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Administration of ursolic acid to new-born pups prevents dietary fructose-induced non-alcoholic fatty liver disease in Sprague Dawley rats

Published online by Cambridge University Press:  19 March 2020

Nyasha C. Mukonowenzou ,
Rachael Dangarembizi ,
Eliton Chivandi ,
Pilani Nkomozepi  and
Kennedy H. Erlwanger Open the ORCID record for Kennedy H. Erlwanger [Opens in a new window]
Nyasha C. Mukonowenzou
Affiliation:
Department of Anatomy and Physiology, Faculty of Medicine, National University of Science and Technology, Box AC 939, Ascot, Bulawayo, Zimbabwe School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, 7 York Road, Parktown, Johannesburg, 2193, South Africa
Rachael Dangarembizi
Affiliation:
Department of Anatomy and Physiology, Faculty of Medicine, National University of Science and Technology, Box AC 939, Ascot, Bulawayo, Zimbabwe School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, 7 York Road, Parktown, Johannesburg, 2193, South Africa
Eliton Chivandi
Affiliation:
School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, 7 York Road, Parktown, Johannesburg, 2193, South Africa
Pilani Nkomozepi
Affiliation:
Department of Human Anatomy and Physiology, Faculty of Health Sciences, University of Johannesburg, 37 Nind Street, Doornfontein, Johannesburg, South Africa
Kennedy H. Erlwanger*
Affiliation:
School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, 7 York Road, Parktown, Johannesburg, 2193, South Africa
*
Address for correspondence: Kennedy H. Erlwanger, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, 7 York Road, Parktown, Johannesburg, 2193, South Africa. Email: Kennedy.Erlwanger@wits.ac.za
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Abstract

Overconsumption of fructose time dependently induces the development of non-alcoholic fatty liver disease (NAFLD). We investigated whether ursolic acid (UA) intake by new-born rats would protect against fructose-induced NAFLD. One hundred and seven male and female Sprague Dawley rat pups were randomly grouped and gavaged (10 ml/kg body weight) with either 0.5% dimethylsulphoxide (vehicle control), 0.05% UA, 50% fructose mixed with UA (0.05%) or 50% fructose alone, from postnatal day 6 (P6) to P20. Post-weaning (P21–P69), the rats received normal rat chow (NRC) and water to drink. On P70, the rats in each group were continued on water or 20% fructose to drink, as a secondary high fructose diet during adulthood. After 8 weeks, body mass, food and fluid intake, circulating metabolites, visceral adiposity, surrogate markers of liver function and indices of NAFLD were determined. Food intake was reduced as a result of fructose feeding in both male and female rats (p < 0.0001). Fructose consumption in adulthood significantly increased fluid intake and visceral adiposity in female rats (p < 0.05) and had no apparent effects in male rats (p > 0.05). In both sexes of rats, fructose had no significant (p > 0.05) effects on body mass, circulating metabolites, total calorie intake and surrogate markers of hepatic function. Fructose consumption in both early life and adulthood in female rats promoted hepatic lipid accumulation (p < 0.001), hypertrophy, microvesicular and macrovesicular steatosis (p < 0.05). Early-life UA intake significantly (p < 0.001) reduced fructose-induced hepatic lipid accumulation in both male and female rats. Administration of UA during periods of developmental plasticity shows prophylactic potential against dietary fructose-induced NAFLD.

Keywords

Ursolic acidfructosenon-alcoholic fatty liver diseasedevelopmental programming
Type
Original Article
Information
Journal of Developmental Origins of Health and Disease , Volume 12 , Issue 1 , February 2021 , pp. 101 - 112
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Copyright
© Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2020

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