Prostaglandin E&lt;sub&gt;2&lt;/sub&gt; Accelerates Enzymatic and Morphological Maturation of the Small Intestine in Suckling Rats

Martí, Amelia; Fernández-Otero, M. P.

doi:10.1159/000244037

Cited by 9 publications

(6 citation statements)

References 17 publications

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“…Prostaglandin E 2 exerts trophic effects on the small bowel of suckling rats (27) and when present in high doses, has been shown to increase brush border enzyme activities, possibly indicating accelerated mucosal maturation (28). This might explain in part why our 0% ARA-supplemented pigs showed lower levels of lactase activity compared with the sow-fed pigs.…”

Section: Discussionmentioning

confidence: 82%

Enrichment of Intestinal Mucosal Phospholipids with Arachidonic and Eicosapentaenoic Acids Fed to Suckling Piglets Is Dose and Time Dependent

Hess

Corl

Lin

et al. 2008

The Journal of Nutrition

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Infant formula companies began fortifying formulas with long-chain PUFA in 2002, including arachidonic acid (ARA) at approximately 0.5% of total fatty acids. The primary objective of this study was to determine the time-specific effects of feeding formula enriched with supra-physiologic ARA on fatty acid composition of intestinal mucosal phospholipids. One-day-old pigs (n = 96) were fed a milk-based formula for 4, 8, or 16 d. Diets contained either no PUFA (0% ARA, negative control), 0.5% ARA, 2.5% ARA, 5% ARA, or 5% eicosapentaenoic acid (EPA) of total fatty acids (wt:wt). Growth (299 +/- 21 g/d) and clinical hematology were unaffected by treatment (P > 0.6). Although minimal on d 4, concentrations of ARA in jejunal mucosa were enriched 47, 272 and 428% by d 8 and 144, 356, and 415% by d 16 in pigs fed the 0.5% ARA, 2.5% ARA, and 5% ARA diets, respectively, compared with the 0% ARA control pigs (P < 0.01). On d 16, ARA enrichment increased progressively with increasing dietary ARA supplementation from 0 to 2.5% but plateaued as dietary ARA rose to 5%. A similar pattern of ARA enrichment was observed in ileal mucosal phospholipids, but maximal enrichment in the ileum exceed that in the jejunum by >50%. As ARA increased, linoleic acid content decreased reciprocally. Although maximal enterocyte enrichment with EPA approached 20-fold by d 8, concentrations were only approximately 50% of those attained for ARA. Negligible effects on gross villus/crypt morphology were observed. These data demonstrate a dose-dependent response of intestinal mucosal phospholipid ARA concentration to dietary ARA with nearly full enrichment attained within 8 d of feeding formula containing ARA at 2.5% of total fatty acids and that supra-physiologic supplementation of ARA is not detrimental to growth.

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Section: Discussionmentioning

confidence: 82%

Enrichment of Intestinal Mucosal Phospholipids with Arachidonic and Eicosapentaenoic Acids Fed to Suckling Piglets Is Dose and Time Dependent

Hess

Corl

Lin

et al. 2008

The Journal of Nutrition

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“…PGE 2 via the actions of EP2/EP4 may regulate mammaryspecific cellular functions during pregnancy, whereas high amounts of PGE 2 secreted into breast milk may modulate infant physiology or immune responses (52,53). Specifically, PGE 2 may promote intestinal maturation or motility in the infant (54,55) or be cytoprotective during postnatal development of the intestinal mucosa. Identifying specific mammary cell populations that express the different PGE synthases and receptors, coupled with the analysis of mammary epithelial proliferation and apoptosis in receptor and mPGES1 Ϫ/Ϫ mice, will help define the normal physiological functions of PGE 2 in the murine mammary gland.…”

Section: Discussionmentioning

confidence: 99%

Coupling of COX-1 to mPGES1 for prostaglandin E2 biosynthesis in the murine mammary gland

