Medium-chain TAG improve energy metabolism and mitochondrial biogenesis in the liver of intra-uterine growth-retarded and normal-birth-weight weanling piglets

Abstract

We previously reported that medium-chain TAG (MCT) could alleviate hepatic oxidative damage in weanling piglets with intra-uterine growth retardation (IUGR). There is a relationship between oxidative status and energy metabolism, a process involved in substrate availability and glucose flux. Therefore, the aim of this study was to investigate the effects of IUGR and MCT on hepatic energy metabolism and mitochondrial function in weanling piglets. Twenty-four IUGR piglets and twenty-four normal-birth-weight (NBW) piglets were fed a diet of either soyabean oil (SO) or MCT from 21 d of postnatal age to 49 d of postnatal age. Then, the piglets' biochemical parameters and gene expressions related to energy metabolism and mitochondrial function were determined (n 4). Compared with NBW, IUGR decreased the ATP contents and succinate oxidation rates in the liver of piglets, and reduced hepatic mitochondrial citrate synthase (CS) activity (P < 0·05). IUGR piglets exhibited reductions in hepatic mitochondrial DNA (mtDNA) contents and gene expressions related to mitochondrial biogenesis compared with NBW piglets (P < 0·05). The MCT diet increased plasma ghrelin concentration and hepatic CS and succinate dehydrogenase activities, but decreased hepatic pyruvate kinase activity compared with the SO diet (P < 0·05). The MCT-fed piglets showed improved mtDNA contents and PPARγ coactivator-1α expression in the liver (P < 0·05). The MCT diet alleviated decreased mRNA abundance of the hepatic PPARα induced by IUGR (P < 0·05). It can therefore be postulated that MCT may have beneficial effects in improving energy metabolism and mitochondrial function in weanling piglets.

Effects of dietary leucine supplementation on the hepatic mitochondrial biogenesis and energy metabolism in normal birth weight and intrauterine growth-retarded weanling piglets

“…Such a decrease may provide a possible explanation for the observed decreases in CS, α-KGDH, and MDH activities. Zhang et al [7] obtained similar findings in another study. Previous studies have also suggested that decreased ATP production might result from the low capacity of the electron transport chain in different IUGR animal models [740].…”

“…TFAM, a key regulator involved in mtDNA replication and transcription, could be regulated by PGC-1α and NRF1 to activate mitochondrial biogenesis [4647]. Similarly, Zhang et al [7] found a decreased transcriptional level of hepatic TFAM in IUGR weanling piglets.…”

“…At birth, the birth weight (BW) and sex of each newborn piglet (Duroc × (Landrace × Yorkshire)) were recorded. In each litter, piglets with a body weight of 1.52 ± 0.06 kg and 0.87 ± 0.04 kg at birth were defined as NBW and IUGR piglets, as previously reported [722]. A total of sixteen pairs of NBW and IUGR piglets from sixteen sows were selected according to their BW.…”

“…Mitochondria, the main sites of adenosine triphosphate (ATP) production in mammalian cells, have an essential role in energy homeostasis, cellular metabolism, and apoptosis [34]. On the basis of several previous observations, we hypothesized that the possible mechanisms responsible for metabolic syndrome in adult IUGR offspring are impairment of mitochondrial biogenesis and energy deficiency [567]. Indeed, it has been demonstrated that IUGR decreases the concentration of ATP and the transcriptional levels of genes involved in mitochondrial biogenesis, and it impairs activities of mitochondrial enzymes related to oxidative phosphorylation (OXPHOS) in the liver of IUGR animals [789].…”

Altered tissue mineralization, increased hepatic lipid and inhibited autophagy in intrauterine growth retardation piglets

“…These findings coincide with those of previous studies (Poore & Fowden, 2004;Attig et al, 2008;Zhang et al, 2014;Li et al, 2015;Zhang et al, 2016).…”