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Peschel G, Weigand K, Grimm J, Müller M, Buechler C. Serum omentin-1 is correlated with the severity of liver disease in patients with chronic hepatitis C. World J Hepatol 2023; 15:1315-1324. [PMID: 38223417 PMCID: PMC10784814 DOI: 10.4254/wjh.v15.i12.1315] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/20/2023] [Revised: 11/03/2023] [Accepted: 11/21/2023] [Indexed: 12/25/2023] Open
Abstract
BACKGROUND Patients with chronic hepatitis C virus (HCV) infection have increased serum omentin-1. Omentin-1 is an anti-inflammatory adipokine, and higher levels may be a direct effect of HCV infection. Successful elimination of HCV by direct acting antivirals almost normalized circulating levels of various molecules with a role in inflammation. AIM To evaluate the effect of HCV infection on serum omentin-1, serum omentin-1 levels of HCV patients were measured before therapy and at 12 wk after therapy end. Associations of serum omentin-1 with parameters of inflammation and liver function were explored at both time points. Serum omentin-1 levels of patients with and without liver cirrhosis, which was defined by ultrasound or the fibrosis-4 (FIB-4) score, were compared. METHODS Serum omentin-1 levels were measured by enzyme-linked immunosorbent assay in 84 chronic HCV patients before therapy and at 12 wk after therapy end where sustained virological response 12 (SVR12) was achieved in all patients. Serum omentin-1 of 14 non-infected controls was measured in parallel. RESULTS In patients with chronic HCV, serum omentin-1 levels were not related to viral load or viral genotype. HCV patients with liver steatosis and HCV patients with diabetes had serum omentin-1 levels comparable to patients not suffering from these conditions. Serum omentin-1 levels at SVR12 were similar in comparison to pretreatment levels. In addition, serum levels did not differ between HCV-infected patients and non-infected controls. Serum omentin-1 levels did not correlate with leukocyte count or C-reactive protein. Positive correlations of serum omentin-1 with bilirubin and the model for end-stage liver disease score (MELD) were detected before therapy and at SVR12 in the whole cohort. Bilirubin and the MELD score also positively correlated with serum omentin-1 levels in the subgroup of patients with ultrasound diagnosed liver cirrhosis before therapy. At SVR12, serum omentin-1 levels of patients with liver cirrhosis negatively correlated with albumin. Before therapy start, patients with high FIB-4 scores had increased serum omentin-1 in comparison to patients with a low score. Serum omentin-1 levels of patients with liver cirrhosis defined by ultrasound were increased at baseline and at SVR12. CONCLUSION Present study showed that liver cirrhosis, but not HCV infection per se, is related to elevated serum omentin-1 levels.
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Affiliation(s)
- Georg Peschel
- Department of Internal Medicine I, University Hospital Regensburg, Regensburg 93053, Germany
- Department of Internal Medicine, Klinikum Fürstenfeldbruck, Fürstenfeldbruck 82256, Germany
| | - Kilian Weigand
- Department of Internal Medicine I, University Hospital Regensburg, Regensburg 93053, Germany
- Department of Gastroenterology, Gemeinschaftsklinikum Mittelrhein, Koblenz 56073, Germany
| | - Jonathan Grimm
- Department of Internal Medicine I, University Hospital Regensburg, Regensburg 93053, Germany
| | - Martina Müller
- Department of Internal Medicine I, University Hospital Regensburg, Regensburg 93053, Germany
| | - Christa Buechler
- Department of Internal Medicine I, University Hospital Regensburg, Regensburg 93053, Germany.
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Ahmed CM, Grams TR, Bloom DC, Johnson HM, Lewin AS. Individual and Synergistic Anti-Coronavirus Activities of SOCS1/3 Antagonist and Interferon α1 Peptides. Front Immunol 2022; 13:902956. [PMID: 35799776 PMCID: PMC9254576 DOI: 10.3389/fimmu.2022.902956] [Citation(s) in RCA: 6] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/23/2022] [Accepted: 05/23/2022] [Indexed: 11/17/2022] Open
Abstract
Suppressors of Cytokine Signaling (SOCS) are intracellular proteins that negatively regulate the induction of cytokines. Amongst these, SOCS1 and SOCS3 are particularly involved in inhibition of various interferons. Several viruses have hijacked this regulatory pathway: by inducing SOCS1and 3 early in infection, they suppress the host immune response. Within the cell, SOCS1/3 binds and inhibits tyrosine kinases, such as JAK2 and TYK2. We have developed a cell penetrating peptide from the activation loop of the tyrosine kinase, JAK2 (residues 1001-1013), denoted as pJAK2 that acts as a decoy and suppresses SOCS1 and 3 activity. This peptide thereby protects against several viruses in cell culture and mouse models. Herein, we show that treatment with pJAK2 inhibited the replication and release of the beta coronavirus HuCoV-OC43 and reduced production of the viral RNA, as measured by RT-qPCR, Western blot and by immunohistochemistry. We confirmed induction of SOCS1 and 3 in rhabdomyosarcoma (RD) cells, and this induction was suppressed by pJAK2 peptide. A peptide derived from the C-terminus of IFNα (IFNα-C) also inhibited replication of OC43. Furthermore, IFNα-C plus pJAK2 provided more potent inhibition than either peptide alone. To extend this study to a pandemic beta-coronavirus, we determined that treatment of cells with pJAK2 inhibited replication and release of SARS-CoV-2 in Calu-3 cells. We propose that these peptides offer a new approach to therapy against the rapidly evolving strains of beta-coronaviruses.