Chandrasekharan

Foley

Jania

et al. 2005

Journal of Lipid Research

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The mammary gland, like most tissues, produces measurable amounts of prostaglandin E 2 (PGE 2 ), a metabolite of arachidonic acid produced by sequential actions of two cyclooxygenases (COX-1 and COX-2) and three terminal PGE synthases: microsomal prostaglandin E 2 synthase-1 (mPGES1), mPGES2, and cytosolic prostaglandin E 2 synthase (cPGES). High PGE 2 levels and COX-2 overexpression are frequently detected in mammary tumors and cell lines. However, less is known about PGE 2 metabolic enzymes in the context of normal mammary development. Additionally, the primary COX partnerships of terminal PGE synthases and their contribution to normal mammary PGE 2 biosynthesis are poorly understood. We demonstrate that expression of COX-1, generally considered constitutive, increases dramatically with lactogenic differentiation of the murine mammary gland. Concordantly, total PGE 2 levels increase throughout mammary development, with highest levels measured in lactating tissue and breast milk. In contrast, COX-2 expression is extremely low, with only a modest increase detected during mammary involution. Expression of the G s -coupled PGE 2 receptors, EP2 and EP4, is also temporally regulated, with highest levels detected at stages of maximal proliferation. PGE 2 production is dependent on COX-1, as PGE 2 levels are nearly undetectable in COX-1 -deficient mammary glands. Interestingly, PGE 2 levels are similarly reduced in lactating glands of mPGES1 -deficient mice, indicating that PGE 2 biosynthesis results from the coordinated activity of COX-1 and mPGES1. We thus provide evidence for the first time of functional coupling between COX-1 and mPGES1 in the murine mammary gland in vivo.

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“…The concentration of CBX required for inhibition of prostaglandin dehydrogenases is much higher than the nanomolar K i for 11␤HSD, and CBX exhibits high nonspecific binding to plasma and cellular proteins (2,(27)(28)(29). In addition, the effect of CBX on morphologic and enzymatic development was different from that of prostaglandin administration in suckling rats (30,31).…”

Section: Discussionmentioning

confidence: 99%

Carbenoxolone Accelerates Maturation of Rat Intestine

2003

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The rat undergoes profound maturational changes in the intestinal structure and function during the third week of its life. To investigate the role of peripheral glucocorticoid metabolism in this process, we studied the postnatal maturation of intestinal structure and function. The peripheral metabolism of glucocorticoids depends on enzyme 11␤-hydroxysteroid dehydrogenase (11␤HSD), which is responsible for the interconversion of corticosterone to 11-dehydrocorticosterone and thus for the modulation of glucocorticoid access to corticosteroid receptors. The pups were treated with carbenoxolone (CBX), an inhibitor of 11␤HSD, for 10 d during the suckling (days 8 -18) or weaning period (days 14 -24 or days 20 -30), and we determined the parameters of intestinal growth and activities of sucrase, alkaline phosphatase, and Na,K-ATPase. The CBX treatment increased plasma concentrations of corticosterone as a result of a significant reduction of peripheral degradation of corticosterone catalyzed by 11␤HSD. This also stimulated intestinal growth without changing somatic growth. The mucosal cell mass was significantly higher in CBX-treated suckling rats, whereas the effect of this treatment was less obvious in weanling animals. CBX increased the crypt depth and villus height in 18-and 24-d-old pups but not in 30-d-old animals. The small intestinal activities of sucrase, alkaline phosphatase, and Na,K-ATPase were not influenced by CBX. In contrast, colonic Na,K-ATPase was stimulated by CBX. We conclude that the administration of CBX results in acceleration of intestinal growth and structural maturation without any influence on the developmental pattern of brush-border hydrolases The concentration of glucocorticoids in the plasma plays an important physiologic role in the promotion of normal ontogeny of the human embryo in utero and of rodents during weaning. The rise of plasma glucocorticoids is associated with an accelerated maturation of various tissues (1). The local action of glucocorticoids in target tissues can be modified by changes in peripheral glucocorticoid metabolism. This metabolism depends on the enzyme 11␤-hydroxysteroid dehydrogenase (11␤HSD), which has been recognized to play a key role in regulating the access of glucocorticoids to corticosteroid receptors. Two isoforms of 11␤HSD with different properties and tissue distribution have been described. Type 2 11␤HSD is a high-affinity NAD-dependent isozyme that catalyzes the conversion of cortisol and corticosterone to cortisone and 11-dehydrocorticosterone, respectively, and thus decreases the local concentration of active glucocorticoids and prevents their binding to mineralocorticoid receptors. In contrast, type 1 11␤HSD is a NADP(H)-dependent isoform that exhibits bidirectional activity in vitro but seems to favor 11-reductase activity in intact cells. Whereas type 2 has been predominantly found in the kidney, colonic epithelium, and placenta, type 1 is the predominant type in the liver, fibroblasts, and cells of lamina propria (2).It has recently been sho...

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

Cited by 9 publications

References 17 publications

Enrichment of Intestinal Mucosal Phospholipids with Arachidonic and Eicosapentaenoic Acids Fed to Suckling Piglets Is Dose and Time Dependent

Enrichment of Intestinal Mucosal Phospholipids with Arachidonic and Eicosapentaenoic Acids Fed to Suckling Piglets Is Dose and Time Dependent

Coupling of COX-1 to mPGES1 for prostaglandin E2 biosynthesis in the murine mammary gland

Carbenoxolone Accelerates Maturation of Rat Intestine

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