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

Abstract

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.

Targeting on Gut Microbial Metabolite Trimethylamine‐N‐Oxide and Short‐Chain Fatty Acid to Prevent Maternal High‐Fructose‐Diet‐Induced Developmental Programming of Hypertension in Adult Male Offspring

“…To our knowledge, this is the first study to examine the potential benefit of maternal supplementation with acetate or 3,3‐dimethyl‐1‐butanol in HFD‐induced programed hypertension. Consumption of various degrees of HFD ranging from 10% to 60% by pregnant dams have been reported to cause hypertension in their adult offspring . Consistent with previous reports, we found that maternal HFD produced elevation of BP in 12‐week‐old male offspring.…”

“…BP was measured in conscious rats on week 3, 4, 8, and 12 using an indirect tail‐cuff method (BP‐2000, Visitech Systems, Inc., Apex, NC, USA), as described previously . To ensure accuracy and reproducibility, the rats were allowed to adapt to restraint and tail‐cuff inflation for 1 week prior to the experiment.…”

“…Consuming a high‐fructose diet (HFD) during pregnancy may cause adverse effects on both mother and their offspring . Our previous reports demonstrated that offspring born to dams exposed to 60% HFD develop hypertension in adulthood …”

Translational insights on developmental origins of metabolic syndrome: Focus on fructose consumption

“…Unlike glucose, which is metabolized widely in the body, fructose is converted into glucose, glycogen, lactate, and fatty acids mainly in the liver [8] . Since fructose can be transported and produced by the placenta [9] , [10] , it is considered that the fetal programming process is driven not only by fructose but also by its metabolites [11] .…”

Liver metabolism in adult male mice offspring: consequences of a maternal, paternal or both maternal and paternal high-fructose diet

“…9 Maternal programming with a high-fructose diet (HFR) has many effects on offspring, including hypertriglyceridemia, hypertension, hyperinsulinemia and liver fat infiltrates. 10,11 However, little is known about the effects on the offspring of a high-fructose diet consumed by the father or both the mother and father. The present study aimed to evaluate the effects of a high-fructose diet consumed by the mother, by the father and by both the mother and father on the metabolism and liver health of adult male offspring, including the β-oxidation, lipogenesis and inflammation pathways.…”