Significance of serum leptin and adiponectin levels in Egyptian patients with chronic hepatitis C virus associated hepatic steatosis and fibrosis

Korah, Tarek E.; El-Sayed, Sawsan; El-Shafie, Maathir Kamel; Hammoda, Ghada E.; Safan, Manal A

doi:10.4254/wjh.v5.i2.74

Cited by 20 publications

(25 citation statements)

References 44 publications

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“…2,22,[25][26][27] This lack of clarity may arise from the heterogeneous hepatic pathologies and metabolic conditions of these patients, as fibrosis and steatosis are associated with hyperadiponectinemia and hypoadiponectinemia, respectively. 18,37 Thus, after SVR, the decrease in adiponectin in G4 CHC patients 22,26 might reflect the reversal of hepatic fibrosis, whereas the increase in adiponectin in G3 CHC patients 25 might indicate an improvement in hepatic steatosis, which is most evident in G3 CHC and regarded as "viral steatosis. "…”

Section: Discussionmentioning

confidence: 99%

“…1,[35][36][37] For all included 747 patients, several baseline factors were evaluated, including sex, age, body mass index (BMI), HCV RNA and genotype, presence of hepatic steatosis and cirrhosis, eGFR, APRI, TC, TGs, HOMA-IR [fasting insulin (mU/mL) £ fasting glucose (mmol/L)/ 22.5], alanine aminotransferase (ALT), adiponectin (i.e., total adiponectin) and HMW adiponectin (R&D Systems, MN, USA) levels. For the 546 patients who completed anti-HCV therapy, the aforementioned factors were evaluated 2 weeks before therapy; after 4, 12 and 24 weeks of therapy; at the end of therapy; and 12 and 24 weeks after the end of therapy.…”

Section: Methods/materialsmentioning

confidence: 99%

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The evolving relationship between adiponectin and insulin sensitivity in hepatitis C patients during viral clearance

et al. 2017

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(2017) The evolving relationship between adiponectin and insulin sensitivity in hepatitis C patients during viral clearance, Virulence, 8:7, 1255-1264, DOI: 10.1080/21505594.2017 ABSTRACT Background: The evolution of the relationship between adiponectin and insulin sensitivity in hepatitis C virus (HCV) patients during viral clearance is unclear and warrants investigation. Methods: A prospective study including 747 consecutive chronic hepatitis C (CHC) patients, of whom 546 had completed a course of anti-HCV therapy and underwent pre-, peri-and post-therapy surveys for anthropomorphic, viral, metabolic and hepatic profiles and adiponectin levels, was conducted in a tertiary care center. Results: Multivariate analyses indicated associations of sex, triglyceride levels and hepatic steatosis with adiponectin levels and of triglyceride levels and interferon λ3 (IFNL3) genotype with homeostasis model assessment-estimated insulin resistance (HOMA-IR) levels before anti-HCV therapy. In patients with a sustained virological response (SVR; n D 455), at 24 weeks post-therapy, sex, BMI, aspartate aminotransferase to platelet ratio index (APRI), HOMA-IR and steatosis were associated with adiponectin levels, and IFNL3 genotype was associated with HOMA-IR levels. GEE analysis demonstrated that SVR affected longitudinal trends in adiponectin levels. Compared with pre-therapy levels, adiponectin and APRI levels decreased 24 weeks post-therapy in SVR patients, regardless of baseline insulin resistance (IR). However, HOMA-IR levels decreased in SVR patients with baseline IR but increased in those without baseline IR. Compared with controls, immunohistochemical studies showed that pre-therapy CHC patients had higher hepatic adiponectin expression associated with hepatic fibrosis. Conclusions: During HCV infection, adiponectin may affect insulin sensitivity through triglycerides. After viral clearance, adiponectin levels were directly associated with insulin sensitivity and decreased upon improved hepatic fibrosis; with a link to the IFNL3 genotype, insulin sensitivity improved only in patients with baseline IR.

