Maternal Fructose Intake Affects Transcriptome Changes and Programmed Hypertension in Offspring in Later Life

Hypertension originates from early-life insults by so-called “developmental origins of health and disease” (DOHaD). Studies performed in the previous few decades indicate that fructose consumption is associated with an increase in hypertension rate. It is emerging field that tends to unfold the nutrient–gene interactions of maternal high-fructose (HF) intake on the offspring which links renal programming to programmed hypertension. Reprogramming interventions counteract disturbed nutrient–gene interactions induced by maternal HF intake and exert protective effects against developmentally programmed hypertension. Here, we review the key themes on the effect of maternal HF consumption on renal transcriptome changes and programmed hypertension. We have particularly focused on the following areas: metabolic effects of fructose on hypertension and kidney disease; effects of maternal HF consumption on hypertension development in adult offspring; effects of maternal HF consumption on renal transcriptome changes; and application of reprogramming interventions to prevent maternal HF consumption-induced programmed hypertension in animal models. Provision of personalized nutrition is still a faraway goal. Therefore, there is an urgent need to understand early-life nutrient–gene interactions and to develop effective reprogramming strategies for treating hypertension and other HF consumption-related diseases.