rats when given intragastri cally [12]. It has also been shown to increase total sucrasc-isomaltase activity in 16-dayold rats [25]. Another previous study failed to demonstrate a trophic effect after only 2 days of treatment [26], In the stomach, change in mucosal mass has been shown to be related to increased cell survival in stud ies utilizing 15,15-dimethyi-PGE2 [27].…”

Section: Discussionmentioning

confidence: 99%

Augmentation of Mucosal Adaptation following Massive Small-Bowel Resection by 16,16-Dimethyl-Prostaglandin E<sub>2</sub> in the Rat

et al. 1987

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Survival following massive resection of the small intestine is often possible due to substantial hyperplasia of the mucosal surface in the remaining small intestine. While nutrients provide the major stimulus for hyperplasia in the clinical setting, the availability of drugs to augment this process would have obvious therapeutic implications. We evaluated the ability of 16,16-dimethyl-prostaglandin E₂ (PGE₂ to augment mucosal hyperplasia following massive small bowel resection in the rat. Three groups of 7 Sprague-Dawley rats, 160g body weight, were subjected to 70% jejunoileal resection. One group was given 150 μg/kg of 16,16-dimethyl-PGE₂ intragastrically twice daily, a second group 75 μg/kg subcutaneously, and a third group was untreated. After 17 days, segmental evaluation of mucosal mass in the remaining small intestine was determined by measuring mucosal protein, DNA, and disaccharidase levels. A significantly greater increase in mucosal mass was developed in the duodenum proximal to the anastomosis in both treatment groups, but neither the proximal nor distal ileum demonstrated significantly more adaptation. Histological examination in the duodenum confirmed the presence of a greater adaptive response in both the intragastrically and subcutaneously treated animals. 16,16-dimethyl-PGE₂ appears to augment mucosal adaptation following massive small bowel resection in the rat, primarily in the very proximal small intestine.

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“…The role of prostaglandins (PGs) has been stressed by ex perimental data. In neonatal rats Neu et al [9] found an increase in sucrase and maltase activities after P G E treatment. Similarly, the administration of a synthetic analog of P G E 2 (16,16-dimethyl-PGE2) induced the develop ment of the small intestine in 11-day-old rats [10] .…”

Section: Introductionmentioning

confidence: 99%

Prostaglandin E<sub>2</sub> Accelerates Enzymatic and Morphological Maturation of the Small Intestine in Suckling Rats

Martí

Fernández-Otero²

1994

Neonatology

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The effect of prostaglandin E₂ (PGE₂) injection on the postnatal maturation of the 16-day-old rodent small intestine was studied. Previous studies have shown that 16,16-dimethyl PGE₂ induced several morphological and biochemical parameters in the small intestine of 11-day-old rats. PGE₂ was given subcutaneously daily at doses of 2 and 4 mg/kg body weight on postnatal days 11–15. After treatment there was a rise in the mean activities of sucrase, maltase, lactase and aminopeptidase. In rats receiving 4 mg/kg PGE₂, sucrase activity was strongly stimulated (p < 0.001) in the proximal and the distal small bowel. In the duodenum, PGE₂ treatment (4 mg/kg body weight) produced a significant increase in crypt depth (35%, p < 0.001), although villus height was not modified. Serum corticosterone levels were significantly increased in PGE₂-treated rats. The results seem to indicate that PGE₂ accelerates enzymatic and morphological intestinal maturation and this effect could be mediated by an increase in corticosterone.

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Prostaglandin-Mediated Effects on Growth and Markers of Biochemical Development in the Rat

Cited by 19 publications

References 6 publications

Comparative Effects of Glucocorticoids and Prostaglandins on Small Intestine of Infant Rats

Comparative Effects of Glucocorticoids and Prostaglandins on Small Intestine of Infant Rats

Augmentation of Mucosal Adaptation following Massive Small-Bowel Resection by 16,16-Dimethyl-Prostaglandin E<sub>2</sub> in the Rat

Prostaglandin E<sub>2</sub> Accelerates Enzymatic and Morphological Maturation of the Small Intestine in Suckling Rats

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