Padmavathi Inagadapa J N, Kishore Yedla Durga, Venu Lagishetty, Ganeshan Manisha, Harishankar Nemani, Giridharan N V, Raghunath Manchala
Division of Endocrinology and Metabolism, National Institute of Nutrition, Hyderabad, India.
Exp Physiol. 2009 Jun;94(6):761-9. doi: 10.1113/expphysiol.2008.045856. Epub 2009 Feb 27.
Maternal undernutrition increases the risk of adult chronic diseases, such as obesity and type 2 diabetes. This study evaluated the effect of maternal zinc restriction in predisposing the offspring to adiposity and altered insulin response in later life. Seventy-day-old female Wistar/NIN rats received a control (ZnC) or zinc-restricted (ZnR) diet for 2 weeks. Following mating with control males, a subgroup of the ZnR dams were rehabilitated with ZnC diet from parturition. Half the offspring born to the remaining ZnR dams were weaned onto the ZnC diet and the other half continued on the ZnR diet throughout their life. Body composition, glucose tolerance, insulin response and plasma lipid profile were assessed in male and female offspring at 3 and 6 months of age. The ZnR offspring weighed less than control offspring at birth and weaning and continued so until 6 months of age. Rehabilitation regimens corrected the body weights of male but not female offspring. Maternal zinc restriction increased the percentage of body fat and decreased lean mass, fat-free mass and fasting plasma insulin levels in both male and female offspring at 6 months of age. Also, glucose-induced insulin secretion was decreased in female but not male offspring. Despite the differences in fasting insulin and the area under the curve for insulin, the fasting glucose and the area under the curve for glucose were in general comparable among offspring of different groups. Rehabilitation from parturition or weaning partly corrected the changes in the percentage of body fat but had no such effect on other parameters. Changes in plasma lipid profile were inconsistent among the offspring of different groups. Thus chronic maternal zinc restriction altered the body composition and impaired the glucose-induced insulin secretion in the offspring.
孕期营养不良会增加成年后患慢性疾病的风险,如肥胖症和2型糖尿病。本研究评估了孕期锌缺乏对后代肥胖倾向及后期胰岛素反应改变的影响。70日龄雌性Wistar/NIN大鼠接受对照(锌充足,ZnC)或锌缺乏(ZnR)饮食2周。与对照雄性大鼠交配后,一部分ZnR母鼠产后恢复锌充足饮食。其余ZnR母鼠所生后代一半断奶后改为锌充足饮食,另一半则终生持续锌缺乏饮食。在雄性和雌性后代3个月和6个月大时评估其身体组成、葡萄糖耐量、胰岛素反应和血浆脂质谱。ZnR后代在出生和断奶时体重低于对照后代,并一直持续到6个月大。恢复方案纠正了雄性后代的体重,但对雌性后代无效。孕期锌缺乏使6个月大的雄性和雌性后代体脂百分比增加,瘦体重、去脂体重和空腹血浆胰岛素水平降低。此外,葡萄糖诱导的胰岛素分泌在雌性后代中减少,但在雄性后代中未减少。尽管空腹胰岛素和胰岛素曲线下面积存在差异,但不同组后代的空腹血糖和葡萄糖曲线下面积总体相当。产后或断奶后恢复饮食部分纠正了体脂百分比的变化,但对其他参数无此作用。不同组后代血浆脂质谱的变化不一致。因此,孕期长期锌缺乏会改变后代的身体组成,并损害葡萄糖诱导的胰岛素分泌。