Prenatal High‐Sucrose Diet Induced Vascular Dysfunction of Renal Interlobar Arteries in the Offspring via PPARγ‐RXRg‐ROS/Akt Signaling

Author:

Feng Xueqin1ORCID,Liu Xinying12,Wang Fuling1,Zhang Xiaoyun1,Zhu Liangxi1,Shu Hua1,Wang Chunxia1,Duan Liting1,Wang Haixia1,Ren Qinggui3,Dong Fangxiang1,Zhang Ziteng4,Man Dongmei1,Qu Miaomiao1

Affiliation:

1. Department of Obstetrics Affiliated Hospital of Jining Medical University Guhuai Road 89 Jining 272001 China

2. Department of Clinical Medicine Jining Medical University Jining 272001 China

3. Department of Mammary gland Surgery Affiliated Hospital of Jining Medical University Jining 272001 China

4. Departments of Thoracic Surgery Qinghai Red Cross Hospital Xining 272001 China

Abstract

ScopePrenatal nutrition imbalance correlates with developmental origin of cardiovascular diseases; however whether maternal high‐sucrose diet (HS) during pregnancy causes vascular damage in renal interlobar arteries (RIA) from offspring still keeps unclear.Methods and resultsPregnant rats are fed with normal drinking water or 20% high‐sucrose solution during the whole gestational period. Swollen mitochondria and distributed myofilaments are observed in vascular smooth muscle cells of RIA exposed to prenatal HS. Maternal HS increases phenylephrine (PE)‐induced vasoconstriction in the RIA from adult offspring. NG‐Nitro‐l‐arginine (L‐Name) causes obvious vascular tension in response to PE in offspring from control group, not in HS. RNA‐Seq of RIA is performed to reveal that the gene retinoid X receptor g (RXRg) is significantly decreased in the HS group, which could affect vascular function via interacting with PPARγ pathway. By preincubation of RIA with apocynin (NADPH inhibitor) or capivasertib (Akt inhibitor), the results indicate that ROS and Akt are the vital important factors to affect the vascular function of RIA exposure to prenatal HS.ConclusionMaternal HS during the pregnancy increases PE‐mediated vasoconstriction of RIA from adult offspring, which is mainly related to the enhanced Akt and ROS regulated by the weakened PPARγ‐RXRg.

Funder

National Natural Science Foundation of China

Natural Science Foundation of Shandong Province

Publisher

Wiley

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