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Neonatal intake of oleanolic acid attenuates the subsequent development of high fructose diet-induced non-alcoholic fatty liver disease in rats

Published online by Cambridge University Press:  24 May 2018

T. T. Nyakudya ,
E. Mukwevho ,
P. Nkomozepi  and
K. H. Erlwanger
T. T. Nyakudya*
Affiliation:
School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa Department of Human Anatomy and Physiology, Faculty of Health Sciences, University of Johannesburg, Johannesburg, South Africa
E. Mukwevho
Affiliation:
Department of Biology, Faculty of Agriculture, Science and Technology, North West University, Mmabatho, Mafikeng, South Africa
P. Nkomozepi
Affiliation:
Department of Human Anatomy and Physiology, Faculty of Health Sciences, University of Johannesburg, Johannesburg, South Africa
K. H. Erlwanger
Affiliation:
School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa
*
Address for correspondence: T. T. Nyakudya, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, 7 York Road, 2193, Johannesburg, South Africa. E-mail: [email protected]
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Abstract

Dietary manipulations during the early postnatal period are associated with the development of metabolic disorders including non-alcoholic fatty liver disease (NAFLD) or long-term protection against metabolic dysfunction. We investigated the potential hepatoprotective effects of neonatal administration of oleanolic acid (OA), a phytochemical, on the subsequent development in adulthood, of dietary fructose-induced NAFLD. Male and female suckling rats (n=112) were gavaged with; distilled water (DW), OA (60 mg/kg), high fructose solution (HF; 20% w/v) and OA+HF (OAHF) for 7 days. The rats were weaned onto normal rat chow on day 21 up to day 55. From day 56, half of the rats in each treatment group were continued on plain water or HF as drinking fluid for 8 weeks. Hepatic lipid accumulation and hepatic histomorphometry were then determined. Fructose consumption in adulthood following neonatal fructose intake (HF+F) caused a 47–49% increase in hepatic lipid content of both male and female rats (P<0.05). However, fructose administered in adulthood only, caused a significant increase (P<0.05) in liver lipid content in females only. NAFLD activity scores for inflammation and steatosis were higher in the fructose-fed rats compared with other groups (P<0.05). Steatosis, low-grade inflammation and fibrosis were observed in rats that received HF+F. NAFLD area fraction for fibrosis was three times higher in rats that received fructose neonatally and in adulthood compared with the rats in the negative control group (P<0.05). Treatment with OA during a critical window of developmental plasticity in rats prevented the development of fructose-induced NAFLD.

Keywords

fructosemetabolic dysfunctionneonatal programmingnon-alcoholic fatty liver diseaseoleanolic acid
Type
Original Article
Information
Journal of Developmental Origins of Health and Disease , Volume 9 , Issue 5 , October 2018 , pp. 500 - 510
Copyright
© Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2018 

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