Abstract
Widespread consumption of high-fructose and high-fat diets relates to the global epidemic of hypertension. Hypertension may originate from early life by a combination of prenatal and postnatal nutritional insults. We examined whether maternal high-fructose diet increases vulnerability to post-weaning high-fructose or high-fat diets induced hypertension in adult offspring and determined the underlying mechanisms. Pregnant Sprague-Dawley rats received regular chow (ND) or chow supplemented with 60% fructose (HFR) during the entire pregnancy and lactation periods. Male offspring were onto either the regular chow, 60% fructose, or high-fat diet (HFA) from weaning to 12 weeks of age and assigned to four groups: ND/ND, HFR/ND, HFR/HFR, and HFR/HFA. Maternal high-fructose diet exacerbates post-weaning high-fat diet-induced programmed hypertension. Post-weaning high-fructose and high-fat diets similarly reduced Sirt4, Prkaa2, Prkag2, Ppara, Pparb, and Ppargc1a mRNA expression in offspring kidneys exposed to maternal high-fructose intake. Additionally, post-weaning high-fat diet significantly reduced renal mRNA levels of Ulk1, Atg5, and Nrf2 and induced greater oxidative stress than did high-fructose diet. Although maternal high-fructose intake increases soluble epoxide hydrolase (SEH) expression in the kidney, which was restored by post-weaning high-fructose and high-fat diets. Maternal high-fructose diet programs differential vulnerability to developing hypertension in male offspring in response to post-weaning high-fructose and high-fat diets. Our data implicated that specific therapy targeting on nutrient sensing signals, oxidative stress, and SEH may be a promising approach to prevent hypertension in children and mothers exposed to high-fructose and high-fat consumption.
Highlights
Over consumption of the Western diet, characterized by high refined sugars and fat content, is a major contributor to the global epidemic of hypertension
As dysfunction of autophagy may result in abnormal mitochondrial function and oxidative stress, we examined whether oxidative stress and autophagy are involved in high-fructose and high-fat-induced programmed hypertension
We examined the alterations of soluble epoxide hydrolase (SEH) in response to post-weaning high-fructose and and high-fat diets, as we previously found that SEH was involved in maternal high-fructose induced high-fat diets, as we previously found that SEH was involved in maternal high-fructose induced programmed hypertension [4,11]
Summary
Over consumption of the Western diet, characterized by high refined sugars and fat content, is a major contributor to the global epidemic of hypertension. Hypertension can be driven by early-life adverse conditions by the so-called developmental origins of health and disease (DOHaD) [2]. While the developing kidney is vulnerable, in particular, to adverse environments in early life, initiating permanent structural and physiological adaptions, namely, renal programming [3]. Our previous reports showed that offspring rats of mothers exposed to 60% high-fructose diet during pregnancy and lactation developed renal programming and hypertension [4,5], which is in agreement with the results of earlier studies involving fructose-fed adult rats [6]
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