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Maternal hypertensive condition alters adipose tissue function and blood pressure sensitivity in offspring
Ren Ozawa1, Hisataka Iwata1, Takehito Kuwayama1
1Laboratory of Animal Reproduction, Department of Animal Science, Tokyo University of Agriculture, 1737 Funako, Atsugi, Kanagawa, 234-0034, Japan.
Insights
Maternal hypertension during pregnancy, induced by angiotensin II (Ang II), leads to placental dysfunction and fetal growth restriction. Offspring exhibit altered lipid metabolism and elevated blood pressure, indicating long-term health impacts.
Area of Science:
- Reproductive biology
- Developmental biology
- Cardiovascular physiology
Background:
- Preeclampsia (PE) involves maternal hypertension and can impact fetal development.
- The intrauterine environment under hypertensive conditions may influence offspring health.
- Lipid metabolism and blood pressure regulation are critical for long-term health.
Purpose of the Study:
- To investigate the effects of maternal hypertension on male offspring growth, focusing on lipid metabolism and blood pressure.
- To determine how angiotensin II (Ang II)-induced maternal hypertension in mice impacts placental function and fetal development.
- To assess the long-term consequences of this intrauterine environment on offspring adipocyte function and cardiovascular health.
Main Methods:
- Induction of maternal hypertension in female mice using angiotensin II (Ang II) infusion from gestational day 12.
- Analysis of placental lipid dysregulation and fetal growth restriction.
- Assessment of birth weight and body weight changes in offspring.
- Evaluation of Pparγ mRNA expression in adipocytes from neonatal and adult offspring.
- Measurement of basal blood pressure and sensitivity to hypertensive stimuli in adult offspring.
Main Results:
- Ang II-induced maternal hypertension caused placental lipid dysregulation and fetal growth restriction, resulting in lower birth weight in offspring.
- Neonatal and adult offspring from hypertensive dams exhibited higher Pparγ mRNA expression in adipose tissue.
- Adult offspring showed increased neutrophils and inflammatory monocytes in adipose tissue.
- Ang II-offspring displayed higher basal blood pressure and increased sensitivity to hypertensive stimuli compared to controls.
- While initially lighter, Ang II-offspring body weight caught up to controls by 16 weeks.
Conclusions:
- Maternal hypertension induced by Ang II disrupts placental function, leading to fetal growth restriction and lower birth weight.
- The altered intrauterine environment impacts offspring adipocyte function, characterized by increased Pparγ expression and inflammation.
- Offspring exposed to maternal hypertension exhibit long-term cardiovascular effects, including elevated blood pressure and heightened sensitivity to hypertensive challenges.
Abstract:
Preeclampsia (PE) is characterized by hypertension, proteinuria, and fetal growth restriction during pregnancy, suggesting that the preeclamptic intrauterine environment may affect the growth and health of the offspring. This study aimed to how maternal hypertension affects male offspring growth, focusing on lipid metabolism and blood pressure in mice. Female mice were infused with angiotensin II (Ang II) on gestational day 12. Dysregulation and accumulation of lipid were observed in the placenta of Ang II-induced maternal hypertensive dams, associating with fetal growth restriction. Ang II-offspring showed lower birth weight than in the control-offspring. Isolated and differentiated adipocyte from neonatal mice of Ang II-dams showed higher Pparγ mRNA expression compared with the control group. Lower body weight tendency had continued in Ang II-offspring during long period, body weight of Ang II-offspring caught up the control-offspring at 16 weeks of age. The adipose tissue of Ang II-offspring in adult also showed higher Pparγ mRNA expression with the accumulation of neutrophils and inflammatory monocytes than in those control. In addition, Ang II-offspring had higher basal blood pressure and higher sensitivity to hypertensive stimuli than in the control-offspring. Taken together, maternal hypertension induced by Ang II changes placental function, causing a lower birth weight. These changes in the intrauterine environment may affect adipocyte function and blood pressure of offspring after growth.
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