Induction of non-alcoholic fatty liver disease and insulin resistance by feeding a high-fat diet in rats: does coenzyme Q monomethyl ether have a modulatory effect?

Safwat, Ghada Mohamed; Pisanò, Stefania; D’Amore, Emanuela; Borioni, Giorgio; Napolitano, Mariarosaria; Amin, Kamal Adel; Ballanti, P.; Botham, Kathleen M.; Bravo, Elena

doi:10.1016/j.nut.2009.02.009

Cited by 40 publications

(37 citation statements)

References 52 publications

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“…Additionally, the observation of reduced systemic coenzyme Q10 levels in patients with NAFLD (223) has lead to limited investigation of the effects of dietary supplementation of coenzyme Q. Coenzyme Q10 supplementation has been observed to lower oxidative stress and markers of inflammation in a mouse, without modulating lipid peroxidation or improving systemic insulin resistance (195). Additionally, coenzyme Q9 monomethyl ether administration increased VLDL assembly in rats with high-fat-diet-induced steatosis (22,182), with no observed improvement in NAFLD or systemic insulin resistance (182).…”

Section: Pharmaceutical and Antioxidant Therapiesmentioning

confidence: 99%

Mitochondria and Redox Signaling in Steatohepatitis

Morris

Rector

Thyfault

et al. 2011

Antioxidants & Redox Signaling

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Alcoholic and nonalcoholic fatty liver diseases are potentially pathological conditions that can progress to steatohepatitis, fibrosis, and cirrhosis. These conditions affect millions of people throughout the world in part through poor lifestyle choices of excess alcohol consumption, overnutrition, and lack of regular physical activity. Abnormal mitochondrial and cellular redox homeostasis has been documented in steatohepatitis and results in alterations of multiple redox-sensitive signaling cascades. Ultimately, these changes in signaling lead to altered enzyme function and transcriptional activities of proteins critical to mitochondrial and cellular function. In this article, we review the current hypotheses linking mitochondrial redox state to the overall pathophysiology of alcoholic and nonalcoholic steatohepatitis and briefly discuss the current therapeutic options under investigation. Antioxid. Redox Signal. 15, 485-504.

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Section: Pharmaceutical and Antioxidant Therapiesmentioning

confidence: 99%

Mitochondria and Redox Signaling in Steatohepatitis

Morris

Rector

Thyfault

et al. 2011

Antioxidants & Redox Signaling

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“…The disease is characterized by the accumulation of triacylglycerols inside liver cells, and the condition can progress into more serious liver disease, such as non alcoholic steatohepatitis, liver fibrosis, cirrhosis, and more rarely, liver carcinoma [23]. Previous works have shown that feeding rats a high fat diet (57% of energy from fat) induces hepatic steatosis and liver damage, which are characteristic of NAFLD and thus provides a suitable model for the early stages of the disease [24,25]. But, in these studies TFAs in the fat diet were not investigated and neglected.…”

Section: Introductionmentioning

confidence: 99%

The intake of high fat diet with different trans fatty acid levels differentially induces oxidative stress and non alcoholic fatty liver disease (NAFLD) in rats

et al. 2011

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BackgroundTrans-fatty acids (TFA) are known as a risk factor for coronary artery diseases, insulin resistance and obesity accompanied by systemic inflammation, the features of metabolic syndrome. Little is known about the effects on the liver induced by lipids and also few studies are focused on the effect of foods rich in TFAs on hepatic functions and oxidative stress. This study investigates whether high-fat diets with different TFA levels induce oxidative stress and liver dysfunction in rats.MethodsMale Wistar rats were divided randomly into four groups (n = 12/group): C receiving standard-chow; Experimental groups that were fed high-fat diet included 20% fresh soybean oil diet (FSO), 20% oxidized soybean oil diet (OSO) and 20% margarine diet (MG). Each group was kept on the treatment for 4 weeks.ResultsA liver damage was observed in rats fed with high-fat diet via increase of liver lipid peroxidation and decreased hepatic antioxidant enzyme activities (superoxide dismutase, catalase and glutathione peroxidase). The intake of oxidized oil led to higher levels of lipid peroxidation and a lower concentration of plasma antioxidants in comparison to rats fed with FSO. The higher inflammatory response in the liver was induced by MG diet. Liver histopathology from OSO and MG groups showed respectively moderate to severe cytoplasm vacuolation, hypatocyte hypertrophy, hepatocyte ballooning, and necroinflammation.ConclusionIt seems that a strong relationship exists between the consumption of TFA in the oxidized oils and lipid peroxidation and non alcoholic fatty liver disease (NAFLD). The extent of the peroxidative events in liver was also different depending on the fat source suggesting that feeding margarine with higher TFA levels may represent a direct source of oxidative stress for the organism. The present study provides evidence for a direct effect of TFA on NAFLD.

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“…The lipid lowering effect of Co-Q10 supplementation was also seen in fructose fed rats [93]. A Co-Q10 analogue, Q monomethyl ether, also showed beneficial effect on progressive non-alcoholic fatty liver (NAFL) in rats fed a high fat diet and improved liver architecture by preventing the fat droplet accumulation in hepatocytes [129]. Increased fatty acid beta oxidation would be the potential mechanism of improving lipid profile in metabolic syndrome.…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial dysfunction in obesity: potential benefit and mechanism of Co-enzyme Q10 supplementation in metabolic syndrome

Alam

Rahman

2014

J Diabetes Metab Disord

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Co-enzyme Q10 (Co-Q10) is an essential component of the mitochondrial electron transport chain. Most cells are sensitive to co-enzyme Q10 (Co-Q10) deficiency. This deficiency has been implicated in several clinical disorders such as heart failure, hypertension, Parkinson’s disease and obesity. The lipid lowering drug statin inhibits conversion of HMG-CoA to mevalonate and lowers plasma Co-Q10 concentrations. However, supplementation with Co-Q10 improves the pathophysiological condition of statin therapy. Recent evidence suggests that Co-Q10 supplementation may be useful for the treatment of obesity, oxidative stress and the inflammatory process in metabolic syndrome. The anti-inflammatory response and lipid metabolizing effect of Co-Q10 is probably mediated by transcriptional regulation of inflammation and lipid metabolism. This paper reviews the evidence showing beneficial role of Co-Q10 supplementation and its potential mechanism of action on contributing factors of metabolic and cardiovascular complications.

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Induction of non-alcoholic fatty liver disease and insulin resistance by feeding a high-fat diet in rats: does coenzyme Q monomethyl ether have a modulatory effect?

Cited by 40 publications

References 52 publications

Mitochondria and Redox Signaling in Steatohepatitis

Mitochondria and Redox Signaling in Steatohepatitis

The intake of high fat diet with different trans fatty acid levels differentially induces oxidative stress and non alcoholic fatty liver disease (NAFLD) in rats

Mitochondrial dysfunction in obesity: potential benefit and mechanism of Co-enzyme Q10 supplementation in metabolic syndrome

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