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Affiliation(s)
- Chulbul M. Ahmed
- Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL, United States
| | - Tristan R. Grams
- Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL, United States
| | - David C. Bloom
- Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL, United States
| | - Howard M. Johnson
- Department of Microbiology and Cell Science, University of Florida, Gainesville, FL, United States
| | - Alfred S. Lewin
- Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL, United States
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Liu Z, Xu L, Xing M, Xu X, Wei J, Wang J, Kang W. Trelagliptin succinate: DPP-4 inhibitor to improve insulin resistance in adipocytes. Biomed Pharmacother 2020; 125:109952. [PMID: 32036216 DOI: 10.1016/j.biopha.2020.109952] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/25/2019] [Revised: 01/18/2020] [Accepted: 01/23/2020] [Indexed: 02/07/2023] Open
Abstract
Trelagliptin inhibits the enzyme dipeptidyl-4 (DPP-4) to treat type 2 diabetes and it may possess the potential to improve insulin resistance. However, the molecular mechanism is not known. In this study, the effect of trelagliptin succinate in improving insulin resistance was investigated. The differentiation system of 3T3-L1 mouse preadipocytes was used to determine the content of adipokines and the content of GLUT4 in the outer membrane. The expression of AKT, P-AKT, IRS-1 and P-IRS-1 in differentiated 3T3-L1 adipocytes was determined by western blotting. Our results demonstrated that trelagliptin succinate increased the expression of AKT, P-AKT, IRS-1 and P-IRS-1 in the PI-3K/AKT insulin signaling pathway. These events promote the trans-membrane function of GLUT4 and concomitant glucose intake in adipocytes. In addition, the secretion of free fatty acids and resistin were decreased. In conclusion, our study suggested that trelagliptin succinate improved insulin resistance in adipocytes via regulation of PI-3K/AKT/GLUT4 insulin signaling pathway.
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Affiliation(s)
- Zhenhua Liu
- National R & D Center for Edible Fungus Processing Technology, Henan University, Kaifeng 475004, China; Joint International Research Laboratory of Food & Medicine Resource Function, Henan Province, Kaifeng 475004, China
| | - Lanting Xu
- National R & D Center for Edible Fungus Processing Technology, Henan University, Kaifeng 475004, China; Joint International Research Laboratory of Food & Medicine Resource Function, Henan Province, Kaifeng 475004, China
| | - Meimei Xing
- National R & D Center for Edible Fungus Processing Technology, Henan University, Kaifeng 475004, China; Joint International Research Laboratory of Food & Medicine Resource Function, Henan Province, Kaifeng 475004, China
| | - Xiaojie Xu
- Zhengzhou Mingze Pharmaceutical Technology Co., Ltd. Zhengzhou, 450000, China
| | - Jinfeng Wei
- National R & D Center for Edible Fungus Processing Technology, Henan University, Kaifeng 475004, China; Joint International Research Laboratory of Food & Medicine Resource Function, Henan Province, Kaifeng 475004, China
| | - Jinmei Wang
- National R & D Center for Edible Fungus Processing Technology, Henan University, Kaifeng 475004, China; Joint International Research Laboratory of Food & Medicine Resource Function, Henan Province, Kaifeng 475004, China.
| | - Wenyi Kang
- National R & D Center for Edible Fungus Processing Technology, Henan University, Kaifeng 475004, China; Joint International Research Laboratory of Food & Medicine Resource Function, Henan Province, Kaifeng 475004, China.
