Prenatal High-Sucrose Diet Induced Vascular Dysfunction of Renal Interlobar Arteries in the Offspring via PPARγ-RXRg-ROS/Akt Signaling.
Mol Nutr Food Res
; 68(10): e2300871, 2024 May.
Article
en En
| MEDLINE
| ID: mdl-38704749
ABSTRACT
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.Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Efectos Tardíos de la Exposición Prenatal
/
Vasoconstricción
/
Transducción de Señal
/
Especies Reactivas de Oxígeno
/
Ratas Sprague-Dawley
/
PPAR gamma
/
Proteínas Proto-Oncogénicas c-akt
Límite:
Animals
/
Pregnancy
Idioma:
En
Revista:
Mol Nutr Food Res
Asunto de la revista:
CIENCIAS DA NUTRICAO
Año:
2024
Tipo del documento:
Article
País de afiliación:
China