Medium-chain TAG attenuate hepatic oxidative damage in intra-uterine growth-retarded weanling piglets by improving the metabolic efficiency of the glutathione redox cycle

Br J Nutr. 2014 Sep 28;112(6):876-85. doi: 10.1017/S000711451400155X. Epub 2014 Aug 1.


The present study investigated the effects of medium-chain TAG (MCT) on hepatic oxidative damage in weanling piglets with intra-uterine growth retardation (IUGR). At weaning (mean 21 (SD 1·06) d of age), twenty-four IUGR piglets and twenty-four normal-birth weight (NBW) piglets were selected according to their birth weight (BW; IUGR: mean 0·95 (SD 0·04) kg; NBW: mean 1·58 (SD 0·04) kg) and weight at the time of weaning (IUGR: mean 5·26 (SD 0·15) kg; NBW: mean 6·98 (SD 0·19) kg) and fed either a soyabean oil (SO) diet (containing 5% SO) or a MCT diet (containing 1% SO and 4% MCT) for 28 d. IUGR piglets exhibited poor (P<0·05) growth performance, lower (P<0·05) metabolic efficiency of hepatic glutathione (GSH) redox cycle, and increased (P<0·05) levels of reactive oxygen species, apoptosis and necrosis in hepatocytes compared with NBW piglets. The MCT diet increased (P<0·05) the average daily gain and feed efficiency of piglets during the first 4 weeks after weaning. Furthermore, MCT diet-fed piglets had a higher (P<0·05) GSH:oxidised glutathione ratio and increased (P<0·05) activities of glucose-6-phosphate dehydrogenase (G6PD) and GSH reductase. The expression of G6PD was up-regulated (P<0·05) by the MCT diet irrespective of BW. Moreover, malondialdehyde concentrations in the liver and apoptosis and necrosis levels in hepatocytes were decreased (P<0·05) by the MCT diet irrespective of BW. These results indicate that MCT might have auxiliary therapeutic potential to attenuate hepatic oxidative damage in IUGR offspring during early life, thus leading to an improvement in the metabolic efficiency of the hepatic GSH redox cycle.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Caprylates / therapeutic use*
  • China
  • Crosses, Genetic
  • Decanoates / therapeutic use*
  • Dietary Supplements*
  • Energy Intake
  • Fetal Growth Retardation / diet therapy*
  • Fetal Growth Retardation / metabolism
  • Fetal Growth Retardation / pathology
  • Fetal Growth Retardation / physiopathology
  • Gene Expression Regulation, Enzymologic
  • Glucosephosphate Dehydrogenase / genetics
  • Glucosephosphate Dehydrogenase / metabolism
  • Glutathione / metabolism*
  • Glutathione Reductase / genetics
  • Glutathione Reductase / metabolism
  • Hepatic Insufficiency / etiology
  • Hepatic Insufficiency / prevention & control*
  • Liver / enzymology
  • Liver / metabolism
  • Liver / pathology
  • Male
  • Necrosis
  • Oxidative Stress
  • Sus scrofa
  • Triglycerides / chemistry
  • Triglycerides / therapeutic use*
  • Weaning
  • Weight Gain


  • Caprylates
  • Decanoates
  • Triglycerides
  • Glucosephosphate Dehydrogenase
  • Glutathione Reductase
  • Glutathione