Diabetes mellitus triggers oxidative stress in the liver of alloxan-treated rats: a mechanism for diabetic chronic liver disease

Lucchesi, Amanda Natália; Freitas, Natália Tavares de; Cassettari, Lucas Langoni; Marques, Silvio Fernando Guideti; Spadella, César Tadeu

doi:10.1590/s0102-86502013000700005

Cited by 93 publications

(67 citation statements)

References 32 publications

(29 reference statements)

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“…Accumulating laboratory evidence suggests that insulin resistance and excess of free fatty acids can trigger the oxidative stress in hepatocytes and lead to chronic inflammation and fibrogenesis [13,14] . Hepatic fibrogenesis is the final consequences of chronic liver disease and constitutes a model of wound-healing process.…”

Section: Hepatic Fibrogenesis Developmentmentioning

confidence: 99%

Proteomic and genomic studies of non-alcoholic fatty liver disease - clues in the pathogenesis

Lim

Dillon

Miller

2014

WJG

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Non-alcoholic fatty liver disease (NAFLD) is a widely prevalent hepatic disorder that covers wide spectrum of liver pathology. NAFLD is strongly associated with liver inflammation, metabolic hyperlipidaemia and insulin resistance. Frequently, NAFLD has been considered as the hepatic manifestation of metabolic syndrome. The pathophysiology of NAFLD has not been fully elucidated. Some patients can remain in the stage of simple steatosis, which generally is a benign condition; whereas others can develop liver inflammation and progress into non-alcoholic steatohepatitis, fibrosis, cirrhosis and hepatocellular carcinoma. The mechanism behind the progression is still not fully understood. Much ongoing proteomic researches have focused on discovering the unbiased circulating biochemical markers to allow early detection and treatment of NAFLD. Comprehensive genomic studies have also begun to provide new insights into the gene polymorphism to understand patientdisease variations. Therefore, NAFLD is considered a complex and mutifactorial disease phenotype resulting from environmental exposures acting on a susceptible polygenic background. This paper reviewed the current status of proteomic and genomic studies that have contributed to the understanding of NAFLD pathogenesis. For proteomics section, this review highlighted functional proteins that involved in: (1) transportation; (2) metabolic pathway; (3) acute phase reaction; (4) antiinflammatory; (5) extracellular matrix; and (6) immune system. In the genomic studies, this review will discuss genes which involved in: (1) lipolysis; (2) adipokines; and (3) cytokines production. Key words: Non-alcoholic fatty liver disease; Proteomics; Genomics; Metabolic syndrome; Pathophysiology Core tip: Non-alcoholic fatty liver disease (NAFLD) is a widely prevalent hepatic disorder in Western populations. NAFLD can occur as a spectrum diseases, from simple steatosis, to non-alcoholic steatohepatitis characterised by hepatocellular injury and inflammation, to cirrhosis and hepatocellular carcinoma. This paper reviewed the current status of proteomic and genomic studies that have contributed to the understanding of NAFLD pathogenesis. This review highlighted several functional proteins and genetic polymoprhisms; particular those involved in insulin resistance, triglycerides metabolism and hepatic inflammation. It is hoped that this review will offer further insights into the pathophysiology of NAFLD.

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Section: Hepatic Fibrogenesis Developmentmentioning

confidence: 99%

Proteomic and genomic studies of non-alcoholic fatty liver disease - clues in the pathogenesis

Lim

Dillon

Miller

2014

WJG

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“…There is a positive relationship between oxidative stress and hyperglycemia. The oxidative unbalance in hepatocytes can cause the development of the liver disease in diabetes (36) . GSH can inhibit free radical-mediated injury by eliminating reactive oxygen species.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Ghrelin Treatment on Cell Survival and Inflammation in Type 2 Diabetic Rat Liver

