Key Laboratory of Animal Disease Resistance Nutrition and Feed Science

China

Key Laboratory of Animal Disease Resistance Nutrition and Feed Science

China

Time filter

Source Type

Che L.,Key Laboratory of Animal Disease Resistance Nutrition and Feed Science | Che L.,Sichuan Agricultural University | Yang Z.G.,Key Laboratory of Animal Disease Resistance Nutrition and Feed Science | Yang Z.G.,Sichuan Agricultural University | And 18 more authors.
BMC Genomics | Year: 2017

Background: Intra-uterine growth restriction (IUGR) and fetal overgrowth increase risks to postnatal health. Maternal nutrition is the major intrauterine environmental factor that alters fetal weight. However, the mechanisms underlying the effects of maternal nutrition on fetal development are not entirely clear. We developed a pig model, and using isobaric tags for relative and absolute quantification (iTRAQ), we investigated alterations in the placental proteome of gilts on a normal-energy-intake (Con) and high-energy-intake (HE) diet. Results: In the Con group, heavy and light fetuses were found at the tubal and cervical ends of the uterus respectively at 90 d of gestation. Moreover, the heavy fetuses had a higher glucose concentration than the light fetuses. However, a higher uniformity was noted in the HE group. Placental promoters between these two positions indicated that 78 and 50 differentially expressed proteins were detected in the Con and HE groups respectively. In the Con group, these proteins were involved in lipid metabolism (HADHA, AACS, CAD), nutrient transport (GLUT, SLC27A1), and energy metabolism (NDUFV1, NDUFV2, ATP5C1). However, in the HE group they mainly participated in transcriptional and translational regulation, and intracellular vesicular transport. Conclusions: Our findings revealed that maternal nutrition may alter birth weight mainly through the modulation of placental lipid and energy metabolism, which also provides a possible mechanism to explain the higher uniformity of fetal weight in gilts fed a HE diet. © 2017 The Author(s).


Yu C.,Sichuan Agricultural University | Yu C.,Key Laboratory of Animal Disease Resistance Nutrition and Feed Science | Jia G.,Sichuan Agricultural University | Jia G.,Key Laboratory of Animal Disease Resistance Nutrition and Feed Science | And 10 more authors.
Asian-Australasian Journal of Animal Sciences | Year: 2014

The glucagon-like peptide 2 (GLP-2) that is expressed in intestine epithelial cells of mammals, is important for intestinal barrier function and regulation of tight junction (TJ) proteins. However, there is little known about the intracellular mechanisms of GLP-2 in the regulation of TJ proteins in piglets' intestinal epithelial cells. The purpose of this study is to test the hypothesis that GLP-2 regulates the expressions of TJ proteins in the mitogen-activated protein kinase (MAPK) signaling pathway in piglets' intestinal epithelial cells. The jejunal tissues were cultured in a Dulbecco's modified Eagle's medium/high glucose medium containing supplemental 0 to 100 nmol/L GLP-2. At 72 h after the treatment with the appropriate concentrations of GLP-2, the mRNA and protein expressions of zonula occludens-1 (ZO-1), occludin and claudin-1 were increased (p<0.05). U0126, an MAPK kinase inhibitor, prevented the mRNA and protein expressions of ZO-1, occludin, claudin-1 increase induced by GLP-2 (p<0.05). In conclusion, these results indicated that GLP-2 could improve the expression of TJ proteins in weaned pigs' jejunal epithelium, and the underlying mechanism may due to the MAPK signaling pathway. Copyright © 2014 by Asian-Australasian Journal of Animal Sciences.


Yu C.,Key Laboratory of Animal Disease Resistance Nutrition and Feed Science | Jia G.,Sichuan Agricultural University | Deng Q.,Sichuan Agricultural University | Zhao H.,Sichuan Agricultural University | And 3 more authors.
Asian-Australasian Journal of Animal Sciences | Year: 2016

Glucagon-like peptide-2 (GLP-2) is important for intestinal barrier function and regulation of tight junction (TJ) proteins, but the intracellular mechanisms of action remain undefined. The purpose of this research was to determine the protective effect of GLP-2 mediated TJ and transepithelial electrical resistance (TER) in lipopolysaccharide (LPS) stressed IPEC-J2 cells and to test the hypothesis that GLP-2 regulate TJ and TER through the phosphatidylinositol 3-kinase (PI3K)-protein kinase B (Akt)-mammalian target of rapamycin (mTOR) signaling pathway in IPEC-J2 cells. Wortmannin and LY294002 are specific inhibitors of PI3K. The results showed that 100 μg/mL LPS stress decreased TER and TJ proteins occludin, claudin-1 and zonula occludens protein 1 (ZO-1) mRNA, proteins expressions (p<0.01) respectively. GLP-2 (100 nmol/L) promote TER and TJ proteins occludin, claudin-1, and zo-1 mRNA, proteins expressions in LPS stressed and normal IPEC-J2 cells (p<0.01) respectively. In normal cells, both wortmannin and LY294002, PI3K inhibitors, prevented the mRNA and protein expressions of Akt and mTOR increase induced by GLP-2 (p<0.01) following with the significant decreasing of occludin, claudin-1, ZO-1 mRNA and proteins expressions and TER (p<0.01). In conclusion, these results indicated that GLP-2 can promote TJ's expression and TER in LPS stressed and normal IPEC-J2 cells and GLP-2 could regulate TJ and TER through the PI3K/Akt/mTOR pathway. Copyright © 2016 by Asian-Australasian Journal of Animal Sciences.

Loading Key Laboratory of Animal Disease Resistance Nutrition and Feed Science collaborators
Loading Key Laboratory of Animal Disease Resistance Nutrition and Feed Science collaborators