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      Effects of Birth Weight and Postnatal Nutritional Restriction on Skeletal Muscle Development, Myofiber Maturation, and Metabolic Status of Early-Weaned Piglets

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          Abstract

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          Light weaning weight piglets have slow post-weaning growth performance and require longer days to reach slaughter weight. Birth weight and early postnatal nutrient intake are the main factors contributing to light weaning weight. Our results suggested that intrauterine growth-retarded (IUGR) piglets fed adequately during the suckling period do not catch up with the same muscle growth and development compared with normal birth weight piglets. Postnatal early nutritional restriction resulted in impaired skeletal muscle growth and delayed myofiber maturation of the piglets.

          Abstract

          Piglets with light weaning weight commonly have a slow post-weaning growth rate due to impaired skeletal muscle development. Therefore, the present study aimed to investigate the impact of birth weight and nutrient intake on skeletal muscle development, myofiber maturation, and metabolic status of early-weaned piglets. Twelve pairs of normal birth weight and intrauterine growth-retarded (IUGR) piglets (seven days old) were randomly assigned to receive adequate nutrient intake or restricted nutrient intake for 21 days. Serum and muscle samples were collected for further analysis. The results indicated that muscle weight, cross-sectional areas, and muscular glycogen were lower ( p < 0.05) in both IUGR and restricted fed piglets. Nutrient restriction decreased the contents of RNA, the RNA to DNA ratio, and the percentages of myosin heavy chain (MyHC) IIx ( p < 0.05), whereas increased the activity of β-hydroxy-acyl-CoA-dehydrogenase (HAD), the ratio of HAD to citrate synthase, as well as the percentages of MyHC I ( p < 0.05). In addition, nutrient restriction significantly decreased muscular glycogen, mRNA levels of fatty acid transport protein 1, cationic amino acid transporter 1, and glucose transporter 4 in IUGR piglets compared with the other groups ( p < 0.05). The results of the present study showed that IUGR impaired skeletal muscle growth and disturbed the hormone and mRNA expression of genes related to energy metabolism, which led to a more severe energy deficit when receiving postnatal nutritional restriction. Postnatal nutritional restriction resulted in delayed myofiber maturation of the piglets, which may be associated with the transformation of MyHC isoform and the change of metabolic status.

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          Fetal origins of hyperphagia, obesity, and hypertension and postnatal amplification by hypercaloric nutrition.

          Environmental factors and diet are generally believed to be accelerators of obesity and hypertension, but they are not the underlying cause. Our animal model of obesity and hypertension is based on the observation that impaired fetal growth has long-term clinical consequences that are induced by fetal programming. Using fetal undernutrition throughout pregnancy, we investigated whether the effects of fetal programming on adult obesity and hypertension are mediated by changes in insulin and leptin action and whether increased appetite may be a behavioral trigger of adult disease. Virgin Wistar rats were time mated and randomly assigned to receive food either ad libitum (AD group) or at 30% of ad libitum intake, or undernutrition (UN group). Offspring from UN mothers were significantly smaller at birth than AD offspring. At weaning, offspring were assigned to one of two diets [a control diet or a hypercaloric (30% fat) diet]. Food intake in offspring from UN mothers was significantly elevated at an early postnatal age. It increased further with advancing age and was amplified by hypercaloric nutrition. UN offspring also showed elevated systolic blood pressure and markedly increased fasting plasma insulin and leptin concentrations. This study is the first to demonstrate that profound adult hyperphagia is a consequence of fetal programming and a key contributing factor in adult pathophysiology. We hypothesize that hyperinsulinism and hyperleptinemia play a key role in the etiology of hyperphagia, obesity, and hypertension as a consequence of altered fetal development.
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            Nuclear control of respiratory gene expression in mammalian cells.

            The mitochondrial respiratory apparatus is the product of both nuclear and mitochondrial genes. The protein coding capacity of mtDNA is restricted to the expression of 13 respiratory subunits and thus nuclear genes play a predominant role in the biosynthesis of the respiratory chain and in the expression of the mitochondrial genome. Transcriptional regulators that act on both nuclear and mitochondrial genes have been implicated in the bi-genomic expression of the respiratory chain. Mitochondrial transcription is directed by a small number of nucleus-encoded factors (Tfam, TFB1M, TFB2M, mTERF). The expression of these factors is coordinated with that of nuclear respiratory proteins through the action of transcriptional activators and coactivators. In particular, environmental signals induce the expression of PGC-1 family coactivators (PGC-1alpha, PGC-1beta, and PRC), which in turn target specific transcription factors (NRF-1, NRF-2, and ERR alpha) in the expression of respiratory genes. This system provides a mechanism for linking respiratory chain expression to environmental conditions and for integrating it with other functions related to cellular energetics. 2005 Wiley-Liss, Inc.
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              Consequences of birth weight for postnatal growth performance and carcass quality in pigs as related to myogenesis.

              In polytocous species such as the pig there is intralitter variation in birth weight and skeletal muscle fiber number. It is commonly recognized that low birth weight in piglets correlates with decreased survival and lower postnatal growth rates. In the majority of low birth weight piglets low numbers of muscle fibers differentiate during prenatal myogenesis, for genetic or maternal reasons, and those low birth weight piglets with reduced fiber numbers are unable to exhibit postnatal catch-up growth. Pigs of low birth weight show the lowest growth performance and the lowest lean percentage at slaughter. In addition, they tend to develop extremely large muscle fibers (giant fibers) and poor meat quality, which results in part from the inverse correlation between fiber number and fiber size. Prenatal growth and myogenesis are under the control of various genetic and environmental factors, which can be targeted for growth manipulation. Genetic selection is considered a suitable tool to improve fetal growth and myogenesis. Prenatal development is mainly dependent on a close interrelation between nutritional supply/use and regulation by hormones and growth factors. In particular, the maternal somatotropic axis plays a significant role in the control of myogenesis. Thus, treatment of sows with GH until mid-gestation was able to increase birth weight and the number of muscle fibers in the small littermates of the progeny that are disadvantaged by insufficient nutrient supply. Growth hormone treatment was associated with increased nutrient availability to the embryos and changes in regulatory proteins of the GH-IGF axis. Interactions between maternal nutrition and the somatotropic axis in determining prenatal growth and myogenesis are worthy of further investigation.
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                Author and article information

                Journal
                Animals (Basel)
                Animals (Basel)
                animals
                Animals : an Open Access Journal from MDPI
                MDPI
                2076-2615
                16 January 2020
                January 2020
                : 10
                : 1
                : 156
                Affiliations
                [1 ]Institute of Animal Nutrition, Sichuan Agricultural University, No.211 Huimin Road, Wenjiang District, Chengdu 611130, Sichuan, China
                [2 ]Department of Animal Science, Aarhus University, DK-8830 Tjele, Denmark
                Author notes
                [* ]Correspondence: zkeying@ 123456sicau.edu.cn (K.Z.); clianqiang@ 123456hotmail.com (L.C.); Tel.: +86-28-86291256 (L.C.); +86-835-2885630 (K.Z.)
                Author information
                https://orcid.org/0000-0001-5263-9314
                Article
                animals-10-00156
                10.3390/ani10010156
                7022288
                31963382
                5e3f5bb7-256a-4786-8a8e-36f5fa41fde7
                © 2020 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
                : 24 October 2019
                : 15 January 2020
                Categories
                Article

                light weaning weight,nutrient intake,piglets,skeletal muscle,suckling

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