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AP-HP Hôpital Pitié-Salpêtrière-Charles Foix, Nutrition Department, Paris, France
AP-HP Hôpital Pitié-Salpêtrière-Charles Foix, Diabetology-Metabolism Department, Paris, France
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AP-HP Hôpital Pitié-Salpêtrière-Charles Foix, Nutrition Department, Paris, France
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Introduction HNF-4 belongs to the nuclear receptor superfamily, and in mammals two paralog genes encode the HNF-4α and HNF-4γ forms. HNF-4α is expressed in the liver, kidney, pancreas and intestine ( Benoit et al. 2006 ). Numerous studies
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opposite sexual dimorphism of DDC in the intestine and kidney of mice, affecting DDC activity and protein. Moreover, we postulate that this DDC dimorphism may have physiological relevance in sodium homeostasis, mainly through the modulation of sodium
Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, ON, Canada
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Department of Medicine, University of Toronto, Toronto, ON, Canada
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Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, ON, Canada
Department of Obstetrics, Gynecology and Pediatrics, McMaster University, Hamilton, ON, Canada
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-related pathways. However, recent discoveries that host-microbe relationships govern glucose regulation in the non-pregnant state, have opened the door to new investigations of the maternal intestine and its bacterial content, as well as to its contribution to
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Laboratory of Intestinal Adaptation and Recovery, Departments of Pediatric Surgery B, Pathology, Section of Pediatric Surgery, The Ruth and Bruce Rappaport Faculty of Medicine, Technion‐Israel Institute of Technology, Haifa, Israel
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. Intestinal mucosal samples The small intestine was removed, stripped of adherent fat and mesentery, washed with normal saline and dried. The removed bowel was divided into two segments: proximal jejunum (10 cm from the ligament of Treitz) and distal ileum (10
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In developmental terms, the endocrine system of neither the gut nor the pancreatic islets has been characterized fully. Little is known about the involvement of cholecystokinin (CCK), a gut hormone, involved in regulating the secretion of pancreatic hormones, and pancreatic growth. Here, we tracked CCK-expressing cells in the intestines and pancreata of normal mice (BALB/c), Non Obese Diabetic (NOD) mice and interferon (IFN)-gamma transgenic mice, which exhibit pancreatic regeneration, during embryonic development, the postnatal period and adulthood. We also questioned whether IFN-gamma influences the expression of CCK. The results from embryonic day 16 showed that all three strains had CCK in the acinar region of pancreata, and specifically in alpha cells that also expressed glucagon. However, in adulthood only BALB/c and NOD mice continued this pattern. By contrast, in IFN-gamma transgenic mice, CCK expression was suppressed from birth to 3 months of age in the pancreata but not intestines. However, by 5 months of age, CCK expression appeared in the regenerating pancreatic ductal region of IFN-gamma transgenic mice. In the intestine, CCK expression persisted from fetus to adulthood and was not influenced by IFN-gamma. Intestinal cells expressing CCK did not co-express glucagon, suggesting that these cells are phenotypically distinct from CCK-expressing cells in the pancreatic islets, and the effect of IFN-gamma on CCK varies depending upon the cytokine's specific microenvironment.
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Abstract
The enzyme 11β-hydroxysteroid dehydrogenase (11β-OHSD) prevents the binding of corticosterone to mineralocorticoid receptors by reversible conversion of biologically active corticosterone to inactive 11-dehydrocorticosterone. To clarify the relationship between high plasma concentrations of corticosterone during weaning and high activity of intestinal transport pathways that are induced by aldosterone in immature intestine, we have studied the distribution, developmental pattern and regulation of 11 β-OHSD in intestinal segments that possess mineralocorticoid target epithelium. Dehydrogenase activity was already high in the caecum, and the proximal and distal colon on the second postnatal day and altered little until adulthood. In contrast, the activity in the ileum was low during the first two weeks of life, rose more than 5-fold in the next 20 days to attain a peak in 30-day-old rats, and thereafter declined to the values of adult animals. There was no significant reductase activity (conversion of 11-dehydrocorticosterone to corticosterone) in any intestinal segment of young and adult rats. The regulation of intestinal 11β-OHSD by corticosteroids and thyroid hormones was studied in the ileum and distal colon. In weanling rats, adrenalectomy or a high-salt diet decreased 11β-OHSD activities in both intestinal segments whereas dexamethasone administration prevented this decline in adrenalectomized rats and administration of deoxycorticosterone acetate led to a significant increase of intestinal 11β-OHSD activities in rats kept on a high-salt diet. Dexamethasone administration to intact adult rats also stimulated 11 β-OHSD activity in the ileum and distal colon. The changes in thyroid status of weanling rats did not change the 11β-OHSD activities. We conclude that (1) the developmental patterns of 11β-OHSD activity in the small and large intestine are not identical and this discrepancy may facilitate the maturation effect of glucocorticoids in the small intestine and the stimulatory effect of aldosterone in the large intestine and (2) corticosteroids but not thyroid hormones can modulate 11β-OHSD activity in the developing intestine.
