Hepatitis C Virus Infection and Human Pancreatic β-Cell Dysfunction

Masini, Matilde; Campani, Daniela; Boggi, Ugo; Menicagli, Michele; Funel, Niccola; Pollera, Maria; Lupi, R; Guerra, S Del; Bugliani, Marco; Torri, S; Prato, Stefano Del; Mosca, Franco; Filipponi, Franco; Marchetti, Piero

doi:10.2337/diacare.28.4.940

Cited by 120 publications

(83 citation statements)

References 8 publications

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“…Additionally, diabetic HCV patients with mixed cryoglobulinemia are more likely to carry non-organ-specific autoantibodies (4). Interestingly, there is evidence to support the hypothesis that HCV directly damages ␤-cells or disturbs their function, which ultimately leads to diabetes (5). Finally, there is no question that HCV, by itself, can induce insulin resistance, disturbing the insulin signaling pathway by the function of HCV core protein (6).…”

mentioning

confidence: 73%

Hepatitis C Virus Infection: Evidence for an Association With Type 2 Diabetes

et al. 2006

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peared to attenuate the negative effect of testosterone on the prostate in that subjects who received the dual regimen had no increase in prostate-specific antigen levels and had a significantly lower increase in prostate volume than those treated with testosterone alone (5). While these data are encouraging, they are based on small patient numbers, and the favorable effects on prostatespecific antigen levels may not necessarily translate to a reduction in prostate cancer risk. In addition, while finasteride was shown to reduce the development of prostate cancer in middle-aged men, the incidence of high-grade prostate tumors and sexual side effects was increased (6).Therefore, I believe that further research is still needed to identify the androgen regimen that confers optimal benefit to older men without compromising prostate health and overall patient safety.

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mentioning

confidence: 73%

Hepatitis C Virus Infection: Evidence for an Association With Type 2 Diabetes

et al. 2006

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“…Some authors have also suggested the in-diagnosed T1DM, raised serum CXCL10 and normal chemokine (C-C motif) ligand 2 concentrations signal a predominantly Th1-driven autoimmune process, which shifts toward Th2 immunity 2 years after diagnosis [172] . Based on the abovementioned concepts, HCV infection of β-cells [106] may act by upregulating CXCL10 gene expression and secretion (as previously shown in human hepatocytes [173] ) and recruiting Th1 lymphocytes that secrete IFN-γ and TNF-α, which induce CXCL10 secretion by β-cells and thus perpetuate the immune cascade. This cascade may lead to the appearance of β-cell dysfunction in genetically predisposed subjects (Figure 2).…”

Section: Hcv-infected Patients With T1dmmentioning

confidence: 99%

“…HCV is hepatotropic and noncytopathic; nevertheless, its genome has been identified in a number of tissues beyond the liver, including pancreatic acinar cells and epithelial cells of the pancreatic duct [105,106] . Although postmortem studies have revealed that HCV replicates in the pancreas [107] and animal models have suggested a direct effect of HCV infection on IR in the liver [108] , the evidence is scanty.…”

Section: Direct Effects Of Hcv and Irmentioning

confidence: 99%

Hepatitis C virus infection and type 1 and type 2 diabetes mellitus

Antonelli

Ferrari

Giuggioli

et al. 2014

WJD

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cytokines, chemokines, and other immune-mediated mechanisms. Few data have been reported on the association of CHC and T1DM and reports on the potential association between T1DM and acute HCV infection are even rarer. A small number of studies indicate that interferon-α therapy can stimulate pancreatic autoimmunity and in certain cases lead to the development of T1DM. Diabetes and CHC have important interactions. Diabetic CHC patients have an increased risk of developing cirrhosis and hepatocellular carcinoma compared with non-diabetic CHC subjects. However, clinical trials on HCV-positive patients have reported improvements in glucose metabolism after antiviral treatment. Further studies are needed to improve prevention policies and to foster adequate and cost-effective programmes for the surveillance and treatment of diabetic CHC patients. AbstractHepatitis C virus (HCV) infection and diabetes mellitus are two major public health problems that cause devastating health and financial burdens worldwide. Diabetes can be classified into two major types: type 1 diabetes mellitus (T1DM) and T2DM. T2DM is a common endocrine disorder that encompasses multifactorial mechanisms, and T1DM is an immunologically mediated disease. Many epidemiological studies have shown an association between T2DM and chronic hepatitis C (CHC) infection. The processes through which CHC is associated with T2DM seem to involve direct viral effects, insulin resistance, proinflammatory Submit a

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“…(17). (18)(19)(20)(21)(22). Some evidence indicates that a predominant effect of the virus is the induction of insulin resistance, caused by inhibitory actions of the virus on insulin regulatory pathways within the liver, possibly mediated by proinflammatory cytokines (18,22).…”

Section: Chronic Hepatitis C Virus (Hcv) Infection Is a Multifaceted mentioning

confidence: 99%

Impaired Insulin Sensitivity as an Underlying Mechanism Linking Hepatitis C and Posttransplant Diabetes Mellitus in Kidney Recipients

Baid-Agrawal¹,

Frei²,

Reinke³

et al. 2009

American Journal of Transplantation

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Aim of this study was to investigate the mechanism/s associating hepatitis C virus (HCV) infection and posttransplant diabetes mellitus in kidney recipients.Twenty HCV-positive and 22 HCV-negative kidney recipients, 14 HCV-positive nontransplant patients and 24 HCV-negative nontransplant (healthy) subjects were analyzed. A 3-h intravenous glucose tolerance test was performed; peripheral insulin sensitivity was assessed by minimal modeling. Pancreatic insulin secretion, hepatic insulin uptake, pancreatic antibodies and proinflammatory cytokines in serum (tumor necrosis factor-a, intereukin-6, high-sensitive C-reactive protein) were also assessed.HCV-positive recipients showed a significantly lower insulin sensitivity as compared to HCV-negative recipients (3.0 ± 2.1 vs. 4.9 ± 3.0 min −1 .lU.mL −1 .10 4 , p = 0.02), however, insulin secretion and hepatic insulin uptake were not significantly different. Pancreatic antibodies were negative in all. HCV status was an independent predictor of impaired insulin sensitivity (multivariate analysis, p = 0.008). The decrease of insulin sensitivity due to HCV was comparable for transplant and non-transplant subjects. No significant correlation was found between any of the cytokines and insulin sensitivity.Our results suggest that impaired peripheral insulin sensitivity is associated with HCV infection irrespective of the transplant status, and is the most likely pathogenic mechanism involved in the development of type 2 diabetes mellitus associated with HCV infection.

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Hepatitis C Virus Infection and Human Pancreatic β-Cell Dysfunction

Cited by 120 publications

References 8 publications

Hepatitis C Virus Infection: Evidence for an Association With Type 2 Diabetes

Hepatitis C Virus Infection: Evidence for an Association With Type 2 Diabetes

Hepatitis C virus infection and type 1 and type 2 diabetes mellitus

Impaired Insulin Sensitivity as an Underlying Mechanism Linking Hepatitis C and Posttransplant Diabetes Mellitus in Kidney Recipients

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