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Zhong H, Li H, Liu G, et al. Increased maternal consumption of methionine as its hydroxyl analog promoted neonatal intestinal growth without compromising maternal energy homeostasis. J Anim Sci Biotechnol. 2016;7:46doi: 10.1186/s40104-016-0103-y.
Zhong, H., Li, H., Liu, G., Wan, H., Mercier, Y., Zhang, X., Lin, Y., Che, L., Xu, S., Tang, L., Tian, G., Chen, D., Wu, & Fang, Z. (2016). Increased maternal consumption of methionine as its hydroxyl analog promoted neonatal intestinal growth without compromising maternal energy homeostasis. Journal of animal science and biotechnology, 746. https://doi.org/10.1186/s40104-016-0103-y
Zhong, Heju, et al. "Increased maternal consumption of methionine as its hydroxyl analog promoted neonatal intestinal growth without compromising maternal energy homeostasis." Journal of animal science and biotechnology vol. 7 (2016): 46. doi: https://doi.org/10.1186/s40104-016-0103-y
Zhong H, Li H, Liu G, Wan H, Mercier Y, Zhang X, Lin Y, Che L, Xu S, Tang L, Tian G, Chen D, Wu, Fang Z. Increased maternal consumption of methionine as its hydroxyl analog promoted neonatal intestinal growth without compromising maternal energy homeostasis. J Anim Sci Biotechnol. 2016 Aug 05;7:46. doi: 10.1186/s40104-016-0103-y. eCollection 2016. PMID: 27499853; PMCID: PMC4975900.
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J Anim Sci Biotechnol. 2016 Aug 05;7:46. doi: 10.1186/s40104-016-0103-y. eCollection 2016.

Increased maternal consumption of methionine as its hydroxyl analog promoted neonatal intestinal growth without compromising maternal energy homeostasis.

Journal of animal science and biotechnology

Heju Zhong, Hao Li, Guangmang Liu, Haifeng Wan, Yves Mercier, Xiaoling Zhang, Yan Lin, Lianqiang Che, Shengyu Xu, Li Tang, Gang Tian, Daiwen Chen, De Wu, Zhengfeng Fang

Affiliations

  1. Key Laboratory for Animal Disease Resistance Nutrition of the Ministry of Education, Animal Nutrition Institute, Sichuan Agricultural University, Ya'an, 625014 China.
  2. Adisseo France S.A.S., CERN, Commentry, France.

PMID: 27499853 PMCID: PMC4975900 DOI: 10.1186/s40104-016-0103-y

Abstract

BACKGROUND: To determine responses of neonatal intestine to maternal increased consumption of DL-methionine (DLM) or DL-2-hydroxy-4-methylthiobutanoic acid (HMTBA), eighteen primiparous sows (Landrace × Yorkshire) were allocated based on body weight and backfat thickness to the control, DLM and HMTBA groups (n = 6), with the nutritional treatments introduced from postpartum d0 to d14.

RESULTS: The DLM-fed sows showed negative energy balance manifested by lost bodyweight, lower plasma glucose, subdued tricarboxylic acid cycle, and increased plasma lipid metabolites levels. Both villus height and ratio of villus height to crypt depth averaged across the small intestine of piglets were higher in the DLM and HMTBA groups than in the control group. Piglet jejunal oxidized glutathione concentration and ratio of oxidized to reduced glutathione were lower in the HMTBA group than in the DLM and control groups. However, piglet jejunal aminopeptidase A, carnitine transporter 2 and IGF-II precursor mRNA abundances were higher in the DLM group than in the HMTBA and control groups.

CONCLUSION: Increasing maternal consumption of methionine as DLM and HMTBA promoted neonatal intestinal growth by increasing morphological development or up-regulating expression of genes responsible for nutrient metabolism. And increasing maternal consumption of HMTBA promoted neonatal intestinal antioxidant capacity without compromising maternal energy homeostasis during early lactation.

