Maternal High-Fructose Intake Induces Multigenerational Activation of the Renin-Angiotensin-Aldosterone System<\/a>\u201d.<\/li>\n<\/ul>\nBackground<\/strong><\/p>\n\n- Seong, et al. investigated whether maternal exposure to high fructose induces hypertension together with RAAS activation, renal tissue oxidative stress, inflammation, and tissue fibrosis in successive multiple generations.<\/li>\n
- Specifically, maternal exposure to high fructose significantly increased blood pressure in the first and second-generation offspring along with increased serum Ren, angiotensin II, and aldosterone levels, as well as abnormal mRNA expression for Ren1, angiotensinogen, Ace, Ace2, Agtr1, Agtr2, and Mas. Furthermore, maternal exposure also induced abnormal renal mRNA expression of sodium transporters Slc9a3, Slc12a1, Slc12a3, and Scnn1b in multiple generations of the adult offspring.<\/li>\n<\/ul>\n
Summary of Comments<\/strong><\/p>\n\n- It is increasingly recognized that high dietary fructose intake, in
\nthe form of high-fructose corn syrup, is a major contributor to the increasing
\nprevalence of obesity and has adverse effect on health outcomes. Recent reports
\nsuggest that consumption of high-fructose diets by mothers during pregnancy and
\nlactation induces renal programming leading to hypertension in adult offspring.<\/li>\n - The mechanisms by which high maternal fructose consumption leads to
\nprogrammed hypertension include excessive oxidative stress, activation of the
\nrenin-angiotensinaldosterone system (RAAS), increased sympathetic nerve
\nactivity, dysregulation of nutrient-sensing signals, increased uric acid,
\nimpaired endothelium-dependent relaxation, abnormal gut microbiota composition
\nwhich are abnormalities impacted by sexual dimorphism.<\/li>\n - Activation of nutrient-sensing signaling pathways, such as adenosine
\nmonophosphate-activated protein kinase and peroxisome proliferator-activated
\nreceptors, increases in uric acid and oxidative stress, and attenuation of the
\nnitric oxide pathway, are also involved in RAAS activation-related hypertension
\nof developmental origin (in adult offspring) induced by maternal and postnatal
\nhigh-fructose intake.<\/li>\n - In concert with RAAS activation and resultant programmed hypertension,
\nmaternal high fructose consumption also induces abnormal expression of renal
\nsodium transporters, excessive oxidative stress, inflammation, and renal
\nfibrosis in adult offspring.<\/li>\n - The data from the present study highlight the role for maternal high
\ndietary fructose intake in increasing the risk of development of hypertension
\nin multigenerational offspring through activation of RAAS, increased
\nvasocontractile peptides, renal sodium transporters, oxidative stress, and
\ninflammation.<\/li>\n - However, clarification is needed regarding the following:\n
\n- The adverse effects of fructose feeding appear
\nto depend on both the amount and duration of fructose consumption. Provision of
\na strong rationale for the maternal 20% high-fructose intake and the 8-month
\ndetermination of blood pressure values in the offspring would have been
\ninstructive.<\/li>\n<\/ul>\n\n- The current study does not identify
\nfundamental sex-specific differences in RAAS activation, sodium transporters,
\noxidative stress factors, and inflammation induced by maternal high-fructose
\nintake in the multigenerational offspring.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\nConclusions<\/strong><\/p>\n\n- The present study is consistent with and extends previous studies in which maternal and post-weaning high-fructose diets induced hypertension of developmental origin.<\/li>\n
- The results show an important role of maternal exposure to high fructose during pregnancy and lactation in development of multigenerational RAAS activation and associated hypertension. Indeed, reductions in maternal fructose consumption may be a novel recommendation and therapeutic strategy for preventing multigenerational hypertension and associated cardiovascular and renal diseases.<\/li>\n
- Additional studies, including in humans, are warranted to more definitively understand the relative role of high fructose consumption in maternal diet-induced cardio-renal metabolic abnormalities and vascular stiffness in conjunction with hypertension.<\/li>\n<\/ul>\n
The post Maternal Exposure to High Fructose and Offspring Health<\/a> appeared first on FructoseFacts<\/a>.<\/p>\n","protected":false},"excerpt":{"rendered":"Jia G, Hill MA and Sowers JR. Hypertension 2019; 74:499-501. DOI: 10.1161\/HYPERTENSIONAHA.119.13017 Download PDF Objective This article is an editorial on a study recently published in the Hypertension journal entitled, \u201cMaternal High-Fructose Intake Induces Multigenerational Activation of the Renin-Angiotensin-Aldosterone System\u201d. Background Seong, et al. investigated whether maternal exposure to high fructose induces hypertension together with […]<\/p>\n","protected":false},"author":7,"featured_media":848,"comment_status":"close","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[24,6,169],"tags":[],"class_list":["post-17557","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-fructose","category-health-profesionals","category-research-summaries"],"yoast_head":"\n
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