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Prenatal High-Sucrose Diet Induced Vascular Dysfunction of Renal Interlobar Arteries in the Offspring via
Xueqin Feng1, Xinying Liu1,2, Fuling Wang1
1Department of Obstetrics, Affiliated Hospital of Jining Medical University, Guhuai Road 89, Jining, 272001, China.
Insights
Maternal high-sucrose diet during pregnancy impairs offspring renal arteries, increasing vasoconstriction. This vascular dysfunction is linked to reduced retinoid X receptor gamma and elevated Akt and reactive oxygen species.
Area of Science:
- Cardiovascular physiology
- Developmental origins of health and disease
- Nutritional science
Background:
- Prenatal nutrition imbalance is linked to cardiovascular disease development.
- The specific impact of a maternal high-sucrose diet on offspring renal artery vascular function remains unclear.
Purpose of the Study:
- To investigate the effects of a maternal high-sucrose diet during pregnancy on the vascular function of renal interlobar arteries (RIA) in adult offspring.
- To identify the molecular mechanisms underlying any observed vascular changes.
Main Methods:
- Pregnant rats were fed either normal water or a 20% high-sucrose solution.
- Vascular responses to phenylephrine were measured in isolated RIA from offspring.
- RNA sequencing (RNA-Seq) was performed on RIA to analyze gene expression.
- Inhibitors of NADPH oxidase (apocynin) and Akt (capivasertib) were used to probe mechanisms.
Main Results:
- Maternal high-sucrose diet induced mitochondrial swelling in RIA vascular smooth muscle cells.
- Offspring exposed to prenatal high-sucrose diet exhibited increased phenylephrine-induced vasoconstriction in RIA.
- RNA-Seq revealed significantly decreased retinoid X receptor gamma (RXRg) expression in the high-sucrose group.
- Enhanced vasoconstriction was attenuated by NADPH and Akt inhibitors, implicating reactive oxygen species (ROS) and Akt signaling.
Conclusions:
- Maternal high-sucrose diet during pregnancy leads to increased phenylephrine-mediated vasoconstriction in offspring RIA.
- This vascular dysfunction is associated with reduced expression of PPARγ-RXRg pathway components.
- Elevated Akt and ROS signaling, regulated by the weakened PPARγ-RXRg pathway, are key contributors to the observed vascular impairment.
Scope:
Prenatal 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 Results:
Pregnant 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.
Conclusion:
Maternal 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.
