Insulin Resistance Provides the Connection Between Hepatitis C Virus and Diabetes

Safi, Sher Zaman; Shah, Humaira; Yan, Gracie Ong Siok; Qvist, Rajes

doi:10.5812/hepatmon.23941

Cited by 13 publications

(11 citation statements)

References 20 publications

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“…More than 20 years ago, Allison et al, demonstrated that T2DM was more frequent in HCV liver cirrhosis compared with other etiologies (20). Currently, it is known that HCV infection is associated with insulin-resistance, T2DM, and liver steatosis (21). In a recent meta-analysis, DM is considered as the second most common extra-hepatic manifestation of HCV (after depression), found in 15% of the patients (22).…”

Section: Discussionmentioning

confidence: 99%

Metabolic Syndrome and Genotype 1 Virus C Compensated Liver Cirrhosis in the Era of Directly Acting Antiviral Therapy

et al. 2017

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Objectives: The current study aimed at evaluating the association between metabolic syndrome (MeS) in patients with hepatitis C virus (HCV) liver cirrhosis (compensated, genotype, 1b) and changes after sustained viral response (SVR) following a 12-week therapy with paritaprevir, ritonavir, ombitasvir, dasabuvir, and ribavirin (PrOD+R). Methods: The current multicenter retrospective study included 809 patients diagnosed with compensated HCV cirrhosis (child class A), all 1b genotype treated for 12 weeks with direct acting antiviral agents -PrOD+R -regimen (according to the protocol practiced in Romania) and achieved SVR. The parameters of MeS (according to the definition of the International Diabetes Federation) were collected from medical records before and 12 weeks after the treatment. The results were collected in a central database and analyzed with SPSS 18.0. Statistical analysis used both descriptive and analytical methods with a significance level of 95% (CI 95%). Results: Out of the 809 patients, 105 (13%) demonstrated 3 out of the 5 criteria for MeS. Based on the MeS criteria, the commonest parameters were abnormal glycaemia (54.1%), followed by visceral obesity (38.6%), raised triglycerides (26.1%), high blood pressure (12.1%), and a low high-density lipoprotein (HDL)-cholesterol (4.6%). The re-assessment of MeS parameters after SVR showed favourable changes, which were statistically significant: a siginficanttly lower serum triglyeride level (182.32 vs. 153.50 mg/dL, P = 0.001), lower systolic arterial blood pressure (130.57 vs. 124.85 mmHg; P = 0.001), lower diastolic arterial blood pressure (80.26 vs. 78.42 mmHg; P = 0.001) and lower glyceamic levels (130.06 vs. 120.71 mg/dL; P = 0.001), as well as a significant rise in HDL-cholesterol levels (48.61 vs. 50.50 mg/dL; P = 0.003). Abdominal circumference was the only parameter, which did not change after SVR. Following the changes sustained after SVR, 26.7% of the patients no longer fulfilled the minimum 3 criteria for MeS. No correlation was observed between the presence of MeS and the risk of severe adverse events, but it was noted that 37.5% of the patients who decompensated, 66.7% of the ones who developed hepatocarcinoma and 100% of the ones that died of abnormal glycaemic levels. Conclusions: Hyperglycemia, and not MeS, is associated with HCV compensated liver cirrhosis genotype 1b, and is a risk factor for severe adverse events. The attainment of SVR through PrOD+R regimen results in short-term improvements in MeS parameters.