Keywords: Energy metabolism; Intestine; Lactating sows; Methionine nutrition; Neonatal pigs

References

  1. J Inherit Metab Dis. 2003;26(2-3):147-69 - PubMed
  2. Annu Rev Nutr. 1986;6:563-97 - PubMed
  3. J Cell Biol. 2009 Dec 14;187(6):889-903 - PubMed
  4. J Nutr. 2004 Mar;134(3):489-92 - PubMed
  5. Am J Physiol Endocrinol Metab. 2009 Jun;296(6):E1239-50 - PubMed
  6. Gene. 1996 Dec 5;182(1-2):71-5 - PubMed
  7. J Physiol. 2002 Nov 15;545(Pt 1):133-44 - PubMed
  8. Methods. 2001 Dec;25(4):402-8 - PubMed
  9. Br J Nutr. 2012 Jun;107(11):1603-15 - PubMed
  10. Br J Nutr. 2011 Aug;106(3):350-6 - PubMed
  11. DNA. 1986 Oct;5(5):357-61 - PubMed
  12. J Nutr. 1996 Oct;126(10):2578-84 - PubMed
  13. J Biol Chem. 1984 Aug 10;259(15):9508-13 - PubMed
  14. Pediatr Res. 1987 Sep;22(3):330-4 - PubMed
  15. Br J Nutr. 2015 Feb 28;113(4):585-95 - PubMed
  16. News Physiol Sci. 2003 Oct;18:201-4 - PubMed
  17. Br J Nutr. 2012 Sep 28;108(6):1069-76 - PubMed
  18. J Biol Chem. 2000 Dec 22;275(51):40064-72 - PubMed
  19. Br J Nutr. 2001 Dec;86(6):661-74 - PubMed
  20. Life Sci. 1986 Jul 14;39(2):103-10 - PubMed
  21. J Anim Sci. 1998 Apr;76(4):1216-31 - PubMed
  22. Prostaglandins Leukot Essent Fatty Acids. 2004 Mar;70(3):243-51 - PubMed
  23. Physiol Rev. 2000 Jul;80(3):1107-213 - PubMed
  24. Appl Microbiol Biotechnol. 2010 Feb;85(5):1383-91 - PubMed
  25. Biochim Biophys Acta. 1981 Mar 13;658(1):148-57 - PubMed
  26. Amino Acids. 2009 Mar;36(3):501-9 - PubMed
  27. FASEB J. 1999 Jul;13(10):1169-83 - PubMed
  28. Biol Neonate. 1994;66(5):280-7 - PubMed
  29. Amino Acids. 2010 Aug;39(3):633-40 - PubMed
  30. Cell Stem Cell. 2011 Feb 4;8(2):188-99 - PubMed
  31. Am J Physiol Lung Cell Mol Physiol. 2009 Jan;296(1):L37-45 - PubMed
  32. Anal Chem. 2005 Jan 15;77(2):517-26 - PubMed
  33. Lancet. 2000 Mar 4;355(9206):827-35 - PubMed
  34. Eur J Biochem. 2004 Nov;271(21):4298-306 - PubMed
  35. Biochim Biophys Acta. 1980 Jun 5;630(1):1-9 - PubMed
  36. J Clin Invest. 1971 Jul;50(7):1536-45 - PubMed
  37. Am J Physiol Regul Integr Comp Physiol. 2001 Dec;281(6):R1986-93 - PubMed
  38. Biochim Biophys Acta. 1965 Dec 16;111(2):384-92 - PubMed
  39. J Anim Sci. 2009 Oct;87(10):3156-66 - PubMed
  40. Br J Nutr. 2014 Sep 28;112(6):855-67 - PubMed
  41. J Nutr. 2008 Jun;138(6):1025-32 - PubMed
  42. Hypertens Res. 2010 May;33(5):511-4 - PubMed
  43. J Nutr Biochem. 2009 Jul;20(7):544-52 - PubMed

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