title: Over-nutrient environment during both prenatal and postnatal development increases severity of islet injury, hyperglycemia, and metabolic disorders in the offspring.
abstract: Prenatal and postnatal over-nutrition has emerged as a new health issue contributing to metabolic disorders in early development of the offspring. Accumulating evidence has suggested that adverse prenatal and postnatal environments gave rise to the predisposition to metabolic syndromes including hyperglycemia, obesity, and diabetes. However, little research has concentrated on the effects of exposures to both adverse conditions before and after birth of the offspring. In this study, we aimed to investigate whether prenatal and postnatal over-nutrition is able to cause metabolic disorders to female mice feed on high-fat/fructose diet (HFFD) as well as their offspring. Female mice were fed on either HFFD or a normal chow diet (NC), while their offspring were divided into four experimental groups as NC/NC, HFFD/NC, NC/HFFD, and HFFD/HFFD (prenatal/postnatal diet order), respectively. Both NC/HFFD and HFFD/HFFD offspring exhibited obvious body weight and fat content gain, hyperglycemia, and severe insulin resistance. Interestingly, when compared to NC/HFFD offspring, the HFFD/HFFD offspring exhibited more severe alterations in their metabolism and dysfunctions on pancreatic β-cells, suggesting a potential impact of prenatal HFFD on the programming of pancreatic β-cell deficiency in the fetus. Meanwhile, the results from HFFD/NC mice indicated that a balance diet after birth partially compensated the adverse prenatal HFFD impact. In conclusion, this study demonstrated that prenatal and postnatal over-nutrition increases severity of islet injury, hyperglycemia, and metabolic disorders in the offspring.
authors.affiliation: Department of Obstetrics, Shandong Provincial Hospital Affiliated to Shandong University, No. 324 Jingwu Road, Jinan, 250021, Shandong, China.
authors.forename: Lei
authors.initials: L
authors.lastname: Li
authors.forename: Jing
authors.initials: J
authors.lastname: Xue
authors.forename: Hongyan
authors.initials: H
authors.lastname: Li
authors.forename: Jian
authors.initials: J
authors.lastname: Ding
authors.forename: Yanyun
authors.initials: Y
authors.lastname: Wang
authors.forename: Xietong
authors.initials: X
authors.lastname: Wang
mesh_terms: D050154:Adiposity; D000818:Animals; D001786:Blood Glucose; D001835:Body Weight; D003920:Diabetes Mellitus / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D002149:Energy Intake; D004734:Energy Metabolism; D005260:Female; D005943:Gluconeogenesis; D050261:Glycogenolysis; D006943:Hyperglycemia / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D007328:Insulin / Q000097:blood / Q000378:metabolism; D007333:Insulin Resistance; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000378:metabolism / Q000473:pathology; D007515:Islets of Langerhans / Q000473:pathology*; D008297:Male; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000209:etiology* / Q000473:pathology
chemical_list: D001786:Blood Glucose; D007328:Insulin