Prenatal High‐Sucrose Diet Induced Vascular Dysfunction in Thoracic Artery of Fetal Offspring. Issue 12 (10th May 2021)

• Record Type: Journal Article
• Authors: Feng, Xueqin; Yu, Tiantian; Zhang, Yumeng; Li, Lijuan; Qu, Miaomiao; Wang, Jishui; Dong, Fangxiang; Zhang, Lihua; Wang, Fengge; Zhang, Fanyong; Zhou, Xiuwen; Xu, Zhice; Man, Dongmei
• Is Part Of: Molecular nutrition & food research. Volume 65:Issue 12(2021)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2021-05-10
• Subjects: fetal offspring -- inositol 1, 4, 5‐trisphosphate receptors -- L‐type calcium channels -- prenatal high‐sucrose -- vascular dysfunction; 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.202100072
• Languages: English
• ISSNs: 1613-4125

Abstract

Abstract : Scope: Maternal nutrition during pregnancy is related to intrauterine fetal development. The authors' previous work reports that prenatal high sucrose (HS) diet impaired micro‐vascular functions in postnatal offspring. It is unclear whether/how prenatal HS causes vascular injury during fetal life. Methods and results: Pregnant rats are fed with normal drinking water or 20% high‐sucrose solution during the whole gestational period. Pregnant HS increases maternal weight before delivery. Fetal thoracic aorta is separated for experiments. Angiotensin II (AII)‐stimulated vascular contraction of fetal thoracic arteries in HS group is greater, which mainly results from the enhanced AT1 receptor (AT1R) function and the downstream signaling. Nifedipine significantly increases vascular tension in HS group, indicating that the L‐type calcium channels (LTCCs) function is strengthened. 2‐Aminoethyl diphenylborinate (2‐APB), inositol 1, 4, 5‐trisphosphate receptors (IP3Rs) inhibitor, increases vascular tension induced by AII in HS group and ryanodine receptors‐sensitive vascular tone shows no difference in the two groups, which suggested that the activity of IP3Rs‐operated calcium channels is increased. Conclusion: These findings suggest that prenatal HS induces vascular dysfunction of thoracic arteries in fetal offspring by enhancing AT1R, LTCCs function and IP3Rs‐associated calcium channels, providing new information regarding the impact of prenatal HS on the functional development of fetal vascular systems. Abstract : A proposed model of how prenatal HS enhanced vascular tension of fetal aortas. Cytoplasmic Ca 2+ ‐induced by AII‐AT1R is abundant in HS vessels, which is mainly due to the increase of Ca 2+ influx through LTCCs and Ca 2+ release from IP3Rs. Eventually, those alterations result in vascular dysfunction in HS fetal offspring.