Effect of sustained virological response to treatment on the incidence of abnormal glucose values in chronic hepatitis C

Romero‐Gómez, Manuel; Fernández-Rodrı́guez, Conrado; Andrade, Raúl J.; Diago, M.; Alonso, Sonia; Planas, Ramón; Solá, Ricard; Pons, J.A.; Salmerón, Javier; Bárcena, Rafael; Pérez, Ramón; Carmona, Isabel; Durán, Santiago

doi:10.1016/j.jhep.2007.11.022

Cited by 165 publications

(137 citation statements)

References 27 publications

(28 reference statements)

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“…Curing HCV results in the amelioration of insulin resistance and decreased incidence of diabetes after the end of therapy [55,56] . In the only trial that used the antidiabetic metformin [57] , only a marginal, nonsignificant increase of the SVR rate was observed, despite an increased virological response after 4 wk of triple therapy.…”

Section: Clinical Implications Of Hcv-mediated Insulin Resistancementioning

confidence: 99%

Hepatitis C virus infection and insulin resistance

Bose¹

2014

WJD

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Approximately 170 million people worldwide are chronically infected with hepatitis C virus (HCV). Chronic HCV infection is the leading cause for the development of liver fibrosis, cirrhosis, hepatocellular carcinoma (HCC) and is the primary cause for liver transplantation in the western world. Insulin resistance is one of the pathological features in patients with HCV infection and often leads to development of type Ⅱ diabetes. Insulin resistance plays an important role in the development of various complications associated with HCV infection. Recent evidence indicates that HCV associated insulin resistance may result in hepatic fibrosis, steatosis, HCC and resistance to anti-viral treatment. Thus, HCV associated insulin resistance is a therapeutic target at any stage of HCV infection. HCV modulates normal cellular gene expression and interferes with the insulin signaling pathway. Various mechanisms have been proposed in regard to HCV mediated insulin resistance, involving up regulation of inflammatory cytokines, like tumor necrosis factor-α, phosphorylation of insulin-receptor substrate-1, Akt, up-regulation of gluconeogenic genes like glucose 6 phosphatase, phosphoenolpyruvate carboxykinase 2, and accumulation of lipid droplets. In this review, we summarize the available information on how HCV infection interferes with insulin signaling pathways resulting in insulin resistance.© 2014 Baishideng Publishing Group Co., Limited. All rights reserved.Key words: Hepatitis C virus; Insulin resistance; Insulin receptor substrate 1; Protein kinase B; mammalian target of rapamycin/S6K1; Suppressor of cytokine signaling 3; Glucose transporter-4; Lipid metabolism; Antiviral therapy Core tip: Insulin resistance is one of the pathological features in patients with hepatitis C virus (HCV) infection and often leads to development of type Ⅱ diabetes. Recent evidence indicates that HCV associated insulin resistance may result in hepatic fibrosis, steatosis, hepatocellular carcinoma and resistance to anti-viral treatment. In this review, we summarize the available information on how HCV infection interferes with insulin signaling pathways.Bose SK, Ray R. Hepatitis C virus infection and insulin resistance. World J Diabetes 2014; 5(1): 52-58 Available from: URL:

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Section: Clinical Implications Of Hcv-mediated Insulin Resistancementioning

confidence: 99%

Hepatitis C virus infection and insulin resistance

Bose¹

2014

WJD

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“…This improvement in insulin sensitivity is maintained for people with a sustained virological response (SVR) [26,30] , and results in a reduced risk of subsequent diabetes [30,31] . However other groups have shown that the apparent reduction in diabetes risk may actually reflect the lower baseline risk of diabetes in patients who respond to interferon treatment, rather than an effect of treatment per se [32] .…”

Section: Chc and Irmentioning

confidence: 99%

Molecular mechanisms of insulin resistance in chronic hepatitis C

Douglas

George²

2009

WJG

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It is now widely recognized that chronic hepatitis C (CHC) is associated with insulin resistance (IR) and type 2 diabetes, so can be considered a metabolic disease. IR is most strongly associated with hepatitis C virus (HCV) genotype 1, in contrast to hepatic steatosis, which is associated with genotype 3 infection. Apart from the well-described complications of diabetes, IR in CHC predicts faster progression to fibrosis and cirrhosis that may culminate in liver failure and hepatocellular carcinoma. More recently, it has been recognized that IR in CHC predicts a poor response to antiviral therapy. The molecular mechanisms for the association between IR and HCV infection are not well defined. This review will elaborate on the clinical associations between CHC and IR and summarize current knowledge regarding the molecular mechanisms that potentially mediate HCV-associated IR.

