Metabolomic Profiles Reveal Potential Factors that Correlate with Lactation Performance in Sow Milk

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Sow milk contains necessary nutrients for piglets; however, the relationship between the levels of metabolites in sow milk and lactation performance has not been thoroughly elucidated to date. In this study, we analysed the metabolites in sow milk from Yorkshire sows with high lactation (HL) or low lactation (LL) performance; these categories were assigned based on the weight gain of piglets during the entire lactation period (D1 to D21). The concentration of milk fat in the colostrum tended to be higher in the HL group (P = 0.05), the level of mannitol was significantly lower in the HL group ( P < 0.05) and the level of glucuronic acid lactone was significantly higher in the HL group ( P < 0.05) compared to those in LL group. In mature milk, the levels of lactose, creatine, glutamine, glutamate, 4-hydroxyproline, alanine, asparagine, and glycine were significantly higher ( P < 0.05) in the HL group than those in LL group. The level of fatty acids showed no significant difference between the two groups in both the colostrum and mature milk. This study suggested that lactation performance may be associated with the levels of lactose and several amino acids in sow milk, and these results can be used to develop new feed additives to improve lactation performance in sows.

Related collections

Most cited references 48

Record: found
Abstract: found
Article: not found

A creatine-driven substrate cycle enhances energy expenditure and thermogenesis in beige fat.

Lawrence Kazak, Edward Chouchani, Mark P. Jedrychowski … (2015)

Thermogenic brown and beige adipose tissues dissipate chemical energy as heat, and their thermogenic activities can combat obesity and diabetes. Herein the functional adaptations to cold of brown and beige adipose depots are examined using quantitative mitochondrial proteomics. We identify arginine/creatine metabolism as a beige adipose signature and demonstrate that creatine enhances respiration in beige-fat mitochondria when ADP is limiting. In murine beige fat, cold exposure stimulates mitochondrial creatine kinase activity and induces coordinated expression of genes associated with creatine metabolism. Pharmacological reduction of creatine levels decreases whole-body energy expenditure after administration of a β3-agonist and reduces beige and brown adipose metabolic rate. Genes of creatine metabolism are compensatorily induced when UCP1-dependent thermogenesis is ablated, and creatine reduction in Ucp1-deficient mice reduces core body temperature. These findings link a futile cycle of creatine metabolism to adipose tissue energy expenditure and thermal homeostasis. PAPERCLIP.

0 comments Cited 351 times – based on 0 reviews      Review now

Record: found
Abstract: found
Article: not found

The mTORC1 pathway stimulates glutamine metabolism and cell proliferation by repressing SIRT4.

Alfred Csibi, Sarah-Maria Fendt, Chenggang Li … (2013)

Proliferating mammalian cells use glutamine as a source of nitrogen and as a key anaplerotic source to provide metabolites to the tricarboxylic acid cycle (TCA) for biosynthesis. Recently, mammalian target of rapamycin complex 1 (mTORC1) activation has been correlated with increased nutrient uptake and metabolism, but no molecular connection to glutaminolysis has been reported. Here, we show that mTORC1 promotes glutamine anaplerosis by activating glutamate dehydrogenase (GDH). This regulation requires transcriptional repression of SIRT4, the mitochondrial-localized sirtuin that inhibits GDH. Mechanistically, mTORC1 represses SIRT4 by promoting the proteasome-mediated destabilization of cAMP-responsive element binding 2 (CREB2). Thus, a relationship between mTORC1, SIRT4, and cancer is suggested by our findings. Indeed, SIRT4 expression is reduced in human cancer, and its overexpression reduces cell proliferation, transformation, and tumor development. Finally, our data indicate that targeting nutrient metabolism in energy-addicted cancers with high mTORC1 signaling may be an effective therapeutic approach. Copyright © 2013 Elsevier Inc. All rights reserved.

0 comments Cited 245 times – based on 0 reviews      Review now

Record: found
Abstract: found
Article: not found

Functional amino acids in nutrition and health.

Guoyao Wu (2013)

The recent years have witnessed growing interest in biochemistry, physiology and nutrition of amino acids (AA) in growth, health and disease of humans and other animals. This results from the discoveries of AA in cell signaling involving protein kinases, G protein-coupled receptors, and gaseous molecules (i.e., NO, CO and H2S). In addition, nutritional studies have shown that dietary supplementation with several AA (e.g., arginine, glutamine, glutamate, leucine, and proline) modulates gene expression, enhances growth of the small intestine and skeletal muscle, or reduces excessive body fat. These seminal findings led to the new concept of functional AA, which are defined as those AA that participate in and regulate key metabolic pathways to improve health, survival, growth, development, lactation, and reproduction of the organisms. Functional AA hold great promise in prevention and treatment of metabolic diseases (e.g., obesity, diabetes, and cardiovascular disorders), intrauterine growth restriction, infertility, intestinal and neurological dysfunction, and infectious disease (including viral infections).

0 comments Cited 190 times – based on 0 reviews      Review now

All references

Author and article information

Contributors

Baichuan Deng: dengbaichuan@scau.edu.cn

Jinping Deng: dengjinping@scau.edu.cn

Yulong Yin: yinyulong@isa.ac.cn

Journal

Journal ID (nlm-ta): Sci Rep

Journal ID (iso-abbrev): Sci Rep

Title: Scientific Reports

Publisher: Nature Publishing Group UK (London )

ISSN (Electronic): 2045-2322

Publication date (Electronic): 16 July 2018

Publication date PMC-release: 16 July 2018

Publication date Collection: 2018

Volume: 8

Electronic Location Identifier: 10712

Affiliations

[1 ]ISNI 0000 0000 9546 5767, GRID grid.20561.30, Guangdong Provincial Key Laboratory of Animal Nutrition Control, Institute of Subtropical Animal Nutrition and Feed, College of Animal Science, , South China Agricultural University, ; Guangzhou, 510642 P.R. China

[2 ]GRID grid.268415.c, Jiangsu Co-Innovation Center for Important Animal Infectious Diseases and Zoonoses, Joint International Research Laboratory of Agriculture and Agri-Product Safety of Ministry of Education of China, College of Veterinary Medicine, , Yangzhou University, ; Yangzhou, 225009 China

[3 ]National Engineering Laboratory for Pollution Control and Waste Utilization in Livestock and Poultry Production, Institute of Subtropical Agriculture, The Chinese Academy of Sciences, Changsha, 410125 P.R. China

Author information

Zhenya Zhai http://orcid.org/0000-0002-7657-8429

Article

Publisher ID: 28793

DOI: 10.1038/s41598-018-28793-0

PMC ID: 6048051

PubMed ID: 30013051

SO-VID: f1b9054d-e2b1-45f0-bbb3-33db54601870

License:

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

History

Date received : 12 October 2017

Date accepted : 25 June 2018

Funding

Funded by: FundRef https://doi.org/10.13039/501100001809, National Natural Science Foundation of China (National Science Foundation of China);

Award ID: 31330075

Award ID: 31572420

Award ID: 31110103909

Award Recipient : Hongrong Long

Custom metadata

ScienceOpen disciplines: Uncategorized

Data availability:

ScienceOpen disciplines: Uncategorized

Comments

Comment on this article

Cited by 18

See all cited by

Most referenced authors 491

See all reference authors