Effect of dietary fat to produce non‐alcoholic fatty liver in the rat

Ahmed, Usman; Redgrave, Trevor G.; Oates, Phillip S.

doi:10.1111/j.1440-1746.2009.05870.x

Cited by 48 publications

(30 citation statements)

References 44 publications

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“…Depending on acute or chronic pathophysiological conditions, the UPR transducer IRE1α may act as an RNase or a scaffold through its cytosolic domain to modulate inflammatory and/or metabolic stress signaling pathways (8, 15). It was previously reported that the IRE1α-XBP1 pathway was activated in the livers of NASH patients or animal models (32–34). However, our study showed that a HFD de-activated IRE1α RNase activity towards both Xbp1 mRNA splicing and select miRNA processing in the liver.…”

Section: Discussionmentioning

confidence: 96%

IRE1α prevents hepatic steatosis by processing and promoting the degradation of select microRNAs

et al. 2018

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Obesity or a high-fat diet represses the endoribonuclease activity of inositol-requiring enzyme 1α (IRE1α), a transducer of the unfolded protein response (UPR) in cells under endoplasmic reticulum (ER) stress. An impaired UPR is associated with hepatic steatosis and non-alcoholic fatty liver disease (NAFLD), which is caused by lipid accumulation in the liver. Here, we found that IRE1α was critical to maintaining lipid homeostasis in the liver by repressing the biogenesis of microRNAs (miRNAs) that regulate lipid mobilization. In mice fed normal chow, the endoribonuclease function of IRE1α processed a subset of precursor miRNAs in the liver, including those of the miR-200 and miR-34 families, such that IRE1α promoted their degradation through the process of regulated IRE1-dependent decay (RIDD). A high-fat diet in mice or hepatic steatosis in patients was associated with the S-nitrosylation of IRE1α and inactivation of its endoribonuclease activity. This resulted in an increased abundance of these miRNA families in the liver and, consequently, a decreased abundance of their targets, which included peroxisome proliferator-activated receptor α (PPARα) and the deacetylase sirtuin 1 (SIRT1), regulators of fatty acid oxidation and triglyceride lipolysis. IRE1α deficiency exacerbated hepatic steatosis in mice. The abundance of the miR-200 and miR-34 families was also increased in cultured, lipid-overloaded hepatocytes and in the livers of patients with hepatic steatosis. Our findings reveal a mechanism by which IRE1α maintains lipid homeostasis through its regulation of miRNAs, a regulatory pathway distinct from the canonical IRE1α-UPR pathway under acute ER stress.

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Section: Discussionmentioning

confidence: 96%

IRE1α prevents hepatic steatosis by processing and promoting the degradation of select microRNAs

et al. 2018

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“…Hence, animals of HA and HL groups could be considered obese since their final body weight was 30 % more than that of either of the other groups, with a body increase significantly higher. In addition, in this study, we chose a nutritional model that has been used previously by other authors [26,27] in which the H diet leads to steatosis, which can be confirmed by plasma levels of ALT and AST, presence of dyslipidemia (Table 3), liver histological examination (Fig. 1) and assessment of total liver fat (Table 3).…”

Section: Discussionmentioning

confidence: 99%

The effect of tomato juice supplementation on biomarkers and gene expression related to lipid metabolism in rats with induced hepatic steatosis

et al. 2014

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“…6 One of the important features of NAFLD is abnormal liver function and nonalcoholic steatosis. 7 Although the pathogenic process of NAFLD is unclear NAFLD has been linked with obesity. Therefore, many chemical agents are used as lipid-lowering medication.…”

Section: Introductionmentioning

confidence: 99%

Beneficial Effects of Red Yeast Rice on High-Fat Diet-Induced Obesity, Hyperlipidemia, and Fatty Liver in Mice

Lee

Chung

et al. 2015

Journal of Medicinal Food

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Obesity is a common cause of hyperlipidemia, which is a major coronary risk factor. Previous studies have shown red yeast rice (RYR) effectiveness in lowering low-density lipoprotein cholesterol. The aim of this study was to investigate the effects of RYR on obesity and hyperlipidemia. Mice were randomly separated into five groups: the control group with a normal diet, the high-fat diet (HFD) group fed a HFD without any treatment, and HFD-fed groups supplemented with RYR (1 g/kg/day for 8 weeks, 1 g/kg/day for 12 weeks, and 2.5 g/kg/day for 8 weeks). Body weight was recorded twice and food intake thrice weekly. Liver and fat pads were surgically removed and weighed. The levels of lipid parameters, liver enzymes, and leptin levels were measured. The HFD feeding resulted in obesity, which was associated with increases in body weight, liver weight, fat pad weight, liver enzymes, and plasma leptin levels with the development of hyperlipidemia. RYR prevented weight gain and fat pad weight in mice fed a HFD. RYR alleviated blood lipid parameters, liver enzymes, and leptin levels, and improved atherogenic index. These findings suggest that RYR has therapeutic potential in treating obesity and hyperlipidemia.

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Effect of dietary fat to produce non‐alcoholic fatty liver in the rat

Cited by 48 publications

References 44 publications

IRE1α prevents hepatic steatosis by processing and promoting the degradation of select microRNAs

IRE1α prevents hepatic steatosis by processing and promoting the degradation of select microRNAs

The effect of tomato juice supplementation on biomarkers and gene expression related to lipid metabolism in rats with induced hepatic steatosis

Beneficial Effects of Red Yeast Rice on High-Fat Diet-Induced Obesity, Hyperlipidemia, and Fatty Liver in Mice

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