Abstract
Nonalcoholic fatty liver diseases (NAFLD) is characterized by accumulation of lipid droplets in the liver. The objective of this study was to evaluate protective effects of fermented Cordyceps militaris extract by Pediococcus pentosaceus ON188 (ONE) against hepatosteatosis and obesity in mice fed a high-fat diet (HFD). Eight-week-old male C57BL/6J mice were fed HFD mixed with ONE for four weeks and its effects on hepatosteatosis and obesity were examined. Although ONE did not change food intake, it reduced body weights of mice at administration dose of 200 mg/kg/day. Activities of lactate dehydrogenase (LDH), aspartate transaminase (AST), and alanine transaminase (ALT) as plasma parameters were reduced by ONE in a dose-dependent manner. Hepatic lipid droplets and triglyceride (TG) levels were also reduced by ONE due to upregulation of fatty acid oxidizing genes such as carnithine palmitoyltransferase (CPT1) and peroxisomal proliferator activated receptor α(PPARα) mediated by induction of sphingosine kinase 2 (SPHK2). In epididymal fat tissue, sizes of adipocytes were significantly reduced by ONE in a dose-dependent manner. This is mainly due to suppression of lipogenesis and upregulation of adipocyte browning genes. Collectively, these results suggest that fermented ONE can activate fatty acid oxidation via SPHK2 in the liver. It can also suppress lipogenesis and activate browning in adipose tissue. Thus, ONE might have potential to be used for the development of functional foods against liver dysfunction and obesity.
Highlights
Western diet and sedentary life-style are associated with development of chronic metabolic disorders including obesity, insulin resistance, and hepatosteatosis
We found that high-fat diet (HFD) feeding increased lipid droplets and pathological states that resembled the occurrence of hepatoseatosis, including accumulation of lipid droplets and ballooning (Figure 3A)
We have previously demonstrated that adenoviral overexpression of hepatic sphingosine kinase 2 with decreased hepatic lipid droplets, we measured expression levels of SPHK2 and fatty acid (FA) oxidizing (SPHK2) can activate FA oxidation in mice [5]
Summary
Western diet and sedentary life-style are associated with development of chronic metabolic disorders including obesity, insulin resistance, and hepatosteatosis. Non-alcoholic fatty liver disease (NAFLD) encompasses a large spectrum of diseases ranging from simple steatosis (accumulation of hepatic triglyceride (TG)), nonalcoholic steatohepatitis (NASH), and fibrosis to cirrhosis [1,2]. Hepatosteatosis represents the very first stage with impaired fatty acid oxidation (FAO), abnormal fatty acid (FA) uptake via circulation, and increased de novo lipogenesis [3]. The following inflammatory stage, called non-alcoholic steatohepatitis (NASH), is characterized by hepatocyte injury, inflammatory infiltrate, and collagen deposition [4,5]. Cirrhosis and hepatocellular carcinoma are developed [6]. To develop therapeutic methods against hepatosteatosis, many studies have been
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