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The protective effect of neonatal oral administration of oleanolic acid against the subsequent development of fructose-induced metabolic dysfunction in male and female rats
BACKGROUND: Consumption of fructose-rich diets has been implicated in the increasing global prevalence of metabolic syndrome (MetS). Interventions during periods of early ontogenic developmental plasticity can cause epigenetic changes which program metabolism for positive or negative health benefits...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6245863/ https://www.ncbi.nlm.nih.gov/pubmed/30479649 http://dx.doi.org/10.1186/s12986-018-0314-7 |
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author | Nyakudya, Trevor T. Mukwevho, Emmanuel Erlwanger, Kennedy H. |
author_facet | Nyakudya, Trevor T. Mukwevho, Emmanuel Erlwanger, Kennedy H. |
author_sort | Nyakudya, Trevor T. |
collection | PubMed |
description | BACKGROUND: Consumption of fructose-rich diets has been implicated in the increasing global prevalence of metabolic syndrome (MetS). Interventions during periods of early ontogenic developmental plasticity can cause epigenetic changes which program metabolism for positive or negative health benefits later in life. The phytochemical oleanolic acid (OA) possesses anti-diabetic and anti-obesity effects. We investigated the potential protective effects of neonatal administration of OA on the subsequent development of high fructose diet-induced metabolic dysfunction in rats. METHOD: Male and female (N = 112) suckling rats were randomly assigned to four groups and administered orally: distilled water (DW), oleanolic acid (OA; 60 mg/kg), high-fructose solution (HF; 20% w/v) or OA + HF for 7 days. The rats were weaned onto normal commercial rat chow up to day 55. From day 56, half of the rats in each treatment group were continued on plain water and the rest on a high fructose solution as drinking fluid for 8 weeks. On day 110, the rats were subjected to an oral glucose tolerance test and then euthanased on day 112. Tissue and blood samples were collected to determine the effects of the treatments on visceral fat pad mass, fasting plasma levels of cholesterol, insulin, glucose, triglycerides, insulin resistance (HOMA-IR) and glucose tolerance. RESULTS: Rats which consumed fructose as neonates and then later as adults (HF + F) and those which consumed fructose only in adulthood (DW + F) had significant increases in terminal body mass (females only), visceral fat mass (males and females), serum triglycerides (females only), epididymal fat (males only), fasting plasma glucose (males and females), impaired glucose metabolism (females only), β-cell dysfunction and insulin resistance (males and females) compared to the other treatment groups (P < 0.05). There were no differences in fasting serum cholesterol levels across all treatment groups in both male and female rats (P > 0.05). CONCLUSION: We conclude that neonatal oral administration of OA during the critical window of developmental plasticity protected against the development of health outcomes associated with fructose-induced metabolic disorders in the rats. |
format | Online Article Text |
id | pubmed-6245863 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-62458632018-11-26 The protective effect of neonatal oral administration of oleanolic acid against the subsequent development of fructose-induced metabolic dysfunction in male and female rats Nyakudya, Trevor T. Mukwevho, Emmanuel Erlwanger, Kennedy H. Nutr Metab (Lond) Research BACKGROUND: Consumption of fructose-rich diets has been implicated in the increasing global prevalence of metabolic syndrome (MetS). Interventions during periods of early ontogenic developmental plasticity can cause epigenetic changes which program metabolism for positive or negative health benefits later in life. The phytochemical oleanolic acid (OA) possesses anti-diabetic and anti-obesity effects. We investigated the potential protective effects of neonatal administration of OA on the subsequent development of high fructose diet-induced metabolic dysfunction in rats. METHOD: Male and female (N = 112) suckling rats were randomly assigned to four groups and administered orally: distilled water (DW), oleanolic acid (OA; 60 mg/kg), high-fructose solution (HF; 20% w/v) or OA + HF for 7 days. The rats were weaned onto normal commercial rat chow up to day 55. From day 56, half of the rats in each treatment group were continued on plain water and the rest on a high fructose solution as drinking fluid for 8 weeks. On day 110, the rats were subjected to an oral glucose tolerance test and then euthanased on day 112. Tissue and blood samples were collected to determine the effects of the treatments on visceral fat pad mass, fasting plasma levels of cholesterol, insulin, glucose, triglycerides, insulin resistance (HOMA-IR) and glucose tolerance. RESULTS: Rats which consumed fructose as neonates and then later as adults (HF + F) and those which consumed fructose only in adulthood (DW + F) had significant increases in terminal body mass (females only), visceral fat mass (males and females), serum triglycerides (females only), epididymal fat (males only), fasting plasma glucose (males and females), impaired glucose metabolism (females only), β-cell dysfunction and insulin resistance (males and females) compared to the other treatment groups (P < 0.05). There were no differences in fasting serum cholesterol levels across all treatment groups in both male and female rats (P > 0.05). CONCLUSION: We conclude that neonatal oral administration of OA during the critical window of developmental plasticity protected against the development of health outcomes associated with fructose-induced metabolic disorders in the rats. BioMed Central 2018-11-20 /pmc/articles/PMC6245863/ /pubmed/30479649 http://dx.doi.org/10.1186/s12986-018-0314-7 Text en © The Author(s). 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Nyakudya, Trevor T. Mukwevho, Emmanuel Erlwanger, Kennedy H. The protective effect of neonatal oral administration of oleanolic acid against the subsequent development of fructose-induced metabolic dysfunction in male and female rats |
title | The protective effect of neonatal oral administration of oleanolic acid against the subsequent development of fructose-induced metabolic dysfunction in male and female rats |
title_full | The protective effect of neonatal oral administration of oleanolic acid against the subsequent development of fructose-induced metabolic dysfunction in male and female rats |
title_fullStr | The protective effect of neonatal oral administration of oleanolic acid against the subsequent development of fructose-induced metabolic dysfunction in male and female rats |
title_full_unstemmed | The protective effect of neonatal oral administration of oleanolic acid against the subsequent development of fructose-induced metabolic dysfunction in male and female rats |
title_short | The protective effect of neonatal oral administration of oleanolic acid against the subsequent development of fructose-induced metabolic dysfunction in male and female rats |
title_sort | protective effect of neonatal oral administration of oleanolic acid against the subsequent development of fructose-induced metabolic dysfunction in male and female rats |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6245863/ https://www.ncbi.nlm.nih.gov/pubmed/30479649 http://dx.doi.org/10.1186/s12986-018-0314-7 |
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