Chitosan Oligosaccharide Attenuates Nonalcoholic Fatty Liver Disease Induced by High Fat Diet through Reducing Lipid Accumulation, Inflammation and Oxidative Stress in C57BL/6 Mice

Abstract

Nonalcoholic fatty liver disease (NAFLD) has become the most common chronic liver disease closely associated with metabolic syndrome, but there are no validated pharmacological therapies. The aim of this study was to investigate the effect of chitosan oligosaccharide (COS) on NAFLD. Mice were fed either a control diet or a high-fat diet (HFD) with or without COS (200 or 400 mg/kg body weight (BW)) by oral gavage for seven weeks. Administration with COS significantly lowered serum lipid levels in the HFD-fed mice. The hepatic lipid accumulation was significantly decreased by COS, which was attributed to decreased expressions of lipogenic genes and increased expressions of fatty β-oxidation-related genes. Moreover, pro-inflammatory cytokines, neutrophils infiltration, and macrophage polarization were decreased by COS in the liver. Furthermore, COS ameliorated hepatic oxidative stress by activating the nuclear factor E2-related factor 2 (Nrf2) pathway and upregulating gene expressions of antioxidant enzymes. These beneficial effects were mediated by the activation of the adenosine monophosphate-activated protein kinase (AMPK) signaling pathway. Therefore, COS might be a potent dietary supplement to ameliorate NAFLD.

Hepatoprotective and Anti-Oxidative Effects of Total Flavonoids From Qu Zhi Qiao (Fruit of Citrus Paradisi cv.Changshanhuyou) on Nonalcoholic Steatohepatitis In Vivo and In Vitro Through Nrf2-ARE Signaling Pathway

“…The pathogenesis of NASH is closely associated with Nrf2-ARE signaling pathway, since Nrf2-ARE plays a key role in response to oxidative stress during NASH progress (Fisher et al, 2008;Lee et al, 2014). Up-regulation of Nrf2-ARE signaling activity is important in reversing many oxidative-stressed diseases, such as NASH (Sampath et al, 2019;Tao et al, 2019). Recently, it becomes a new target of treatment in liver injury and liver fibrosis (Shin et al, 2013).…”

Modeling Diet‐Induced Metabolic Syndrome in Rodents

“…All data presented herein were obtained from refs. [70,72,74,77,78,88,95,96,98,104,105,107,109–112,114–128,130,132,133,135–142,144–146,148,150,151,153,154,157,159,161–168,174,176–184,187,188,190,191,194,196–198,200–204,206,208–212,215,217,219–226,229,230,232–235,237,239–242,244,250–253,257,258,263,264,266–268,270–276,278,285,287–290,292,295,296,298–301,303,304,308–310,314,316,317,319,321,322,324,325,329,331–342].…”

Effects of Chitosan Oligosaccharide on Plasma and Hepatic Lipid Metabolism and Liver Histomorphology in Normal Sprague-Dawley Rats

“…Chitosan oligosaccharide can also regulate lipid metabolism, improving obesity and dyslipidemia [ 9 , 10 , 11 ]. Chitosan oligosaccharide has been shown to inhibit adipocyte differentiation and reduce lipid accumulation [ 12 ], improve obesity-related glucolipid metabolism disorder in mouse liver [ 13 ], and attenuate nonalcoholic fatty liver in mice [ 14 ].…”