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Visfatin serum concentration and hepatic mRNA expression in chronic hepatitis C. Clin Exp Hepatol 2019; 5:147-154. [PMID: 31501791 PMCID: PMC6728865 DOI: 10.5114/ceh.2019.85074] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/09/2018] [Accepted: 12/26/2018] [Indexed: 12/15/2022] Open
Abstract
Aim of the study Chronic hepatitis C (CHC) is a viral disease with metabolic disturbances involved in its pathogenesis. Adipokines may influence the inflammatory response and contribute to development of metabolic abnormalities in CHC. Visfatin exerts immunomodulatory and insulin-mimetic effects. The aim was to measure visfatin serum concentrations and its mRNA hepatic expression in non-obese CHC patients and to assess the relationships with metabolic and histological parameters. Material and methods In a group of 63 non-obese CHC patients (29 M/34 F) infected with genotype 1b aged 46.6 ±14.6 years, body mass index (BMI) 24.8 ±3.0 kg/m2, serum visfatin levels and its mRNA hepatic expression were examined and the subsequent associations with metabolic and histopathological features were assessed. Results Serum visfatin levels were significantly higher in CHC patients compared to controls (22.7 ±5.7 vs. 17.8 ±1.5 ng/ml, p < 0.001). There was no difference in serum visfatin and its mRNA hepatic expression regardless of sex, BMI, insulin sensitivity and lipids concentrations. There was no mutual correlation between serum visfatin and visfatin mRNA hepatic expression. Hepatic visfatin mRNA levels but not visfatin serum levels were higher in patients with steatosis (1.35 ±0.75 vs. 0.98 ±0.34, p = 0.009). Conclusions Serum visfatin levels may reflect its involvement in chronic inflammatory processes accompanying HCV infection. Increased visfatin mRNA hepatic expression in patients with steatosis seems to be a compensatory mechanism enabling hepatocytes to survive metabolic abnormalities resulting from virus-related lipid droplet deposition prerequisite to HCV replication.
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Crisan D, Radu C, Suciu A, Leach N, Stefanescu H, Avram L, Crisan N, Grigorescu M. Hepatitis C in nonobese nondiabetic patients: Insulin resistance and the metabolic syndrome make a difference. J Viral Hepat 2017; 24:86-87. [PMID: 27700001 DOI: 10.1111/jvh.12610] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/09/2022]
Affiliation(s)
- D Crisan
- 5th Medical Clinic, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania.,Clinical Municipal Hospital, Cluj-Napoca, Romania
| | - C Radu
- 3rd Medical Clinic, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania.,Hepatology Unit, Regional Institute of Gastroenterology and Hepatology, Cluj-Napoca, Romania
| | - A Suciu
- 3rd Medical Clinic, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania
| | - N Leach
- 4th Medical Clinic, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania
| | - H Stefanescu
- Hepatology Unit, Regional Institute of Gastroenterology and Hepatology, Cluj-Napoca, Romania
| | - L Avram
- Clinical Municipal Hospital, Cluj-Napoca, Romania
| | - N Crisan
- Clinical Municipal Hospital, Cluj-Napoca, Romania.,Department of Surgery, Iuliu-Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania
| | - M Grigorescu
- Hepatology Unit, Regional Institute of Gastroenterology and Hepatology, Cluj-Napoca, Romania
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Jamali R, Razavizade M, Arj A, Aarabi MH. Serum adipokines might predict liver histology findings in non-alcoholic fatty liver disease. World J Gastroenterol 2016; 22:5096-5103. [PMID: 27275102 PMCID: PMC4886385 DOI: 10.3748/wjg.v22.i21.5096] [Citation(s) in RCA: 44] [Impact Index Per Article: 4.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/05/2016] [Revised: 02/25/2016] [Accepted: 03/18/2016] [Indexed: 02/06/2023] Open
Abstract
AIM To assess significance of serum adipokines to determine the histological severity of non-alcoholic fatty liver disease. METHODS Patients with persistent elevation in serum aminotransferase levels and well-defined characteristics of fatty liver at ultrasound were enrolled. Individuals with a history of alcohol consumption, hepatotoxic medication, viral hepatitis or known liver disease were excluded. Liver biopsy was performed to confirm non-alcoholic liver disease (NAFLD). The degrees of liver steatosis, lobular inflammation and fibrosis were determined based on the non-alcoholic fatty liver activity score (NAS) by a single expert pathologist. Patients with a NAS of five or higher were considered to have steatohepatitis. Those with a NAS of two or lower were defined as simple fatty liver. Binary logistic regression was used to determine the independent association of adipokines with histological findings. Receiver operating characteristic (ROC) analysis was employed to determine cut-off values of serum adipokines to discriminate the grades of liver steatosis, lobular inflammation and fibrosis. RESULTS Fifty-four participants aged 37.02 ± 9.82 were enrolled in the study. Higher serum levels of visfatin, IL-8, TNF-α levels were associated independently with steatosis grade of more than 33% [β = 1.08 (95%CI: 1.03-1.14), 1.04 (95%CI: 1.008-1.07), 1.04 (95%CI: 1.004-1.08), P < 0.05]. Elevated serum IL-6 and IL-8 levels were associated independently with advanced lobular inflammation [β = 1.4 (95%CI: 1.09-1.8), 1.07 (95%CI: 1.003-1.15), P < 0.05]. Similarly, higher TNF-α, resistin, and hepcidin levels were associated independently with advanced fibrosis stage [β = 1.06 (95%CI: 1.002-1.12), 19.86 (95%CI: 2.79-141.19), 560.72 (95%CI: 5.98-5255.33), P < 0.05]. Serum IL-8 and TNF-α values were associated independently with the NAS score, considering a NAS score of 5 as the reference value [β = 1.05 (95%CI: 1.01-1.1), 1.13 (95%CI: 1.04-1.22), P < 0.05]. CONCLUSION Certain adipokines may determine the severity of NAFLD histology accurately.
