Modulation of hepatic sterol regulatory element-binding protein-1c-mediated gene expression contributes to Salacia oblonga root-elicited improvement of fructose-induced fatty liver in rats

Oct 26, 2013Journal of ethnopharmacology

Salacia oblonga root may improve fructose-caused fatty liver in rats by changing liver gene activity that controls fat production

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Abstract

Treatment with Salacia oblonga root (20 mg/kg) significantly reduced fructose-induced fatty liver in rats.

Fructose intake led to excess triglyceride accumulation and changes in liver structure in rats.
Salacia oblonga root treatment decreased the overexpression of sterol regulatory element-binding protein (SREBP)-1/1c and its target genes involved in fat synthesis.
Key genes such as fatty acid synthase and acetyl-CoA carboxylase-1 were downregulated following SOR treatment.
No significant changes were observed in the expression of carbohydrate response element binding protein or peroxisome proliferator-activated receptors.
These findings indicate that SOR may improve fatty liver conditions through modulation of specific gene expressions.

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ETHNOPHARMACOLOGICAL RELEVANCE: Salacia oblonga root (SOR) is a traditionally herbal medicine for obesity and diabetes, which are closely associated with fatty liver. To investigate the molecular mechanisms of SOR in the treatment of dietary-induced fatty liver.

MATERIALS AND METHODS: Male rats were co-administered with fructose in drinking water and vehicle or the aqueous-ethanolic extract of SOR (by gavage, once daily) for 10 weeks. Biochemical variables were determined enzymatically or by ELISA. Gene expression was analyzed by Real-Time PCR and/or Western blot.

RESULTS: SOR treatment (20mg/kg) diminished fructose-induced fatty liver indicated by decreases in excess triglyceride accumulation and the increased vacuolization and Oil Red O staining area in the livers of rats. Importantly, Hepatic gene expression profile revealed that SOR suppressed fructose-stimulated overexpression of sterol regulatory element-binding protein (SREBP)-1/1c mRNA and nuclear protein. In accord, overexpression of SREBP-1c-responsive genes, such as fatty acid synthase, acetyl-CoA carboxylase-1 and stearoyl-CoA desaturase-1, was also downregulated. In contrast, overexpressed nuclear protein of carbohydrate response element binding protein and mRNA of its target gene liver pyruvate kinase were not altered. Additionally, SOR also did not affect expression of peroxisome proliferator-activated receptor-gamma- and -alpha, as well as their target genes, such as carnitine palmitoyltransferase-1a, acyl-CoA oxidase and CD36.

CONCLUSIONS: These results suggest that modulation of hepatic sterol regulatory element-binding protein-1c-mediated gene expression contributes to SOR-elicited improvement of fructose-induced fatty liver in rats. Our findings provide a better understanding of SOR in the treatment of obesity and diabetes.

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Modulation of hepatic sterol regulatory element-binding protein-1c-mediated gene expression contributes to Salacia oblonga root-elicited improvement of fructose-induced fatty liver in rats

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