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Exogenous Leptin Controls the Development of the Small Intestine in Neonatal Piglets

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215 Exogenous leptin controls the development of the small intestine in neonatal piglets J Wolin´ ski, M Biernat, P Guilloteau1, B R Weström2 and R Zabielski The Kielanowski Institute of Animal Physiology and Nutrition, Polish Academy of Sciences, 05-110 Jabłonna, Instytucka 3, Poland 1Unité Mixte de Recherches sur le Veau et le Porc, INRA, 35590 Rennes, France 2Institute of Cell and Organism Biology, Lund University, Lund, Sweden (Requests for offprints should be addressed to R Zabielski; Email: [email protected]) Abstract Leptin, a hormone produced and secreted by adipose absorption in vivo. Feeding milk formula slowed the tissue, muscles and stomach, is involved in the regulation maturation of small intestinal mucosa compared with of adipose tissue mass, food intake and body weight in feeding sow’s milk. However, after leptin treatment the neonatal animals. It is also produced in the mammary length of the small intestine was increased, and intestinal glands and secreted into the colostrum and milk. Since villi length, but not crypt size, was reduced compared with leptin receptors are widely distributed in the small intes- controls. The mitotic index was increased and the per- tine mucosa, the aim of the present study was to investi- centage of vacuolated enterocytes was reduced in the gate the effect of exogenous leptin on the development of entire small intestine. Enterocyte brush border protease the small intestine in neonatal piglets. Male neonatal and lactase activities were reduced in the jejunum. Na- piglets were fed with sow’s milk or artificial milk formula. fluorescein marker molecule absorption did not change but Every 8 h the latter received either vehicle or leptin (2 or that of BSA was reduced 3·8-fold. In conclusion, exogen- 10 µg/kg body weight). The animals were either killed ous leptin administered in physiological doses reversed the after 6 days of treatment and the small intestine sampled maturation of the small intestinal mucosa to the range for histology and brush border enzyme activities or were found in sow-reared piglets. tested for marker molecule (Na-fluorescein and BSA) Journal of Endocrinology (2003) 177, 215–222 Introduction leptin concentrations. Silva and co-workers (1999) showed that leptin is synthesized in the mammary gland and Leptin is a 167 amino acid protein, first discovered in excreted with milk. In contrast, Casabiell and co-workers adipose tissue (Zhang et al. 1994) and after that in a wide (1997) demonstrated that leptin is transferred from the variety of tissues, including the mammary gland (Smith- circulation to the mammary gland, then without loss of Kirwin et al. 1998, Aoki et al. 1999, Silva & VandeHaar biological activity, to the milk and after that to the infant’s 1999, Bonnet et al. 2002). Smith-Kirwin and co-workers stomach and general blood circulation. The biologically (1998) demonstrated the biosynthesis of leptin in human active form of the leptin receptor (OB-Rb) (Cioffi et al. placenta and suggested a plausible role of the hormone in 1996, Lee et al. 1996) is widespread, and has been localized foetal growth. After birth, colostrum and milk take over in the entire length of the small intestine (Morton et al. some of the placenta’s functions, especially in regard to the 1998). Using immunostaining, Barrenetxe et al. (2002) delivery of maternal hormones and growth factors to the demonstrated the leptin receptor within the cytoplasm of neonate. This is true also for leptin, which has been enterocytes located on both intestinal villi and crypts in the identified in human, mouse, rat and pig colostrum and human, rat and mouse small intestine. In human entero- milk (Casabiell et al. 1997, Houseknecht et al. 1997, Aoki cytes, the OB-Rb receptor (long form of the leptin et al. 1999, Estienne et al. 2000, Ucar et al. 2000). It is receptor) was also found in the brush border plasma noteworthy that in humans, leptin is present in whole membrane (Barrenetxe et al. 2002). breast milk at 30- to 150-fold higher concentrations than These studies suggest that ‘milk-borne’ leptin may play in milk formula (Houseknecht et al. 1997, Smith-Kirwin aroleintheoffspring, although its effect on the develop- et al. 1998), and its concentration in breast milk is ment of the neonatal gastrointestinal tract has never been positively correlated with maternal and/or infant plasma experimentally verified. The aim of the present study was Journal of Endocrinology (2003) 177, 215–222 Online version via http://www.endocrinology.org 0022–0795/03/0177–215 2003 Society for Endocrinology Printed in Great Britain Downloaded from Bioscientifica.com at 09/28/2021 04:44:30PM via free access 216 J WOLINuSKI and others · Leptin controls small intestinal development to investigate the role