Coşkun¹,

Beydogan²,

Bolkent³

2017

Okmeydani Medical Journal

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, nuclear factor kappa B (NF-κB), peroxisome proliferatoractivated receptor gamma and proliferating cell nuclear antigen (PCNA) expressions were determined by immunohistochemical methods. Results: The number of MMP-2, MMP-9, NF-κB, PPAR-γ and IL-6 immunopositive cells increased in the diabetic rat liver as compared to control. The ghrelin treatment significantly reduced the numbers of MMP-2, MMP-9, NF-κB, PPAR-γ and IL-6 immunopositive cells in diabetic rat

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“…The results showed that compared with the model group, CCPW could inhibit JNK expression and improve Glut4 at the mRNA level, inhibit JNK and phospho-IRS1 (Ser 307 ) expression, and improve the expression of PI3Kp85 and Glut4 at the protein level, but could not affect the expression of IRS1 and PI3K obviously. Many studies have demonstrated that oxidative stress is closely related to diabetes and insulin resistance (Lucchesi & Freitas, 2013;Venkatasamy et al, 2013). Oxidative stress can promote the production of JNK, thus make IRS1 phosphorylated, and finally result in diabetes mellitus (Kaneto et al, 2005(Kaneto et al, , 2007.…”

Section: Discussionmentioning

confidence: 99%

Antidiabetic mechanism ofCoptis chinensispolysaccharide through its antioxidant property involving the JNK pathway

Jiang

Wang²,

Ren

et al. 2015

Pharmaceutical Biology

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Context: Antidiabetic activity of Coptis chinensis Franch (Ranunculaceae) polysaccharide (CCPW) has been reported. However, its molecular mechanism remains unclear. Objective: An attempt was made to further verify the antidiabetic activity of CCPW on type 2 diabetes mellitus (T2DM) and elucidate the mechanism of antidiabetic activity. Materials and methods: Male Wistar rats were fed with high-fat diet (HFD) and injected with streptozotocin (STZ) to generate a T2DM model. Effects of CCPW on fasting blood glucose (FBG), triglyceride (TG), total cholesterol (TC), glutathione (GSH), glutathione peroxidases (GSH-Px), superoxide dismutases (SOD), catalase (CAT), malondialdehyde (MDA), c-jun n-terminal kinase (JNK), phosphorylated insulin receptor substrate 1 (phospho-IRS1), phosphorylated phosphatidylinositol 3 kinase (phospho-PI3Kp85) and glucose transporter 4 (Glut4) were investigated. Results: FBG level of diabetic rats could be significantly inhibited by 51.2, 42.7, and 23.3% through administration of CCPW at doses of 200, 100, and 50 mg/kg b.w., respectively (p50.01). CCPW also could significantly reduce TG by 19.2, 12.1, and 7.4%, and TC by 24.2, 20.9, and 18.7%, respectively (p50.05 or p50.01). CCPW showed an obvious antioxidant effect through increasing GSH-Px, SOD, and CAT activities, and decreasing GSH and MDA contents (p50.05 or p50.01). Furthermore, CCPW could inhibit JNK and phospho-IRS1 expression and promote the expression of phospho-PI3Kp85 and Glut4 compared with those in the DM group (p50.05 or p50.01). Discussion and conclusion: CCPW can produce antidiabetic activity in rats with T2DM through its antioxidative effect, which is closely related to the JNK/IRS1/PI3K pathway.

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Diabetes mellitus triggers oxidative stress in the liver of alloxan-treated rats: a mechanism for diabetic chronic liver disease

Cited by 93 publications

References 32 publications

Proteomic and genomic studies of non-alcoholic fatty liver disease - clues in the pathogenesis

Proteomic and genomic studies of non-alcoholic fatty liver disease - clues in the pathogenesis

The Effect of Ghrelin Treatment on Cell Survival and Inflammation in Type 2 Diabetic Rat Liver

Antidiabetic mechanism ofCoptis chinensispolysaccharide through its antioxidant property involving the JNK pathway

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