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“…Two other studies have indirectly demonstrated the cause-effect relationship between chronic HCV infection and IR. Patients with HCV-related hepatitis who had sustained virological responses after antiviral therapy were less likely to develop type 2 diabetes mellitus (DM2) and glycemic alterations, compared with non-responders (15,16). Although the mechanisms underlying the development of IR in patients with HCV chronic infection have not been fully elucidated, the following factors have been recently considered: changes in insulin signaling pathways due to viral proteins; chronic inflammation with overproduction of tumor necrosis factor (TNF) and consequent phosphorylation of ISR-1 serine residues, lower expression of genes related to glucose metabolism, and degradation of insulin receptor substrates (17).…”

Section: Introductionmentioning

confidence: 99%

Insulin resistance in non-diabetic patients with chronic hepatitis C: what does it mean?

Souza

Pace²,

Chebli³

et al. 2011

Arq Bras Endocrinol Metab

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Objectives: To determine the prevalence of insulin resistance (IR) in non-diabetic patients with chronic hepatitis C, and to assess the association between IR, laboratory parameters and histological findings. Subjects and methods: Eighty-two patients had their serum analyzed for glucose, lipid profile, C-reactive protein (CRP), ferritin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), HOMA-IR, viral load and HCV genotype. Patients with HOMA-IR levels > 2.5 were considered as carriers of insulin resistance. Results: IR was observed in 27% of patients and was associated with age, waist circumference and body mass index. IR patients were more likely to have more advanced hepatic fibrosis and necroinflammatory activity, higher levels of aminotransferases and liver steatosis than patients without IR. Conclusions: Insulin resistance is often present in patients with chronic hepatitis C, and this parameter is associated with more advanced HCV-related hepatic fibrosis. Arq Bras Endocrinol Metab. 2011;55(6):412-8 Keywords Chronic hepatitis C; liver fibrosis; insulin resistance; HOMA-IR RESUMO Objetivos: Em portadores de hepatite crônica C não diabéticos, verificar a prevalência de resistência insulínica (RI) e analisar a associação desta com os parâmetros laboratoriais e histológicos. Sujeitos e métodos: Foram incluídos no estudo 82 pacientes, e amostras de sangue foram coletadas para determinação de glicose, perfil lipídico, alanina aminotransferase (ALT), aspartato aminotransferase (AST), ferritina, HOMA-IR, carga viral e genótipo do VHC. HOMA--IR superior a 2,5 foi considerado resistência insulínica. Resultados: RI foi observada em 27% dos pacientes e foi associada a idade, circunferência abdominal e índice de massa corpórea. Quando comparado a pacientes sem RI, aqueles com HOMA-IR superior a 2,5 apresentaram graus mais acentuados de fibrose hepática e atividade necroinflamatória, maiores níveis de aminotransferases e esteatose hepática mais frequente. Conclusões: É comum a presença de RI em portadores de hepatite crônica C e esta se associa com graus mais avançados de fibrose hepática induzida pelo vírus da hepatite C. Arq Bras Endocrinol Metab. 2011;55(6):412-8 Descritores

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Effect of sustained virological response to treatment on the incidence of abnormal glucose values in chronic hepatitis C

Cited by 165 publications

References 27 publications

Hepatitis C virus infection and insulin resistance

Hepatitis C virus infection and insulin resistance

Molecular mechanisms of insulin resistance in chronic hepatitis C

Insulin resistance in non-diabetic patients with chronic hepatitis C: what does it mean?

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