Oxidative stress is independently associated with non-alcoholic fatty liver disease (NAFLD) in subjects with and without type 2 diabetes

Sandhya, Narasimhan; Gokulakrishnan, Kuppan; Rangasamy, Sampathkumar; Syed, Farooq; Radhakrishnan, Ramalingam; Mohan, Viswanathan; Balasubramanyam, Muthuswamy

doi:10.1016/j.clinbiochem.2010.04.003

Cited by 100 publications

(77 citation statements)

References 45 publications

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“…In fact, protection by A. orientale extracts against lipid peroxidation and nitric oxide production has been documented in high-fat diet, experimental NAFLD model rats and in lipopolysaccharide-activated macrophages (Matsuda et al, 1999;Hong et al, 2006). Consistent with these findings, recent studies demonstrated pivotal roles for oxidative stress in FFA-induced insulin resistance of hepatocytes and NAFLD with type 2 diabetes (Nakamura et al, 2009;Narasimhan et al, 2010). Although we cannot exclude the possibility that AEAO activates intracellular defense mechanisms other than antioxidant systems, our present findings indicate that the primary role of AEAO in protection against palmitate-induced cellular injury is an antioxidant.…”

Section: Discussionsupporting

confidence: 70%

Antioxidative effects ofAlisma orientaleextract in palmitate-induced cellular injury

Han

Kang

Ham

et al. 2012

Pharmaceutical Biology

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Section: Discussionsupporting

confidence: 70%

Antioxidative effects ofAlisma orientaleextract in palmitate-induced cellular injury

Han

Kang

Ham

et al. 2012

Pharmaceutical Biology

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“…T2DM is also characterized by the presence of oxidative stress (Davi et al 1999), and diabetic patients with NAFLD have higher levels of markers of oxidative stress compared to diabetic patients without NAFLD (Narasimhan et al 2010). Recently, several studies have demonstrated that IHG can generate more ROS than SHG in endothelial cells (Quagliaro et al 2003, Piconi et al 2006, islet cell (Del Guerra et al 2007, Kim et al 2012 and Schwann cells (Sun et al 2012a,b).…”

Section: Discussionmentioning

confidence: 99%

Glucose fluctuation increased hepatocyte apoptosis under lipotoxicity and the involvement of mitochondrial permeability transition opening

Yin¹,

Zheng²,

Pan³

et al. 2015

Journal of Molecular Endocrinology

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Oxidative stress is considered to be an important factor in producing lethal hepatocyte injury associated with nonalcoholic fatty liver disease (NAFLD). Glucose fluctuation, more pronounced in patients with diabetes, has been recognized as an even stronger oxidative stress inducer than the sustained hyperglycemia. Here, we investigated the role of glucose variability in the development of the NAFLD based on hepatocyte apoptosis and possible mechanisms. To achieve this goal we studied C57BL/6J mice that were maintained on a high fat diet (HFD) and injected with glucose (3 g/kg) twice daily to induce intermittent high glucose (IHG). We also studied hepatic L02 cells incubated with palmitic acid (PA) to induce steatosis. The following experimental groups were compared: normal glucose (NG), sustained high glucose (SHG) and IHG with or without PA. We found that, although hepatic enzyme levels and liver lipid deposition were comparable between HFD mice injected with glucose or saline, the glucose injected mice displayed marked hepatocyte apoptosis and inflammation, accompanied by increased lipid peroxide in liver. In vitro, in the presence of PA, IHG increased L02 cell apoptosis and oxidative stress and produced pronounced mitochondrial dysfunction relative to the NG and SHG groups. Furthermore, treatment with the mitochondrial permeability transition (MPT) inhibitor, cyclosporin A (1.5 mmol/l), prevented mitochondrial dysfunction, oxidative stress and hepatocyte apoptosis. Our data suggests that IHG under lipotoxicity might contribute to the development of NAFLD by increasing oxidative stress and hepatocyte apoptosis via MPT and its related mitochondrial dysfunction.

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“…In fact, in many clinical studies, elevated systemic markers of oxidative stress and lipid peroxidation have been found in patients with NAFLD [53][54][55][56][57][58][59] . Recently, in two studies carried out in patients with NAFLD [60,61] , we found increased oxidative stress in vivo, by measuring urinary 8-iso-prostaglandin F2α (8-iso-PGF2α), which derives from the non-enzymatic oxidation of arachidonic acid [62] , and serum levels of soluble NOX2-derived peptide (sNOX2-dp), which is an indicator of NOX2 activation, a NADPH oxidase isoform involved in ROS generation [63,64] .…”

Section: Imtmentioning

confidence: 99%

Oxidative stress: New insights on the association of non-alcoholic fatty liver disease and atherosclerosis

Polimeni

Ben

Baratta

et al. 2015

WJH

174

137

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Non-alcoholic fatty liver disease (NAFLD) represents the most common and emerging chronic liver disease worldwide. It includes a wide spectrum of liver diseases ranging from simple fatty liver to non-alcoholic steatohepatitis (NASH), which may progress to fibrosis and more severe liver complications such as cirrhosis, hepatocellular carcinoma and liver mortality. NAFLD is strongly associated with obesity, insulin resistance, hypertension, and dyslipidaemia, and is now regarded as the liver manifestation of the metabolic syndrome. The increased mortality of patients with NAFLD is primarily a result of cardiovascular disease and, to a lesser extent, to liver related diseases. Increased oxidative stress has been reported in both patients with NAFLD and patient with cardiovascular risk factors. Thus, oxidative stress represents a shared pathophysiological disorder between the two conditions. Several therapeutic strategies targeting oxidative stress reduction in patients with NAFLD have been proposed, with conflicting results. In particular, vitamin E supplementation has been suggested for the treatment of non-diabetic, non-cirrhotic adults with active NASH, although this recommendation is based only on the results of a single randomized controlled trial. Other antioxidant treatments suggested are resveratrol, silybin, L-carnitine and pentoxiphylline. No trial so far, has evaluated the cardiovascular effects of antioxidant treatment in patients with NAFLD. New, large-scale studies including as end-point also the assessment of the atherosclerosis markers are needed.

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Oxidative stress is independently associated with non-alcoholic fatty liver disease (NAFLD) in subjects with and without type 2 diabetes

Cited by 100 publications

References 45 publications

Antioxidative effects ofAlisma orientaleextract in palmitate-induced cellular injury

Antioxidative effects ofAlisma orientaleextract in palmitate-induced cellular injury

Glucose fluctuation increased hepatocyte apoptosis under lipotoxicity and the involvement of mitochondrial permeability transition opening

Oxidative stress: New insights on the association of non-alcoholic fatty liver disease and atherosclerosis

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