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RISS 인기검색어
- 검색키워드
- 저자 : TRANSONGNGUYENKHOI (검색결과 2 건)
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Preventive Effects of Fermented Cordyceps militaris on Obesity and Hepatosteatosis
TRANSONGNGUYENKHOI Gachon University, Gachon University 2018 국내박사
Various studies have shown that nonalcoholic fatty liver diseases (NAFLD), the aggregation of lipid droplets in the liver (hepatosteatosis) followed by inflammatory complication, appears to be chronic consequences of overnutrition. In the present research, we examined the anti-hepatosteatosis effects of fermented Cordyceps militaris (CM) extracts in AML-12 hepatocytes as well as in mice with short-term high-fat diet (HFD) via activation of fatty acid oxidation (FAO). The chemical components, adenosine and cordycepin, of CM extract (CME), CM grown on germinated soybean (GSCE) and fermented GSC by Pediococcus pentosaceus ON188 (ON188E) were assessed. In hepatocytes, the expression of CPT1α and PPARα, FAO genes were upregulated only by ON188E treatment. In contrast, SCD1, a lipogenic gene was downregulated by ON188E within no cytotoxic range. Regardless of oleic acid treatment to mimic fatty liver condition, mRNA and proteins of FAO genes were upregulated by ON188E in a dose-dependent manner. Formation of intracellular lipid droplets by addition of oleic acid was reduced by ON188E to the levels in WY14643-treated cells. When cells were treated with ON188E, SPHK2 and its phosphorylated product sphingosine 1-phosphate (S1P) elevation activated FAO in hepatocytes. In consistent with this, in animal results, ON188E extract did not alter the food intake while body weight and inflammatory factors in plasma of HFD mice were controlled comparable to those of NCD mice. Moreover, ON188E treatment significantly upregulated hepatic SPHK2 level in mice fed HFD. The elevated SPHK2 activated hepatic FAO genes such as CPT1α and PPARα but downregulated DGAT2, a triglyceride biosynthetic gene. We found that ON188E treatment reduced lipid droplets in liver and the hypertrophy of adipocytes in epididymal white adipose tissue (WAT) in a dose-dependent manner. Activation of SIRT1and PPARγ in WAT suggests that ON188E could modulate browning process of adipocytes which induces body thermogenesis. Collectively, the fermented CM extracts not only reduce risk of tissue damage but activate hepatic FAO via elevation of S1P synthesis in hepatocytes and induce WAT browning as well. This suggests ON188E can be applied as a potential functional food preventing obesity and hepatosteatosis.
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Suppression of Sptlc2 expression by oyster shell extracts modulates hepatic lipid metabolism
TRAN SONG NGUYEN KHOI Graduate School, Gachon University 2014 국내석사
Studies on rodent models revealed the contributed roles of sphingolipids in the onset of diabetes, cardiomyopathy, insulin resistance, atherosclerosis, hepatic steatosis, liver injury, and hepatocarcinogenesis. In cardiovascular system, sphingolipids are implicated in atherogenesis, lipoprotein metabolism and insulin resistance leading to etiology of cardiovascular or metabolic dysfunction. We hypothesized that suppression of serine palmitoyltransferase (SPT) inhibits ceramide/sphingomyelin biosynthesis as well as de novo cholesterol/triglyceride (TG) biosynthesis. In this study, we examined the Sptlc2 suppressing effects of various natural extracts in Hepa1c1c7 cells. Among them, oyster (Ostrea gigas Thunb.) shell extract significantly down regulated expression of Sptlc2 with no toxicity to liver cell. Further extraction of oyster shell by various concentrations of ethanol was performed in order to examine the specific components having SPT subunits (Sptlc1 and Sptlc2) suppressing effects. By using 50% ethanol, the oyster shell extract has the highest SPT suppressing effects, Sptlc2 mRNA and protein expressions were reduced in a dose-dependent manner. In addition, oyster shell extract down regulated HMG-CoA reductase (HMG-CR), diglyceride acyltransferase (DGAT2), fatty acid synthase (FAS), carnitine palmitoyltransferase alpha (CPT1a), stearoyl-CoA desaturase 1 (SCD1), acyl-CoA carboxylase (ACC), and acyl-CoA oxidase (ACO) gene expression, which are involved in fatty acid and cholesterol biosynthesis. These results indicate that suppression of Sptlc2 by oyster shell extracts reduces de novo ceramide synthesis leading to inhibition of de novo synthesis of cholesterol/triacylglycerol (TG). In brief, our investigation suggests the possible therapeutic application of oyster shell extracts for cardiovascular/metabolic disease treatment.
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