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Published on: March 25, 2016
Murine aortic reactivity is programmed equally by maternal low protein diet or late gestation dexamethasone
Robert D Roghair1, Jeffrey L Segar, Robert A Kilpatrick
1Department of Pediatrics, University of Iowa, Iowa City, IA, USA.
Insights
Maternal low protein diet and dexamethasone exposure in late gestation program offspring for endothelial dysfunction. Only low protein diet impaired growth and glucose clearance in adult offspring.
Area of Science:
- Developmental biology
- Endocrinology
- Cardiovascular science
Background:
- Maternal nutrition and prenatal exposures can program offspring for long-term health outcomes.
- Low protein diets during pregnancy are linked to fetal growth restriction and later-life disease.
- Glucocorticoid exposure in utero can impact fetal development and adult physiology.
Purpose of the Study:
- To investigate the effects of maternal low protein diet and late gestation dexamethasone on murine offspring.
- To determine if these exposures program offspring for hypertension, vascular dysfunction, and glucose intolerance.
Main Methods:
- Maternal mice were fed a low protein (LP) diet or normal protein (NP) diet.
- Dams received dexamethasone (NP-Dex) or saline (NP-NS) during late gestation.
- Offspring were assessed for birth weight, blood pressure, glucose tolerance, and aortic ring vasodilatation.
Main Results:
- Offspring from LP dams had lower birth weight compared to NP offspring.
- Both LP and NP-Dex offspring exhibited impaired vasodilatation to acetylcholine, indicating endothelial dysfunction.
- Offspring from LP dams showed impaired glucose clearance, correlated with perinatal weight.
Conclusions:
- Maternal low protein diet and late gestation dexamethasone exposure program offspring for endothelial dysfunction.
- Hypertension was not observed in offspring under these experimental conditions.
- Maternal low protein diet uniquely impacted perinatal growth and adult glucose metabolism.
Objective:
In rats, maternal low protein diet induces growth restriction, increases fetal glucocorticoid exposure and programs cardiovascular and endocrine dysfunction in adult offspring. We hypothesized that both maternal low protein diet and late gestation dexamethasone program murine offspring to develop hypertension, vascular dysfunction, and glucose intolerance.
Methods:
An iso-caloric low protein diet (LP) was provided to dams from E0 to E19. Additional dams received a normal protein diet without (NP) or with either dexamethasone (NP-Dex, 0.1 mg/kg/d sc) or normal saline (NP-NS) from E10 to E18.
Results:
Offspring of dams given LP weighed less at 10 days than NP offspring, while Dex administration did not alter pup weight. At 4 months, all four groups had similar systolic blood pressures and no detectable differences were evoked by oral L-NAME. Offspring of LP mice had impaired glucose clearance that was directly correlated with their weight at 10 days. Aortic rings from offspring of both LP and NP-Dex exposed dams had impaired vasodilatation to acetylcholine.
Conclusions:
These findings demonstrate that both maternal low protein diet and late gestation dexamethasone program murine offspring to develop endothelial dysfunction in the absence of hypertension, while only maternal LP impaired perinatal growth and glucose clearance in adult offspring.
Keywords:
Acetylcholine; blood pressure; developmental biology; fetal programming
