No abstract

Neonates with intrauterine growth restriction (IUGR) are prone to suffer from digestive diseases. Using neonatal pigs with IUGR, we tested the hypothesis that IUGR may induce alterations in the developmental pattern of intestinal barrier and thereby may be responsible for IUGR-associated increased morbidity. Piglets with a birth weight near the mean birth weight (+/-0.5 SD) were identified as normal birth weight (control) and piglets with a mean -2 SD lower birth weight (-30%) were defined as piglets with IUGR. The developmental pattern of intestinal structure, transcriptomic profile, and bacterial colonization was investigated from birth to d 5 postnatal. At birth, intestinal weight and length, ileal and colonic weight per unit of length, and villous sizes were lower (P < 0.05) in piglets with IUGR than in same-age control piglets. These IUGR-induced intestinal alterations further persisted, although they were less marked at d 5. Counts of adherent bacteria to ileal and colonic mucosa were greater (P < 0.05) in 2-d-old piglets with IUGR than in same-age control piglets. Dynamic analyses of the transcriptomic profile of the intestine revealed molecular evidence of IUGR-induced intestinal growth impairment that may result from a change in the cell proliferation-apoptosis balance during the first days of life, while a protective process would occur later on. In addition, changes in the expression of several genes suggest a pivotal role of both glucocorticoids and microbiota in driving IUGR intestinal development during the neonatal period.

Predicting aspects of pork quality becomes increasingly important from both a nutritional and technological point of view. The aim of the present study was to provide quantitative information on the relation between nutrient intake and whole-body fatty acid (FA) deposition. This information is essential to develop mechanistic models predicting the FA content of tissues. A serial slaughter study was carried out in which thirty pigs were slaughtered between 90 and 150 kg. The diet included 15 g/kg soyabean oil and contained 44 g/kg fat. Only 0·31 and 0·40 of the digested n-6 and n-3 FA were deposited, respectively. Approximately one-third of the n-3 supply that was deposited resulted from the conversion of 18 : 3 to other metabolites (i.e. EPA, docosapentaenoic acid and DHA). This proportion was affected by the pig genotype. De novo-synthesised FA represented 0·86 of the total non-essential FA deposition, and its average composition corresponded to 0·017, 0·286, 0·025, 0·217 and 0·454 for 14 : 0, 16 : 0, 16 : 1, 18 : 0 and 18 : 1, respectively. Although the average whole-body FA composition was relatively constant during the finishing period, this was not so for the tissues. In the carcass (without backfat), the content of 18 : 1 increased during the finishing period, whereas that of 16 : 0 and 18 : 0 decreased. Backfat captured a proportionally greater fraction of 18 : 2 than did the carcass or the residual tissues. In contrast, a proportionally greater fraction of the dietary 18 : 3 supply was deposited in the carcass compared to other tissues.

This article is available online at http://www.jlr.org derived from the biosynthetic pathways resulting in the conversion of essential precursors to their respective elongated polyenoic products.The availability of PUFA in mammalian cells greatly depends on the activity of enzymes involved in FA metabolism. In animals and humans, the ⌬ 5-and ⌬ 6-desaturases are the pivotal enzymes introducing de novo unsaturations in the carbon chain of precursors leading to the synthesis of long-chain PUFA (LC-PUFA). These enzymes were cloned 10 years ago from mammals ( 2-5 ). In parallel, Marquardt et al. ( 6 ) described the human genomic structure of the fatty acid desaturase ( FADS ) cluster including the FADS1 and FADS2 genes coding, respectively, for the ⌬ 5-and ⌬ 6-desaturases. A third gene, named FADS3 , was identifi ed, revealing 62% and 70% nucleotide sequence identity with FADS1 and FADS2 , respectively. Further studies showed a signifi cant correlation between FADS3 polymorphism and lipid metabolism markers such as PUFA, high density-or low density-lipoprotein cholesterol, and triglyceride levels ( 7-10 ). The newly discovered gene was thereafter integrated into a serial analysis of gene expression and a DNA microarray succeeding in more physiological data. FADS3 was therefore found to be highly expressed at the implantation site of the embryo in mouse uterus ( 11 ) and downregulated during human neurogenic differentiation ( 12 ). More recently, Park et al. described, in baboon, different alternative transcripts of FADS3 generated by alternative splicing, which suggests the occurrence of multiple FADS3 gene products ( 13 ). This study also showed a different pattern of expression in response to human neuroblastoma SK-N-SH cell differentiation. All data together only concern the FADS3 gene with no description of the functional role of the putative FADS3 protein. PUFAs are key components involved in a variety of physiological functions ( 1 ). Some of them, belonging to the n-6 or n-3 families, have to be fulfi lled from the diet or This work was supported by the Région Bretagne, the Groupe Lipides et Nutrition, Valorex (Combourtillé, France), and Polaris (Pleuven, France).