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Catch-up growth following food restriction exacerbates adulthood glucose intolerance in pigs exposed to intrauterine undernutrition

Wang, Jun, Cao, Meng, Zhuo, Yong, Che, Lianqiang, Fang, Zhengfeng, Xu, Shengyu, Lin, Yan, Feng, Bin, Wu, De
Nutrition 2016 v.32 no.11-12 pp. 1275-1284
adulthood, blood glucose, cafeterias, compensatory growth, enzymes, gene expression, gluconeogenesis, glucose, glucose tolerance, glucose tolerance tests, glucose transporters, insulin, malnutrition, messenger RNA, muscles, pregnancy, progeny, refeeding, sows, triacylglycerols
The aim of this study was to evaluate the effects of food restriction followed by controlled refeeding on glucose tolerance in pigs exposed to intrauterine malnutrition.Pregnant sows (n = 11) were assigned to either a control (C) group or an undernutrition (U) group (75% of C) during gestation. At postnatal 68 d, the offspring (n = 16) were placed on either a cafeteria feeding (CF) group or a food-restricted (FR) group (75% of CF) for 6 wk. After that, all offspring were fed ad libitum until 189 d (dpn189).The results showed that maternal malnutrition induced offspring glucose intolerance, which was demonstrated by increased serum glucose and triacylglycerol content at dpn189, as well as increased area under the blood glucose curve (AUC) during the intravenous glucose tolerance test (i.v.GTT) (P < 0.05). Interestingly, food restriction followed by controlled refeeding further increased serum glucose content at dpn189 and AUC during i.v.GTT in pigs born from U sows (P < 0.05), which was accompanied by catch-up growth during the refeeding period. These changes were associated with increased mRNA levels of hepatic gluconeogenesis (PC, PEPCK) enzymes (P < 0.05), decreased mRNA level of muscle glucose transporter (GLUT4; P = 0.07), and reduced mRNA level of insulin signaling protein (IRS1, P < 0.05) in the liver.Our results indicate that catch-up growth following food restriction can exacerbate glucose intolerance in offspring exposed to intrauterine malnutrition. This may be caused by increased hepatic gluconeogenesis, decreased muscle glucose transport, and impaired hepatic insulin signaling.