Insulin resistance and oxidative stress interdependency in non-alcoholic fatty liver disease

Videla, Luis A.; Rodrigo, Ramón; Araya, Julia; Poníachik, Jaime

doi:10.1016/j.molmed.2006.10.001

Cited by 139 publications

(152 citation statements)

References 19 publications

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“…Persistent OS can diminish insulin action through the activation of serine-threonine kinase cascades, which in turn phosphorylate several targets, including insulin receptor and insulin receptor substrate (IRS) proteins, with consequent decrease of insulin-stimulated tyrosine phosphorylation (33). As suggested by Videla et al (34), the onset of IR could further increase ROS generation through CYP2E1 induction, mitochondrial dysfunction and pro-inflammation, all of which lead to the progression from steatosis to steatohepatitis. This observation was also supported by another study that showed an exacerbation of OS in patients with both NAFLD and T2DM (35).…”

Section: Köroğlu Et Al Oxidative Stress and Insulin Resistance In Nomentioning

confidence: 99%

Role of oxidative stress and insulin resistance in disease severity of non-alcoholic fatty liver disease

Köroğlu

Canbakan²,

Atay³

et al. 2016

Turk J Gastroenterol

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Section: Köroğlu Et Al Oxidative Stress and Insulin Resistance In Nomentioning

confidence: 99%

Role of oxidative stress and insulin resistance in disease severity of non-alcoholic fatty liver disease

Köroğlu

Canbakan²,

Atay³

et al. 2016

Turk J Gastroenterol

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“…Normally, FAs absorbed in the liver are esterified to triglycerides (TGs) for transportation to extrahepatic tissues by lipoproteins, and are oxidized via β-oxidation in the mitochondria or peroxisomes. With an increase in nutrient intake, the hepatic FA level is significantly increased, which may result in mitochondrial oxidation of FAs and oxidative stress in the liver (2,3), with subsequent development of metabolic disease. For example, diabetes is commonly associated with changes in hepatic glucose and lipid metabolism (4), which may be partly attributed to the altered expression levels of hepatic genes involved in glucose and lipid metabolism (5).…”

Section: Introductionmentioning

confidence: 99%

Effects of individual and multiple fatty acids (palmitate, oleate and docosahaexenoic acid) on cell viability and lipid metabolism in LO2 human liver cells

Chen

Wang

Huang

et al. 2014

Molecular Medicine Reports

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Abstract. This study was designed to investigate the direct effects of fatty acids (FAs) on the cell viability and the expression levels of genes involved in lipid metabolism in LO2 human liver cells. Palmitate (PA), oleate (OA) and docosahaexenoic acid (DHA) were used to represent saturated, mono-unsaturated and polyunsaturated FAs, respectively. At concentrations of ≤3.2 µg/ml, treatment with single FAs increased the viability of the LO2 cells. At FA concentrations of >3.2 µg/ml, cell viability following OA treatment was increased, but PA or DHA treatment at these concentrations reduced cell viability. Administration of mixtures of these FAs in three ratios (PA:OA:DHA = 1:2:1, 1:1:1 and 1:1:2, respectively) increased the cell viability compared with the control group. The intracellular triglyceride (TG) levels following all types of treatment were significantly increased and the accumulation of TGs was markedly increased with high doses of DHA. In addition, peroxisome proliferator-activated receptor-γ was significantly upregulated in all groups, with the exception of the 1:1:1 group at 3.2 µg/ml and the 1:1:2 group at 12.8 µg/ml. The expression levels of sterol regulatory-element binding protein-1c, liver X receptor α and apolipoprotein C-I were significantly reduced in all groups with the exception of the DHA-treated group and the 1:2:1 groups at 3.2 and 12.8 µg/ml. In conclusion, these results indicate that the type, concentration and mixture ratios of FAs are all important in determining the cell viability and lipid metabolism-related gene expression in LO2 hepatocytes.

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“…As a result, abnormal ROS production at complex I of the mitochondrial electron-transport chain is induced, leading to the mitochondrial oxidative damage. Under such condition, the redox imbalance, lower antioxidant potential, and an enhanced free-radical activity lead to a signiicant reduction in systemic antioxidant capacity of plasma [91]. These conditions are indeed considered as a trigger of "second hit," which then induces NASH.…”

Section: Oxidative Stress Theorymentioning

confidence: 99%

Role of Lipid Droplet Proteins in the Development of NAFLD and Hepatic Insulin Resistance

Minehira¹,

Gual²

2018

Non-Alcoholic Fatty Liver Disease - Molecular Bases, Prevention and Treatment

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NAFLD is diagnosed, when the liver fat exceeds more than 5% of liver weight. Inside of hepatocytes, these fats are stored in cytosolic lipid droplets. The lipid droplets can be formed from a bud, vesicles of the lipid bilayer, which lines at a vicinity of the endoplasmic reticulum (ER). On the surface of droplets, there are several structural/ functional proteins such as lipid droplet proteins, lipogenic enzymes, and lipases. Interestingly, the lipid droplet proteins seem to have great impact on a development of NAFLD. Some proteins can interact with transcriptional factors such as SREBP1c and PPAR-alpha/gamma, and some proteins strongly impact a mitochondrial structure. As a result, the lipid droplet proteins highly inluence lipid handling and faty acid oxidation in hepatocytes. This chapter will elucidate our recent understanding of the role of each lipid droplet protein in faty liver formation and in hepatic insulin resistance. Existing information on genetically modiied animals as well as on human NAFLD was reviewed on Perilipin families, CIDE proteins, Seipin, and PNPLAs. Finally, the chapter will discuss how the lipid droplet proteins could potentially lead/protect from hepatic insulin resistance via abnormal accumulation of ceramides and diacylglycerols, autophagy, ER stress, and oxidative stress.

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Insulin resistance and oxidative stress interdependency in non-alcoholic fatty liver disease

Cited by 139 publications

References 19 publications

Role of oxidative stress and insulin resistance in disease severity of non-alcoholic fatty liver disease

Role of oxidative stress and insulin resistance in disease severity of non-alcoholic fatty liver disease

Effects of individual and multiple fatty acids (palmitate, oleate and docosahaexenoic acid) on cell viability and lipid metabolism in LO2 human liver cells

Role of Lipid Droplet Proteins in the Development of NAFLD and Hepatic Insulin Resistance

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