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      Metabolomic Profiling Reveals the Difference on Reproductive Performance between High and Low Lactational Weight Loss Sows

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          Abstract

          Sows suffering excess weight loss during lactation may delay weaning to estrus interval (WEI) and have a detrimental effect on subsequent reproductive performance, however, the underlying mechanism is not completely clear. Therefore, the goal of this study was to investigate physiological profiles manifested in plasma originating from high (HWL) and low lactational weight loss (LWL) sows. The plasma biochemical parameters, hormones, antioxidant parameters, and milk compositions were assessed. Furthermore, plasma metabolites were analyzed using ultrahigh-performance liquid chromatography/time-of-flight mass spectrometry in positive and negative ion modes. Results showed that HWL sows had a lower feed intake and higher lactational weight loss and prolonged WEI, but had similar litter performance and milk composition compared to LWL sows. These changes were associated with lower plasma insulin-like growth factor 1 and higher fibroblast growth factor 21 levels in the HWL sows. Moreover, HWL led to a severe oxidative stress and metabolic damage, as accompanied by excessive protein breakdown and lipids mobilization at weaning. Metabolomic analysis revealed differences in 46 compounds between HWL and LWL sows, and the identified compounds were enriched in metabolic pathways related to amino acids metabolism, fatty acids oxidation metabolism, bile acids biosynthesis, and nucleoside metabolism. These results provide the evidence for physiological mechanism in sows with excessive lactational weight loss that delayed the WEI. Metabolomic data provides essential information and gives rise to potential targets for the development of nutritional intervention strategies.

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          Most cited references53

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          Metabolomics activity screening for identifying metabolites that modulate phenotype

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            FGF21 contributes to neuroendocrine control of female reproduction

            Preventing reproduction during nutritional deprivation is an adaptive process that is conserved and essential for the survival of species. In mammals, the mechanisms that inhibit pregnancy during starvation are complex and incompletely understood 1–7 . Here we show that exposure of female mice to FGF21, a fasting-induced hepatokine, mimics infertility secondary to starvation. Mechanistically, FGF21 acts on the suprachiasmatic nucleus (SCN) in the hypothalamus to suppress the vasopressin-kisspeptin signaling cascade, thereby inhibiting the proestrus surge in luteinizing hormone. Mice lacking the FGF21 co-receptor, β-Klotho, in the SCN are refractory to the inhibitory effect of FGF21 on female fertility. Thus, FGF21 defines an important liver-neuroendocrine axis that modulates female reproduction in response to nutritional challenge.
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              Adenosine, energy metabolism and sleep homeostasis.

              Adenosine is directly linked to the energy metabolism of cells. In the central nervous system (CNS) an increase in neuronal activity enhances energy consumption as well as extracellular adenosine concentrations. In most brain areas high extracellular adenosine concentrations, through A1 adenosine receptors, decrease neuronal activity and thus the need for energy. Adenosine may be a final common pathway for various sleep factors. We have identified a relatively specific area, the basal forebrain (BF), which appears to be central in the regulation/execution of recovery sleep after sleep deprivation (SD), or prolonged wakefulness. Adenosine concentration increases in this area during SD, and this increase induces sleep while prevention of the increase during SD abolishes recovery sleep. The increase in adenosine is associated with local changes in energy metabolism as indicated by increases in levels of pyruvate and lactate and increased phosphorylation of AMP-activated protein kinase. The increases in adenosine and sleep are associated with intact cholinergic system since specific lesion of the BF cholinergic cells abolishes both. Whether adenosine during SD is produced by the cholinergic neurons or astrocytes associated with them remains to be explored. An interesting, but so far unexplored question regards the relationship between the local, cortical regulation of sleep homeostasis and the global regulation of the state of sleep as executed by lower brain mechanisms, including the BF. The increase in adenosine concentration during SD also in cortical areas suggests that adenosine may have a role in the local regulation of sleep homeostasis. The core of sleep need is probably related to primitive functions of life, like energy metabolism. It can be noted that this assumption in no way excludes the possibility that later in evolution additional functions may have developed, e.g., related to complex neuronal network functions like memory and learning. Copyright © 2010. Published by Elsevier Ltd.
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                Author and article information

                Journal
                Metabolites
                Metabolites
                metabolites
                Metabolites
                MDPI
                2218-1989
                04 December 2019
                December 2019
                : 9
                : 12
                : 295
                Affiliations
                [1 ]Key Laboratory for Animal Disease-Resistance Nutrition of China Ministry of Education, Institute of Animal Nutrition, Sichuan Agricultural University, No. 211, Huimin Road, Wenjiang District, Chengdu 611130, Sichuan, China; huliangsau90@ 123456hotmail.com (L.H.); clianqiang@ 123456hotmail.com (L.C.); 18283581065@ 123456163.com (C.W.); 15008318848@ 123456163.com (F.W.); fangzhengfeng@ 123456hotmail.com (Z.F.); linyan936@ 123456163.com (Y.L.); shengyu_x@ 123456hotmail.com (S.X.); fengb123d@ 123456163.com (B.F.); lijian522@ 123456hotmail.com (J.L.); zhuoyong@ 123456sicau.edu.cn (Y.Z.)
                [2 ]Department of Animal Science, Faculty of Science and Technology, Aarhus University, DK-8830 Tjele, Denmark; mihai.curtasu@ 123456anis.au.dk (M.V.C.); peter.theil@ 123456anis.au.dk (P.K.T.)
                Author notes
                [* ]Correspondence: wude@ 123456sicau.edu.cn ; Tel.: +86-835-288-5107
                [†]

                These authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0001-5263-9314
                https://orcid.org/0000-0003-1844-194X
                https://orcid.org/0000-0002-4415-8542
                https://orcid.org/0000-0001-6258-2729
                https://orcid.org/0000-0002-8348-4199
                Article
                metabolites-09-00295
                10.3390/metabo9120295
                6950487
                31817081
                95ad4075-6ff1-47d2-847c-5d39a6e776d9
                © 2019 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 25 October 2019
                : 28 November 2019
                Categories
                Article

                lactational weight loss,metabolites,oxidative stress,reproductive performance,sow

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