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Vanni E, Bugianesi E, Saracco G. Treatment of type 2 diabetes mellitus by viral eradication in chronic hepatitis C: Myth or reality? Dig Liver Dis 2016; 48:105-11. [PMID: 26614641 DOI: 10.1016/j.dld.2015.10.016] [Citation(s) in RCA: 49] [Impact Index Per Article: 5.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/13/2015] [Revised: 10/05/2015] [Accepted: 10/16/2015] [Indexed: 12/15/2022]
Abstract
Chronic hepatitis C is a systemic disease inducing metabolic alterations leading to extrahepatic consequences. In particular, hepatitis C virus (HCV) infection seems to increase the risk of incident type 2 diabetes mellitus in predisposed individuals, independently of liver disease stage. The mechanisms through which hepatitis C induces T2DM involve direct viral effects, insulin resistance, pro-inflammatory cytokines and other immune-mediated processes. Many studies have reported the clinical consequences of type 2 diabetes mellitus on hepatitis C outcome, but very few studies have addressed the issue of microangiopathic complications among patients with hepatitis C only, who develop type 2 diabetes mellitus. Moreover, clinical trials in HCV-positive patients have reported improvement in glucose metabolism after antiviral treatment; recent studies have suggested that this metabolic amelioration might have a clinical impact on type 2 diabetes mellitus-related complications. These observations raise the question as to whether the HCV eradication may also have an impact on the future morbidity and mortality due to type 2 diabetes mellitus. The scope of this review is to summarise the current evidence linking successful antiviral treatment and the prevention of type 2 diabetes mellitus and its complications in hepatitis C-infected patients.
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Affiliation(s)
- Ester Vanni
- Gastro-hepatology Unit, Department of Medical Sciences, University of Turin, Turin, Italy
| | - Elisabetta Bugianesi
- Gastro-hepatology Unit, Department of Medical Sciences, University of Turin, Turin, Italy
| | - Giorgio Saracco
- Gastroenterology Unit, Oncology Department, University of Turin, Italy.
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Liu D, Li S, Li Z. Adiponectin: A biomarker for chronic hepatitis C? Cytokine 2015; 89:27-33. [PMID: 26683021 DOI: 10.1016/j.cyto.2015.10.016] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/19/2015] [Revised: 10/30/2015] [Accepted: 10/30/2015] [Indexed: 12/14/2022]
Abstract
Adiponectin, a hormone primarily synthesized and secreted by adipose tissue, plays a pivotal role in lipid metabolism. Chronic hepatitis C (CHC) infection is characterized by disordered lipid metabolism, which may potentially evolve into steatosis over a period of time. A growing body of evidence appears to link decreased adiponectin plasma levels with severe CHC-related steatosis, which suggests a potential role of this adipokine as a diagnostic and therapeutic target for clinical application. In this review, we have attempted to summarize the current status of adiponectin research in the context of CHC, concentrating predominantly on its roles in CHC, and its potential relevance as a biomarker for CHC.
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Affiliation(s)
- Ding Liu
- Department of Orthopaedics, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China
| | - Shengyu Li
- Department of General Surgery, The Xiangya Hospital of Central South University, Changsha, Hunan, China
| | - Zhihong Li
- Department of Orthopaedics, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
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Liu N, Mu H, Liang CD, Zheng JM, Zhang J. Effect of norepinephrine on expression of leptin and leptin receptor in hepatic stellate cells. Shijie Huaren Xiaohua Zazhi 2015; 23:1052-1058. [DOI: 10.11569/wcjd.v23.i7.1052] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
AIM: To investigate the effect of sympathetic neurotransmitter norepinephrine (NE) on the expression of leptin and leptin receptor in hepatic stellate cells (HSCs) in vitro.
