Abstract:Emerging evidence suggests that mitochondrial dysfunction mediates the pathogenesis for non-alcoholic fatty liver disease (NAFLD). Hydroxytyrosol (HT) is a key component of extra virgin olive oil which can exert beneficial effects on NAFLD through modulating mitochondria. However, the mechanism of the impacts of HT still remains elusive. Thus, an in vivo and a series of in vitro experiments were carried out to examine the impacts of hydroxytyrosol (HT) on lipid metabolism and mitochondrial function in fish. Fo… Show more
“…Stress-induced mitochondrial dysfunction is prevented by PTEN-induced kinase 1 (PINK1). Ultimately, HT boosted PINK1 and AMPK expressions in the HFD zebrafish liver model, which suggested a reduction in hepatic lipid accumulation and mitochondrial dysfunction, activating the AMPK/PINK1 pathway [157].…”
Non-alcoholic fatty liver disease (NAFLD), with a global prevalence of 25%, continues to escalate, creating noteworthy concerns towards the global health burden. NAFLD causes triglycerides and free fatty acids to build-up in the liver. The excessive fat build-up causes inflammation and damages the healthy hepatocytes leading to non-alcoholic steatohepatitis (NASH). Dietary habits, obesity, insulin resistance, type 2 diabetes, and dyslipidemia influence NAFLD progression. The disease burden is complicated due to the paucity of therapeutic interventions. Obeticholic acid is the only approved therapeutic agent for NAFLD. With more scientific enterprise being directed towards understanding of underlying mechanisms of NAFLD, novel targets like lipid synthase, farnesoid X receptor signalling, peroxisome proliferator-activated receptors associated with inflammatory signalling and hepatocellular injury have played a crucial role in progression of NAFLD to NASH. Phytocompounds have shown promising results in modulating hepatic lipid metabolism and de novo lipogenesis suggesting their possible role in managing NAFLD. This review discusses the ameliorative role of different classes of phytochemicals with molecular mechanisms in different cell lines and established animal models. These compounds may lead to the development of novel therapeutic strategies for NAFLD progression to NASH. This review also deliberates on phytomolecules undergoing clinical trials for effective management of NAFLD.
“…Stress-induced mitochondrial dysfunction is prevented by PTEN-induced kinase 1 (PINK1). Ultimately, HT boosted PINK1 and AMPK expressions in the HFD zebrafish liver model, which suggested a reduction in hepatic lipid accumulation and mitochondrial dysfunction, activating the AMPK/PINK1 pathway [157].…”
Non-alcoholic fatty liver disease (NAFLD), with a global prevalence of 25%, continues to escalate, creating noteworthy concerns towards the global health burden. NAFLD causes triglycerides and free fatty acids to build-up in the liver. The excessive fat build-up causes inflammation and damages the healthy hepatocytes leading to non-alcoholic steatohepatitis (NASH). Dietary habits, obesity, insulin resistance, type 2 diabetes, and dyslipidemia influence NAFLD progression. The disease burden is complicated due to the paucity of therapeutic interventions. Obeticholic acid is the only approved therapeutic agent for NAFLD. With more scientific enterprise being directed towards understanding of underlying mechanisms of NAFLD, novel targets like lipid synthase, farnesoid X receptor signalling, peroxisome proliferator-activated receptors associated with inflammatory signalling and hepatocellular injury have played a crucial role in progression of NAFLD to NASH. Phytocompounds have shown promising results in modulating hepatic lipid metabolism and de novo lipogenesis suggesting their possible role in managing NAFLD. This review discusses the ameliorative role of different classes of phytochemicals with molecular mechanisms in different cell lines and established animal models. These compounds may lead to the development of novel therapeutic strategies for NAFLD progression to NASH. This review also deliberates on phytomolecules undergoing clinical trials for effective management of NAFLD.
“…Intestinal lipase and trypsin activities were measured by competition method using commercial kits (Nanjing Jiancheng Biological Company, Nanjing, China) according to the manufacturerâs instructions. Quantification of proteins was performed with a total protein quantitative kit (Beijing Solarbio Science and Technology Company, Beijing, China) according to our previous study [ 34 ].…”
This study was conducted to investigate the effects of Tenebrio molitor meal (TM) replacement for fish meal (FM) on growth performance, humoral immunity, and intestinal health of juvenile large yellow croakers (Larimichthys crocea). Four experimental diets were formulated by replacing FM with TM at different levelsâ0% (TM0), 15% (TM15), 30% (TM30), and 45% (TM45). Triplicate groups of juveniles (initial weight = 11.80 ± 0.02 g) were fed the test diets to apparent satiation two times daily for eight weeks. There was no significant difference in final body weight (FBW) and weight gain rate (WG) among TM0, TM15, and TM30, while TM45 feeding significantly reduced the FBW and WG. Compared with TM0, AKP activity in serum was significantly decreased in TM45, while the TM15 group remarkably increased LZM activity. TM30 showed significantly higher serum C3 levels compared to the TM0 group, while the TM addition groups decreased the C4 levels significantly in the serum. In terms of intestinal histology, the addition of TM increased the height and thickness of the intestinal villus and also increased the thickness of the intestinal muscles significantly. The addition of TM significantly reduced the serum DAO and D-lactate concentrations. The results of 16S rRNA gene sequencing showed that the addition of TM significantly enhanced the relative abundance of Bacilli and Lactobacillus and contributed to the decrease in the relative abundance of Plesiomonas. In addition, the TM30 and TM45 groups significantly reduced the abundance of Peptostreptococcaceae. Overall, our results indicated that TM could be a viable alternative protein source, 6.7% TM supplantation (replacing 15% FM) in large yellow croaker feed improved humoral immunity and intestinal health with no adverse effects on growth. Furthermore, the replacement of FM with 30% and 45% TM adversely affects growth and humoral immunity.
“…Dong et al examined hydroxytyrosol, derived from olive oil, in the setting of NASH. This study showed hydroxytyrosol can alleviate NASH by inducing mitophagy upon mitochondrial activation through the AMPK/PINK1 pathway ( Van Gisbergen et al, 2020 ).…”
Section: How Boosting Mitochondria Can Protect Liver From Covid-induc...mentioning
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