Wang Jun, Cao Meng, Zhuo Yong, Che Lianqiang, Fang Zhengfeng, Xu Shengyu, Lin Yan, Feng Bin, Wu De
Key Laboratory for Animal Disease-Resistance Nutrition of the Ministry of Education of China, Institute of Animal Nutrition, Sichuan Agricultural University, Ya'an, China.
Key Laboratory for Animal Disease-Resistance Nutrition of the Ministry of Education of China, Institute of Animal Nutrition, Sichuan Agricultural University, Ya'an, China.
Nutrition. 2016 Nov-Dec;32(11-12):1275-84. doi: 10.1016/j.nut.2016.03.010. Epub 2016 Mar 24.
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.
本研究旨在评估限食后进行可控再喂养对宫内营养不良仔猪葡萄糖耐量的影响。
怀孕母猪（n = 11）在妊娠期被分为对照组（C组）或营养不良组（U组，摄入量为C组的75%）。出生后68天，子代仔猪（n = 16）被分为自助餐喂养组（CF组）或限食组（FR组，摄入量为CF组的75%），持续6周。之后，所有子代仔猪自由采食直至189天（出生后第189天，dpn189）。
结果显示，母体营养不良会导致子代葡萄糖不耐受，表现为dpn189时血清葡萄糖和三酰甘油含量增加，以及静脉葡萄糖耐量试验（i.v.GTT）期间血糖曲线下面积（AUC）增加（P < 0.05）。有趣的是，限食后进行可控再喂养会使U组母猪所产仔猪在dpn189时血清葡萄糖含量进一步增加，且i.v.GTT期间的AUC也增加（P < 0.05），同时在再喂养期间出现追赶生长。这些变化与肝脏中糖异生（PC、PEPCK）酶的mRNA水平升高（P < 0.05）、肌肉葡萄糖转运蛋白（GLUT4）的mRNA水平降低（P = 0.07）以及肝脏中胰岛素信号蛋白（IRS1）的mRNA水平降低（P < 0.05）有关。
我们的结果表明，限食后的追赶生长会加剧宫内营养不良子代的葡萄糖不耐受。这可能是由于肝脏糖异生增加、肌肉葡萄糖转运减少以及肝脏胰岛素信号受损所致。
