Synergetic Effects of Prenatal and Postnatal High Sucrose Intake on Glucose Tolerance and Hepatic Insulin Resistance in Rat Offspring. Issue 5 (19th February 2018)

• Record Type: Journal Article
• Authors: Zhang, Pengjie; Zhu, Di; Zhang, Yueming; Li, Lingjun; Chen, Xionghui; Zhang, Wenna; Shi, Ruixiu; Tao, Jianying; Han, Bing; Xu, Zhice
• Is Part Of: Molecular nutrition & food research. Volume 62:Issue 5(2018)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2018-02-19
• Subjects: high sucrose exposure -- insulin resistance -- offspring -- pregnancy -- rat; Food -- Biotechnology -- Periodicals; Food -- Microbiology -- Periodicals; Nutrition -- Periodicals; Food -- Toxicology -- Periodicals; Nutrition -- Periodicals; Food Microbiology -- Periodicals; Food Technology -- Periodicals; Molecular Biology -- Periodicals; 664.0705
• DOI: 10.1002/mnfr.201700771
• Languages: English
• ISSNs: 1613-4125

Abstract

Abstract : 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. Abstract : Prenatal plus postnatal high sucrose feeding (HH) in rats led to worse insulin resistance, including increased GTT, FBG, and decreased pancreatic islets, in the offspring. This could be attributed to the dysregulation of insulin signaling pathway, including up‐regulation of IRS‐1(Ser612) and down‐regulation of AKT (Ser473), GSK‐3β(ser9) in HH offspring.