of exogenous leptin in the develop- (Leptin Mouse Recombinant; Sigma, St Louis, MO, USA) ment of the small intestine of neonatal piglets fed artificial at a dose of 2 µg/kg body weight – group L2 (n=6), or milk formula. Development was evaluated in regard to the 10 µg/kg body weight – group L10 (n=6) every 8 h via a microscopic structure of the intestinal mucosa, brush stomach tube. The pH of the vehicle was 5·8, which is border-specific enzyme activities and in vivo intestinal optimal for leptin bioactivity and similar to that of the absorption of marker molecules. ingested milk replacer. After 6 days of vehicle or leptin treatment the animals were killed by pentobarbiturate (Vetbutal; Biowet, Poland) overdose, and the gastro- Materials and Methods intestinal tract was removed for morphometric analysis and tissue sampling. The stomach and pancreas were weighed Animal experiments and the small intestine’s weight and length determined. The experiments and treatments were conducted in com- Whole-thickness samples of the duodenum, proximal pliance with the European Union regulations concerning (25%), middle (50%) and distal (75%) jejunum and ileum the protection of experimental animals. The Local Ethics were harvested and fixed in Bouin’s solution for histologi- Committee approved the study protocol. A total of 44 cal analysis. The corresponding 15 cm long intestine male neonatal piglets (Polish LandracePietrain) from segments were gently scraped to collect the mucosa for nine different litters were purchased from a commercial enzyme activity analysis. In the second series, eight piglets pig farm. The average birth weight was 1·600·15 kg. were divided into two groups receiving saline (CM, n=4) The piglets were delivered healthy and without compli- or leptin at a dose of 10 µg/kg body weight (LM, n=4) cations, and were kept with their sows for 24 h, except six using an identical schedule as in the first series. On day 6 of them that were kept with their sows for 7 days (control they were implanted with Silastic catheters in the left group of sow-reared piglets (CSR)). Six animals were jugular vein under general halothane anaesthesia, and on killed by pentobarbiturate overdose 24 h after birth, and the day after, a test of in vivo intestinal absorptive capacity another six were killed 7 days after birth (CSR), and was performed. In the morning, the CM and LM groups sampled like those described below. The other 26 animals received a marker molecule cocktail by a stomach tube. were installed (initially in groups of four piglets) in the The cocktail contained: 500 mg/kg BSA (67 kDa, Cat. laboratory in a special cage equipped with an ‘artificial No. A-4503; Sigma) and 9·4 mg/kg Na-fluorescein sow’. The laboratory provided a 12 h light:12 h darkness (376 Da; Merck, Darmstadt, Germany). The components cycle and an ambient temperature that was decreased from were dissolved in 0·9% NaCl immediately before admin- 32 Cto28C over the 6 days of the experiment to ensure istration and given to the pigs in a volume of 4 ml/kg body a comfortable environment for neonatal piglets. At the weight. For marker molecule analysis, 4 ml venous blood beginning of each trial, four piglets were kept together for samples were taken just before administration (0 h) and an approximately 12 h period of adaptation. After that, the after 0·5, 1, 2, 4, 8 and 24 h. After the last blood sample piglets were housed individually in a manner providing was taken, the animals were killed by pentobarbiturate social contact with each other. Milk-replacer formula for overdose. The blood samples were centrifuged at 3000 g piglets (protein 19·8%; fat 19·7%; ash 8·2%; Milky Farm, (4 C) for 15 min and the plasma harvested and stored Nukamel Olen, Belgium) was distributed to each piglet frozen (20 C) until analysis. every 75 min (20 times per 24 h) in equal amounts by means of an artificial sow (Research Centre Foulum- Mucosa histology and laser scanning cytometry (LSC) model, Pig’s oline; Boss’ Produkter a/s, Denmark). The daily amount of milk replacer was calculated on the basis of Serial histological sections of 5 µm thickness were cut and daily body weight gain and protein intake. Body weight stained with haematoxylin and eosin for morphometric was recorded every morning. Protein intake in neonatal analysis under a light microscope. After staining, the depth pigs rose gradually from 11·0 to 11·3 g/kg body weight of crypts, length of villi and thickness of the tunica mucosa during the first 7 days of life. The concentration of protein were measured in the small intestine preparations at a low in milk formula was 20% of dry matter (V Lesniewska & magnification with a Nikon type 104 (Nikon Corporation, M Hedemann, unpublished observations). Sow colostrum Yokohama, Japan) optical binocular microscope coupled and milk, artificial milk formula and plasma blood samples via a camera to a computer.
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