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Synergetic Effects of Prenatal and Postnatal High Sucrose Intake on Glucose Tolerance and Hepatic Insulin Resistance in Rat Offspring
Author(s) -
Zhang Pengjie,
Zhu Di,
Zhang Yueming,
Li Lingjun,
Chen Xionghui,
Zhang Wenna,
Shi Ruixiu,
Tao Jianying,
Han Bing,
Xu Zhice
Publication year - 2018
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201700771
Subject(s) - offspring , insulin resistance , medicine , endocrinology , insulin , sucrose , glucose homeostasis , pregnancy , diabetes mellitus , triglyceride , biology , cholesterol , biochemistry , genetics
Scope High sucrose intake during pregnancy is linked to type 2 diabetes mellitus and altered insulin resistance. Methods and results This study attempts to ascertain whether prenatal high sucrose intake (20% sucrose) alleviates the detrimental effects of high postnatal sugar consumption in the offspring, and the molecular mechanisms are investigated using a rat model. High prenatal sucrose exposure increases the body weight of the offspring at 1–3 weeks of age. Exposure to both prenatal and postnatal high sucrose increases glucose tolerance in the 4‐month‐old adult offspring compared with offspring receiving other treatments. Postnatal high sucrose exposure suppresses food intake but increases the total daily caloric and fluid intake. Both fasting blood glucose and plasma triglyceride levels are increased, but the fasting insulin level is unaffected. Prenatal high sucrose intake enlarges pancreatic islet area; however, prenatal‐plus‐postnatal high sucrose exposure induces smaller pancreatic islets. IRS‐1(S612) protein phosphorylation is significantly increased, and the GSK‐3β (S9) phosphorylation level is reduced. Conclusion Both prenatal and prenatal‐plus‐postnatal high sucrose exposure substantially affect biological functions related to insulin homeostasis. IRS‐1(S612) protein phosphorylation appears to be a part of the molecular mechanism underlying these effects. These results add to the understanding of how high sucrose intake contributes to insulin resistance and diabetes pathogenesis and how postnatal nutrition and lifestyle may mitigate detrimental prenatal exposures.