Journal of Endocrinology (1996) 148, 561–566
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Leptin, a hormone produced and secreted by adipose tIssue, muscles and stomach, is involved in the regulation of adipose tIssue mass, food intake and body weight in neonatal animals. It is also produced in the mammary glands and secreted into the colostrum and milk. Since leptin receptors are widely distributed in the small intestine mucosa, the aim of the present study was to investigate the effect of exogenous leptin on the development of the small intestine in neonatal piglets. Male neonatal piglets were fed with sow's milk or artificial milk formula. Every 8 h the latter received either vehicle or leptin (2 or 10 microg/kg body weight). The animals were either killed after 6 days of treatment and the small intestine sampled for histology and brush border enzyme activities or were tested for marker molecule (Na-fluorescein and BSA) absorption in vivo. Feeding milk formula slowed the maturation of small intestinal mucosa compared with feeding sow's milk. However, after leptin treatment the length of the small intestine was increased, and intestinal villi length, but not crypt size, was reduced compared with controls. The mitotic index was increased and the percentage of vacuolated enterocytes was reduced in the entire small intestine. Enterocyte brush border protease and lactase activities were reduced in the jejunum. Na-fluorescein marker molecule absorption did not change but that of BSA was reduced 3.8-fold. In conclusion, exogenous leptin administered in physiological doses reversed the maturation of the small intestinal mucosa to the range found in sow-reared piglets.
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SUMMARY
Using a new technique for determining transmucosal electrical potential difference (p.d.) and short-circuit current (Isc.) in the rat small intestine in vivo it would appear that aldosterone had no direct effect on these parameters of intestinal activity. However, adrenalectomy decreased the Isc. while after adrenalectomy aldosterone and cortisol (hydrocortisone) restored the lowered independent and probably also the lowered dependent (hexose) Isc.
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SUMMARY
The absorption of calcium from duodenal and jejunal segments of the small intestine was studied in rats using an in-vivo loop technique. Previous parathyroidectomy decreased calcium absorption from both segments in rats fed a normal diet. Reduced calcium transport was greater in rats fed a calcium-deficient diet after parathyroidectomy. The slower clearance of radioactive calcium from the lumen of the intestine was not due to increased endogenous calcium excretion. Thyroidectomy, either alone or combined with parathyroidectomy, decreased calcium absorption but the effect of thyroidectomy alone requires further study. The decrease in calcium absorption after removal of the parathyroids was minimal or absent when the animals were fed a high calcium, low phosphorus, vitamin D-deficient diet or fasted 48 hr. before the experiment.
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The villous epithelial cells of the terminal part of the rat small intestine readily absorb maternal antibodies and certain other macromolecules up to the 18th day after birth. Between 18 and 21 days, however, these cells are progressively replaced by more mature cells, and the uptake of macromolecules declines to zero (Clarke & Hardy, 1969a, b). This process has been termed 'closure'.
Closure can be induced at least 9 days before the normal time by the administration of deoxycorticosterone acetate or cortisone acetate (Halliday, 1959). Furthermore, bilateral adrenalectomy at 15–18 days after birth has been shown to delay the time of closure (Daniels & Hardy, 1971). These results suggest that the functional development of the adrenal cortex may determine the maturation of the small intestine with respect to its ability to absorb macromolecules.
In order to investigate further the possible role of the adrenal gland in the mechanism of
