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Author Xing, Xiaomang ♦ Li, Danyang ♦ Chen, Dilong ♦ Zhou, Liang ♦ Chonan, Ritsu ♦ Yamahara, Johji ♦ Wang, Jianwei ♦ Li, Yuhao
Source United States Department of Energy Office of Scientific and Technical Information
Content type Text
Language English
Subject Keyword APPLIED LIFE SCIENCES ♦ ADIPOSE TISSUE ♦ BIOSYNTHESIS ♦ BLOOD PRESSURE ♦ CARBOXYLASE ♦ CHOLESTEROL ♦ COENZYMES ♦ FRUCTOSE ♦ GENES ♦ GLUCOSE ♦ HERBS ♦ INSULIN ♦ INTAKE ♦ LIVER ♦ MESSENGER-RNA ♦ METABOLISM ♦ MUTATIONS ♦ OXIDATION ♦ RATS ♦ RECEPTORS ♦ TRIGLYCERIDES
Abstract Mangiferin, a xanthone glucoside, and its associated traditional herbs have been demonstrated to improve abnormalities of lipid metabolism. However, its underlying mechanisms remain largely unclear. This study investigated the anti-steatotic effect of mangiferin in fructose-fed spontaneously hypertensive rat (SHR)s that have a mutation in sterol regulatory element binding protein (SREBP)-1. The results showed that co-administration of mangiferin (15 mg/kg, once daily, by oral gavage) over 7 weeks dramatically diminished fructose-induced increases in hepatic triglyceride content and Oil Red O-stained area in SHRs. However, blood pressure, fructose and chow intakes, white adipose tissue weight and metabolic parameters (plasma concentrations of glucose, insulin, triglyceride, total cholesterol and non-esterified fatty acids) were unaffected by mangiferin treatment. Mechanistically, mangiferin treatment suppressed acyl-coenzyme A:diacylglycerol acyltransferase (DGAT)-2 expression at the mRNA and protein levels in the liver. In contrast, mangiferin treatment was without effect on hepatic mRNA and/or protein expression of SREBP-1/1c, carbohydrate response element binding protein, liver pyruvate kinase, fatty acid synthase, acetyl-CoA carboxylase-1, stearoyl-CoA desaturase-1, DGAT-1, monoacyglycerol acyltransferase-2, microsomal triglyceride transfer protein, peroxisome proliferator-activated receptor-alpha, carnitine palmitoyltransferase-1 and acyl-CoA oxidase. Collectively, our results suggest that mangiferin treatment ameliorates fatty liver in fructose-fed SHRs by inhibiting hepatic DGAT-2 that catalyzes the final step in triglyceride biosynthesis. The anti-steatotic effect of mangiferin may occur independently of the hepatic signals associated with de novo fatty acid synthesis and oxidation. - Highlights: • We investigated the anti-steatotic effect of mangiferin (MA) in fructose-fed SHR. • MA (15 mg/kg/day for 7 weeks) ameliorated fructose-induced fatty liver in SHR. • MA inhibited hepatic DGAT2 expression at the mRNA and protein levels. • MA did not affect expression of the genes responsible for fatty acid synthesis. • MA ameliorates fructose-induced fatty liver by inhibiting hepatic DGAT2 in rats.
ISSN 0041008X
Educational Use Research
Learning Resource Type Article
Publisher Date 2014-10-15
Publisher Place United States
Journal Toxicology and Applied Pharmacology
Volume Number 280
Issue Number 2


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