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Section: Discussionmentioning

confidence: 99%

Metabolic Syndrome and Genotype 1 Virus C Compensated Liver Cirrhosis in the Era of Directly Acting Antiviral Therapy

et al. 2017

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“…HCV infections can trigger autoimmune reactions against pancreatic β-cellsin genetically susceptible subjects leading to direct destruction of b cells thereby causing type 1 diabetes 32 . Conversely, a complex interaction between insulin resistance (IR), hepatic steatosis and inflammatory cytokines have been implicated for the development of type 2 diabetes in HCV infected individuals 33 . HCV causes alteration in hepatic carbohydrate and lipid metabolism and has also been linked with modifications of molecular mechanisms like oxidative stress, mitochondrial function, signalling in the insulin receptor substrate-1 pathway and influences on the activities of proinflammatory cytokines and adipokines 34 .…”

Section: Hepatitis C Virus and Insulin Resistance /Diabetes Mellitusmentioning

confidence: 99%

B (Reg) Cells in Hepatitis C Virus and Diabetes

Hassanin

Bakr

Hetta

et al. 2019

Bulletin of Pharmaceutical Sciences. Assiut

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Over the last decade it has become evident that in addition to producing antibody, B cells activate the immune system by producing cytokines and via antigen presentation. In addition, B cells also exhibit immunosuppressive functions via diverse regulatory mechanisms. This subset of B cells, known as regulatory B cells (B regs), contributes to the maintenance of tolerance, primarily via the production of IL-10. Studies in experimental animal models, as well as in patients with autoimmune diseases, have identified multiple B(reg) subsets exhibiting diverse mechanisms of immune suppression. In this review, we describe the different B(reg) subsets identified in humans, and their diverse mechanisms of suppression in HCV and diabetic patients. Aims:The main objectives of the study are to identify the role of B (reg) in the hepatitis C virus infected patients and diabetes.

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“…The association between HCV and diabetes was initially perceived to be a non‐specific consequence of liver inflammation but several mechanisms have now been cited . HCV infections can trigger auto‐immune reactions against pancreatic β cells in genetically susceptible subjects leading to direct destruction of β cells thereby causing type 1 diabetes .…”

Section: Introductionmentioning

confidence: 99%

“…HCV infections can trigger auto‐immune reactions against pancreatic β cells in genetically susceptible subjects leading to direct destruction of β cells thereby causing type 1 diabetes . Conversely, a complex interaction between insulin resistance (IR), hepatic steatosis and inflammatory cytokines have been implicated for the development of type 2 diabetes in HCV infected individuals . HCV causes alteration in hepatic carbohydrate and lipid metabolism and has also been linked with modifications of molecular mechanisms like oxidative stress, mitochondrial function, signalling in the insulin receptor substrate‐1 pathway and influences on the activities of pro‐inflammatory cytokines and adipokines .…”

Section: Introductionmentioning

confidence: 99%

Hepatitis C virus infection and diabetes

Das

Bolusani

2016

Pract Diab

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Hepatitis C virus (HCV) infection is the leading cause of chronic liver disease resulting in end-stage cirrhosis and liver cancer, and it remains the primary cause for liver transplantation in the western countries. Chronic HCV infection is believed to be a multi-faceted systemic disease which not only influences the hepatic environment causing inflammation, steatosis and fibrosis but also alters the metabolism of glucose and lipids, leading to metabolic sequelae such as insulin resistance, diabetes and dyslipidaemia. HCV has been identified as an independent risk factor for the development of diabetes in predisposed individuals (with family history and visceral obesity) and it is more prevalent with certain HCV genotypes.Moreover, it can also induce direct destruction of pancreatic b cells and trigger auto-immune reactions by molecular mimicry in the pancreas, leading to auto-immune diabetes. Its immunological effects can also lead to the development of diabetes in patients who had undergone liver transplantation for HCV infection which is further made worse by intense immunosuppression used in such settings.This article provides an overview of the intriguing relationship between HCV infection and diabetes, the two major public health challenges which lead to widespread health and financial burden worldwide.

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Insulin Resistance Provides the Connection Between Hepatitis C Virus and Diabetes

Cited by 13 publications

References 20 publications

Metabolic Syndrome and Genotype 1 Virus C Compensated Liver Cirrhosis in the Era of Directly Acting Antiviral Therapy

Metabolic Syndrome and Genotype 1 Virus C Compensated Liver Cirrhosis in the Era of Directly Acting Antiviral Therapy

B (Reg) Cells in Hepatitis C Virus and Diabetes

Hepatitis C virus infection and diabetes

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