| The inhibitory effect of genistein on hepatic steatosis is linked to visceral adipocyte metabolism in mice with diet-induced non-alcoholic fatty liver disease. | |
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MedLine Citation:
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PMID: 20687969 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Non-alcoholic fatty liver disease (NAFLD) has been deeply associated with visceral adiposity, adipose tissue inflammation and a variety of adipocytokines. We reported previously that genistein inhibited NAFLD by enhancing fatty acid catabolism. However, this molecular approach focused on hepatic metabolism. Thus, we have attempted to determine whether this anti-steatotic effect of genistein is linked to visceral adipocyte metabolism. C57BL/6J mice were fed on normal-fat (NF) diet, high-fat (HF) diet and HF diet supplemented with genistein (1, 2 and 4 g/kg diet) for 12 weeks. Mice fed on the HF diet gained body weight, exhibited increased visceral fat mass and elevated levels of serum and liver lipids, and developed NAFLD, unlike what was observed in mice fed on the NF diet. However, genistein supplementation (2 and 4 g/kg diet) normalised these alternations. In the linear regression analysis, visceral fat (R 0·77) and TNFα (R 0·62) were strongly correlated with NAFLD among other NAFLD-related parameters. Genistein supplementation suppressed the hypertrophy of adipocytes via the up-regulation of genes involved in fatty acid β-oxidation, including PPARα, 5'-AMP-activated protein kinase and very long-chain acyl CoA dehydrogenase, as well as through the down-regulation of genes associated with adipogenesis or lipogenesis, including liver X receptor-α, sterol-regulatory element-binding protein-1c, PPARγ, retinoid X receptor-α and acetyl CoA carboxylase 2. Moreover, genistein supplementation augmented an anti-steatohepatitic adiponectin TNF and reduced a steatohepatitic TNFα. Collectively, these findings show that genistein may prevent NAFLD via the regulation of visceral adipocyte metabolism and adipocytokines. |
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Authors:
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Mi-Hyun Kim; Kyung-Sun Kang; Yeon-Sook Lee |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-08-06 |
Journal Detail:
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Title: The British journal of nutrition Volume: 104 ISSN: 1475-2662 ISO Abbreviation: Br. J. Nutr. Publication Date: 2010 Nov |
Date Detail:
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Created Date: 2010-10-29 Completed Date: 2010-11-12 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0372547 Medline TA: Br J Nutr Country: England |
Other Details:
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Languages: eng Pagination: 1333-42 Citation Subset: IM |
Affiliation:
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Department of Food and Nutrition, College of Human Ecology, Seoul National University, 599 Gwanangno, Gwanak-gu, Seoul 151-742, South Korea. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adipocytes
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metabolism,
pathology Adipogenesis / genetics Animals Antilipemic Agents / pharmacology*, therapeutic use Dietary Fats / metabolism Fatty Liver / drug therapy, genetics, metabolism* Gene Expression Regulation / drug effects Genistein / pharmacology*, therapeutic use Hypertrophy Intra-Abdominal Fat / metabolism* Linear Models Lipid Metabolism* Lipogenesis / genetics Male Mice Mice, Inbred C57BL Phytoestrogens / pharmacology, therapeutic use Plant Extracts / pharmacology*, therapeutic use Soybeans / chemistry Tumor Necrosis Factors / metabolism Weight Gain / drug effects |
| Chemical | |
Reg. No./Substance:
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0/Antilipemic Agents; 0/Dietary Fats; 0/Phytoestrogens; 0/Plant Extracts; 0/Tumor Necrosis Factors; 446-72-0/Genistein |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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