Umekawa Takashi, Sugiyama Takashi, Du Qinwen, Murabayashi Nao, Zhang Lingyun, Kamimoto Yuki, Yoshida Toshimichi, Sagawa Norimasa, Ikeda Tomoaki
Department of Obstetrics and Gynecology, Mie University Graduate School of Medicine, Tsu, Japan; Department of Women's and Children's Health, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Department of Obstetrics and Gynecology, Tohoku University Graduate School of Medicine, Sendai, Japan.
J Nutr Biochem. 2015 Mar;26(3):259-66. doi: 10.1016/j.jnutbio.2014.10.012. Epub 2014 Dec 3.
The impact of an increase in maternal fat consumption on fetal metabolic programming separately from maternal obesity remains unclear. The purpose of this study was to document the effect of in utero high-fat diet exposure on the development of metabolic syndrome characteristics in offspring. C57BL/6 female mice were fed either a control diet (10% fat) or a moderately high-fat (MHF) diet (45% fat) until delivery. All pups were fostered to mothers fed with the control diet. Pups were raised on the control diet and assessed until 35 weeks of age. The caloric intake from fat was significantly increased in the MHF dams compared with the control dams. There were no significant differences in the maternal weight at mating or at gestational Day 18 between the two groups. The MHF offspring did not become obese, but they developed hypertension and glucose intolerance. Moreover, the MHF offspring had significantly higher serum non-esterified fatty acid and triglyceride levels during the refeeding state following fasting as compared with the control offspring. Serum adiponectin levels were significantly lower, and the cell size of the mesenteric adipose tissue was significantly larger in the MHF offspring than in the control offspring. The mRNA levels of the proinflammatory macrophage markers in the mesenteric adipose tissue were significantly higher in the MHF offspring than those of the control offspring. These results suggest that in utero high-fat diet exposure causes hypertension and glucose intolerance resulting from mesenteric adipose tissue dysfunction in offspring, independently of maternal obesity.
母体脂肪摄入量增加对胎儿代谢编程的影响，独立于母体肥胖之外，目前仍不清楚。本研究的目的是记录子宫内高脂饮食暴露对后代代谢综合征特征发展的影响。将C57BL/6雌性小鼠分为两组，一组喂食对照饮食（10%脂肪），另一组喂食中度高脂（MHF）饮食（45%脂肪），直至分娩。所有幼崽均寄养于喂食对照饮食的母鼠。幼崽以对照饮食饲养，并评估至35周龄。与对照母鼠相比，MHF母鼠从脂肪中摄入的热量显著增加。两组在交配时或妊娠第18天的母体体重无显著差异。MHF组后代并未变得肥胖，但出现了高血压和葡萄糖不耐受。此外，与对照后代相比，MHF后代在禁食后的再喂养状态下血清非酯化脂肪酸和甘油三酯水平显著更高。MHF后代的血清脂联素水平显著降低，肠系膜脂肪组织的细胞大小显著大于对照后代。MHF后代肠系膜脂肪组织中促炎巨噬细胞标志物的mRNA水平显著高于对照后代。这些结果表明，子宫内高脂饮食暴露会导致后代因肠系膜脂肪组织功能障碍而出现高血压和葡萄糖不耐受，与母体肥胖无关。
