Kjaergaard M, Nilsson C, Secher A, Kildegaard J, Skovgaard T, Nielsen M O, Grove K, Raun K
Diabetes and Obesity Pharmacology, Novo Nordisk A/S, Måløv, Denmark.
Department of Large Animal Science, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg C, Denmark.
Nutr Diabetes. 2017 Jan 16;7(1):e242. doi: 10.1038/nutd.2016.53.
BACKGROUND/OBJECTIVE: Intake of high-energy foods and maternal nutrient overload increases the risk of metabolic diseases in the progeny such as obesity and diabetes. We hypothesized that maternal and postnatal intake of chocolate and soft drink will affect leptin sensitivity and hypothalamic astrocyte morphology in adult rat offspring.
Pregnant Sprague-Dawley rats were fed ad libitum chow diet only (C) or with chocolate and high sucrose soft drink supplement (S). At birth, litter size was adjusted into 10 male offspring per mother. After weaning, offspring from both dietary groups were assigned to either S or C diet, giving four groups until the end of the experiment at 26 weeks of age.
As expected, adult offspring fed the S diet post weaning became obese (body weight: P<0.01, %body fat per kg: P<0.001) and this was due to the reduced energy expenditure (P<0.05) and hypothalamic astrogliosis (P<0.001) irrespective of maternal diet. Interesting, offspring born to S-diet-fed mothers and fed the S diet throughout postnatal life became obese despite lower energy intake than controls (P<0.05). These SS offspring showed increased feed efficiency (P<0.001) and reduced fasting pSTAT3 activity (P<0.05) in arcuate nucleus (ARC) compared with other groups. The findings indicated that the combination of the maternal and postnatal S-diet exposure induced persistent changes in leptin signalling, hence affecting energy balance. Thus, appetite regulation was more sensitive to the effect of leptin than energy expenditure, suggesting differential programming of leptin sensitivity in ARC in SS offspring. Effects of the maternal S diet were normalized when offspring were fed a chow diet after weaning.
Maternal intake of chocolate and soft drink had long-term consequences for the metabolic phenotype in the offspring if they continued on the S diet in postnatal life. These offspring displayed obesity despite lowered energy intake associated with alterations in hypothalamic leptin signalling.
背景/目的：摄入高能量食物以及母体营养过剩会增加后代患代谢性疾病的风险，如肥胖症和糖尿病。我们推测母体孕期及产后摄入巧克力和软饮料会影响成年大鼠后代的瘦素敏感性和下丘脑星形胶质细胞形态。
将怀孕的斯普拉格-道利大鼠随意分为仅喂食普通饲料组（C组）或添加巧克力和高蔗糖软饮料组（S组）。出生时，将每窝幼崽数量调整为每位母亲10只雄性后代。断奶后，将两组饮食组的后代分别分配至S组或C组饮食，直至26周龄实验结束，共形成四组。
正如预期，断奶后喂食S组饮食的成年后代变得肥胖（体重：P<0.01，每千克体脂百分比：P<0.001），这是由于能量消耗减少（P<0.05）和下丘脑星形胶质细胞增生（P<0.001），与母体饮食无关。有趣的是，出生于喂食S组饮食母亲且在出生后一直喂食S组饮食的后代尽管能量摄入量低于对照组（P<0.05），但仍变得肥胖。与其他组相比，这些SS后代的饲料效率增加（P<0.001），弓状核（ARC）中的空腹pSTAT3活性降低（P<0.05）。研究结果表明，母体和产后S组饮食暴露的组合导致瘦素信号传导持续变化，从而影响能量平衡。因此，食欲调节对瘦素的影响比对能量消耗更敏感，这表明SS后代的ARC中瘦素敏感性存在差异编程。当后代断奶后喂食普通饲料时，母体S组饮食的影响恢复正常。
如果后代在出生后继续食用S组饮食，母体摄入巧克力和软饮料会对其代谢表型产生长期影响。这些后代尽管能量摄入量降低，但仍表现出肥胖，同时伴有下丘脑瘦素信号传导改变。
