Abstract
Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease globally and there is a pressing need for effective treatment. Lipotoxicity and oxidative stress are the important mediators in NAFLD pathogenesis. Lingonberry (Vaccinium vitis-idaea L.) is rich in anthocyanins that have antioxidant and anti-inflammatory properties. The present study investigated the effect of lingonberry supplementation on liver injury in C57BL/6J male mice fed a high-fat diet (HFD) for 12 weeks. Mice fed HFD displayed liver injury with steatosis, increased lipid peroxidation and inflammatory cytokine expression in the liver as compared to mice fed a control diet. Lingonberry supplementation for 12 weeks alleviated HFD-induced liver injury, attenuated hepatic lipid accumulation, and inflammatory cytokine expression. Lingonberry supplementation inhibited the expression of sterol regulatory element-binding protein-1c (SREBP-1c) and acetyl-CoA carboxylase-1 (AAC-1) as well as activated AMP-activated protein kinase (AMPK) in the liver. It also decreased HFD-induced hepatic oxidative stress and aggregation of inflammatory foci. This was associated with a restoration of nuclear factor erythroid 2–related factor 2 (Nrf2) and glutathione level in the liver. These results suggest that lingonberry supplementation can protect against HFD-induced liver injury partly through attenuation of hepatic lipid accumulation, oxidative stress, and inflammatory response.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is a major cause of chronic liver injury worldwide [1,2]
Results from the present study suggested that attenuation of SREBP-1c and restoration of AMPK by lingonberry supplementation at a lower dose might account for a reduction of hepatic lipid accumulation, which was independent of weight gain change
Our results suggested that lingonberry supplementation attenuated HFDinduced oxidative stress through increased nuclear factor erythroid 2–related factor 2 (Nrf2)/glutathione antioxidant defense
Summary
Non-alcoholic fatty liver disease (NAFLD) is a major cause of chronic liver injury worldwide [1,2]. It is defined as the hepatic accumulation of excess fat (>5% of hepatocytes) in people who drink little or no alcohol [2,3]. The prevalence of NAFLD in general populations has increased up to 25% worldwide [1,2,4]. This is presumptively due to a strong association of NAFLD with metabolic syndrome as NAFLD patients often develop dyslipidemia, hyperglycemia, insulin resistance, and hypertension [5,6].
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