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

You-Lin Tain,Chien-Ning Hsu,Julie Chan

doi:10.3390/nu8120757

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.

Highlights

Fructose consumption has grown over the past several decades and its growth has been paralleled by an increase in hypertension [1,2,3]
We examined major organs that control blood pressure (BP), including the heart and brain, and observed that maternal HF consumption increased the mRNA levels of Pfkl, hexokinase 2 (Hk2), 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (Pfkfb3), suppressor of cytokine signaling 3 (Socs3), NFκB inhibitor α (Nfkbia), Ppargc1a, liver glycogen phosphorylase (Pygl), and forkhead box protein O1 (Foxo1) in the heart
Maternal nutrition and its association with nutrient–gene interactions remains a challenging area of research

Summary

Introduction

Fructose consumption has grown over the past several decades and its growth has been paralleled by an increase in hypertension [1,2,3]. Nutrition during pregnancy and lactation exerts long-term effects on the health of offspring. Developmental origins of health and disease (DOHaD) is an emerging branch of science that assesses the effects of these early insults on the health of offspring [4]. Adult-onset hypertension develops from nutritional insults in early life [5]. Because the developing kidney is vulnerable to insults of programming in early life, renal programming plays an essential role in the developmental programming of hypertension [6]. The DOHaD concept offers a novel approach to prevent programmed hypertension through reprogramming [7]. Nutrients 2016, 8, 757 maternal HF consumption on programmed hypertension; effects of maternal HF consumption on renal transcriptome changes; and application of reprogramming interventions to prevent maternal

Metabolic Effects of Fructose on Renal Biology and Hypertension

Effect of Maternal Fructose Consumption on Programmed Hypertension

HF Consumption Induces Renal Transcriptome Changes

Reprogramming Strategy to Prevent Maternal HF Consumption-Induced

Conclusions