METHODS: Different concentrations of NE were applied on HSCs for 24, 48 or 72 h. Immunohistochemical staining was used to detect the expression of α-smooth muscle actin (α-SMA) in activated HSCs. Western blot was used to detect the expression of leptin and soluble leptin receptor (sOB-R) proteins. Real-time PCR was used to examine the effect of NE on mRNA expression of leptin and sOB-R in HSCs.
RESULTS: Immunohistochemistry results showed that after 1, 10, or 100 μmol/L NE was used on HSCs, the expression of α-SMA increased significantly at 24 h (14.1 ± 4.4, 17.5 ± 5.2, 19.8 ± 4.1 vs 11.3 ± 4.5; P < 0.05), suggesting that NE could activate HSCs and promote their proliferation. When 10 μmol/L NE was applied for 24, 48 or 72 h, α-SMA expression gradually increased (17.5 ± 5.2; 18.5 ± 5.4; 19.2 ± 6.2, P < 0.05), indicating that NE induced HSC proliferation in a time-dependent manner. Western blot analysis showed that leptin protein expression was significantly higher in HSCs after treatment with 1, 10 and 100 μmol/L NE for 24 h compared with the control group (1.54 ± 0.08, 2.72 ± 0.09, 2.84 ± 0.18 vs 0.85 ± 0.12, P < 0.05); the expression of leptin receptor protein was also significantly higher than that in the control group (1.57 ± 0.18, 2.51 ± 0.17, 2.89 ± 0.19 vs 0.98 ± 0.15, P < 0.05). Real-time PCR was used to detect mRNA expression of leptin and leptin receptor, and the results showed that leptin mRNA expression was significantly higher than that in the control group (1.51 ± 0.08, 2.58 ± 0.09, 3.63 ± 0.12 vs 1.00 ± 0.07, P < 0.05); the expression of leptin receptor mRNA was also significantly higher than that in the control group (1.71 ± 0.08, 2.87 ± 0.10, 4.01 ± 0.14 vs 1.00 ± 0.08, P < 0.05).
CONCLUSION: The sympathetic neurotransmitter NE plays a role in the process of liver fibrosis possibly by promoting leptin and sOB-R expression in activated HSCs.
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Iwane S, Mizuta T, Kawaguchi Y, Takahashi H, Oza N, Oeda S, Nakashita S, Kuwashiro T, Otsuka T, Kawazoe S, Eguchi Y, Anzai K, Ozaki I, Fujimoto K. Impact of Body Weight Reduction via Diet and Exercise on the Anti-Viral Effects of Pegylated Interferon Plus Ribavirin in Chronic Hepatitis C Patients with Insulin Resistance: A Randomized Controlled Pilot Trial. Intern Med 2015; 54:3113-9. [PMID: 26666596 DOI: 10.2169/internalmedicine.54.5574] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/06/2022] Open
Abstract
OBJECTIVE Insulin resistance (IR) modifies the anti-viral effects of interferon (IFN) therapy in patients with chronic hepatitis C (CHC). This prospective study evaluated whether lifestyle interventions improve the anti-viral response to treatment with pegylated (PEG)-IFN plus ribavirin (RBV) in patients with CHC. METHODS The study cohort consisted of 60 patients chronically infected with a high viral load of hepatitis C virus genotype 1b and a homeostasis model assessment of IR (HOMA-IR) value above 2. The patients were divided into two groups, an intervention group (n=26) and a control group (n=34). The patients in the intervention group were prescribed diet and exercise treatment for 3-6 months to reduce their body weight by ≥5% before starting treatment with PEG-IFN plus RBV. RESULTS Diet and exercise significantly reduced the HOMA-IR values in the intervention group, from 3.4 to 2.5 (p=0.0009), especially among the 15 patients who achieved a body weight reduction of ≥5%. The viral disappearance rate at 12 weeks was significantly higher in the intervention group among the patients with a ≥5% weight reduction than in the control group (53.3% vs. 23.5%, p=0.01). However, the sustained viral response (SVR) rates were similar. CONCLUSION Improvements in IR achieved through weight reduction via lifestyle interventions may enhance the early viral response to PEG-IFN plus RBV in patients with CHC. However, this intervention program has no effect on the SVR rate.
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Affiliation(s)
- Shinji Iwane
- Department of Internal Medicine, Saga University Hospital, Japan
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