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The Impact of Nutrient Intake and Metabolic Wastes during Pregnancy on Offspring Hypertension: Challenges and Future Opportunities

期刊

METABOLITES
卷 13, 期 3, 页码 -

出版社

MDPI
DOI: 10.3390/metabo13030418

关键词

hypertension; nutrient-sensing signal; developmental origins of health and disease (DOHaD); asymmetric dimethylarginine; uremic toxin; short chain fatty acid; trimethylamine-N-oxide; AMP-activated protein kinase (AMPK)

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Hypertension can be influenced by metabolic disturbances during pregnancy, leading to programmed hypertension later in life. Maternal dietary nutrients and disrupted nutrient-sensing signals play a role in fetal programming of hypertension. Metabolism-modulated metabolites and nutrient-sensing signals are potential targets for new drug discovery to prevent and treat hypertension.
Hypertension can have its origin in early life. During pregnancy, many metabolic alterations occur in the mother that have a crucial role in fetal development. In response to maternal insults, fetal programming may occur after metabolic disturbance, resulting in programmed hypertension later in life. Maternal dietary nutrients act as metabolic substrates for various metabolic processes via nutrient-sensing signals. Different nutrient-sensing pathways that detect levels of sugars, amino acids, lipids and energy are integrated during pregnancy, while disturbed nutrient-sensing signals have a role in the developmental programming of hypertension. Metabolism-modulated metabolites and nutrient-sensing signals are promising targets for new drug discovery due to their pathogenic link to hypertension programming. Hence, in this review, we pay particular attention to the maternal nutritional insults and metabolic wastes affecting fetal programming. We then discuss the role of nutrient-sensing signals linking the disturbed metabolism to hypertension programming. This review also summarizes current evidence to give directions for future studies regarding how to prevent hypertension via reprogramming strategies, such as nutritional intervention, targeting nutrient-sensing signals, and reduction of metabolic wastes. Better prevention for hypertension may be possible with the help of novel early-life interventions that target altered metabolism.

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