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Abstract Title:

β-sitosterol mitigates the progression of high-fructose diet-induced non-alcoholic fatty liver disease in growing male Sprague-Dawley rats.

Abstract Source:

Can J Physiol Pharmacol. 2019 Sep 27. Epub 2019 Sep 27. PMID: 31560861

Abstract Author(s):

Nontobeko Gumede, Busisani Lembede, Pilani Nkomozepi, Richard Brooksbank, Kennedy Honey Erlwanger, Eliton Chivandi

Article Affiliation:

Nontobeko Gumede

Abstract:

Fructose contributes to the development of non-alcoholic fatty liver disease (NAFLD).β-sitosterol (Bst), a naturally occurring phytosterol, has antihyperlipidaemic and hepatoprotective properties. This study interrogated the potential protective effect of β-sitosterol against NAFLD in growing rats fed a high-fructose diet, modelling children fed obesogenic diets. Forty-four 21-dayold male rat pups were randomly allocated to and administered the following treatments for 12 weeks: group I- standard rat chow (SRC) + plain drinking water (PW) + plain gelatine cube (PC); group II- SRC+ 20% w/v fructose solution (FS) as drinking fluid + PC; group III- SRC + FS + 100 mg/kg fenofibrate in gelatine cube; group IV- SRC + FS + 20 mg/kg β-sitosterol gelatine cube (Bst) and group V- SRC + PW + Bst. Terminally, the livers were dissected out, weighed, total liver lipid content determined and histological analyses were done. Harvested plasma was used to determine the surrogate biomarkers of liver function. The high-fructose diet caused increased (p<0.05) hepatic lipid (total) accretion (>10% liver mass), micro- and macro-vesicular hepatic steatosis and hepatic inflammation.β-sitosterol and fenofibrate prevented the high-fructose diet-induced macrovesicular steatosis and prevented the progression of NAFLD to steatohepatitis. β-sitosterol can prospectively be used to mitigate diet-induced NAFLD.

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