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Section: Discussionmentioning

confidence: 99%

Section: Methods/materialsmentioning

confidence: 99%

The evolving relationship between adiponectin and insulin sensitivity in hepatitis C patients during viral clearance

et al. 2017

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“…The ability of adipokines to signify the loss of liver function is controversial . Adiponectin levels alone did not correspond to liver damage.…”

Section: Resultsmentioning

confidence: 99%

“…However, NS3induced IL-6 production correlated with AST levels (r = 0.476, P = 0.022) and grade of inflammation (r = 0.699, P = 0.004, Table S3). The ability of adipokines to signify the loss of liver function is controversial (15)(16)(17)(18)(19)(20)(21). Adiponectin levels alone did not correspond to liver damage.…”

Section: Cytokine Activity and Disease Parametersmentioning

confidence: 99%

HCV protein‐induced cytokine predicts treatment outcomes in chronic hepatitis C virus infection

Krueger

Collister

Minuk

et al. 2013

Liver International

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Background & Aims Immune‐mediated processes are thought to influence the efficacy of treatment in chronic hepatitis C virus (HCV) infection. This study evaluated the association of baseline immune responses with the achievement of a sustained viral response (SVR) upon pegylated interferon and ribavirin treatment. Methods Baseline serum and peripheral blood mononuclear cells (PBMC) cytokine activity was assessed. Metabolic and liver injury parameters were evaluated as underlying factors. Results Baseline demographics and disease parameters did not differ between the SVR− (n = 14) and SVR+ (n = 25) cohorts except for body mass index (BMI) values and liver injury scores. Baseline circulating TNF‐α levels were three‐fold higher with subsequent treatment failure vs. success (P = 0.124). Baseline peripheral blood mononuclear cells (PBMC, n = 25) were cultured with HCV core and non‐structural (NS)3 proteins. Core (P = 0.0003) and NS3 (P = 0.018) induced greater TNF‐α production within the SVR−, compared with the SVR+, cohorts. Similar findings were noted for interleukin (IL)‐1β and IL‐10 synthesis. Furthermore, HCV core‐induced TNF‐α synthesis correlated with patient BMI values (r = 0.489, P = 0.015). Core (r = 0.432, P = 0.065) and NS3 (r = 0.530, P = 0.020)‐induced TNF‐α displayed a positive relationship with serum adiponectin concentrations. In addition, lipopolysaccharide stimulated cytokine synthesis associated with BMI and adiponectin levels. Although unable to predict treatment outcomes, NS3‐induced IL‐6 synthesis and serum leptin concentrations corresponded to liver injury scores. Conclusion An enhanced PBMC susceptibility to core and NS3‐induced TNF‐α synthesis at baseline was associated with treatment failure. This phenomenon appeared to involve the interaction of virally generated TNF‐α activity and metabolic disease. In contrast, IL‐6 activity and leptin levels may indicate liver damage.

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“…More relevant, positive immunostaining for the leptin receptor (ObR) was found to co‐localize with VEGF and α‐SMA in fibrotic rat livers after chronic CCl 4 administration. The profibrogenic action of leptin has been mainly involved in the pathogenesis of non‐alcoholic steatohepatitis, a very common condition in Western countries, mostly found in obese and diabetic patients carrying metabolic syndrome, and potentially able to progress towards cirrhosis and even hepatocellular carcinoma (HCC) . Leptin, interacting with ObR, stimulates several signal pathways and transcription factors, including signal transducing and activator 3, nuclear factor‐κB and, as also shown by others, ERK1/2 and c‐Akt .…”

Section: Main Mechanisms Of Prevention and Treatment Of Liver Fibrosimentioning

confidence: 96%

Update on implications and mechanisms of angiogenesis in liver fibrosis

Zhang

et al. 2014

Hepatology Research

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Liver fibrosis occurs as a compensatory response to the process of tissue repair in a wide range of chronic liver injures. It is characterized by excessive deposition of extracellular matrix in liver tissues. As the pathogenesis progresses without effective management, it will lead to formation of liver fiber nodules and disruption of normal liver structure and function, finally culminating in cirrhosis and hepatocellular carcinoma. A new discovery shows that liver angiogenesis is strictly associated with, and may even favor fibrogenic progression of chronic liver diseases. Recent basic and clinical investigations also demonstrate that liver fibrogenesis is accompanied by pathological angiogenesis and sinusoidal remodeling, which critically determine the pathogenesis and prognosis of liver fibrosis. Inhibition of pathological angiogenesis is considered to be a new strategy for the treatment of liver fibrosis. This review summarizes current knowledge on the process of angiogenesis, the relationships between angiogenesis and liver fibrosis, and on the molecular mechanisms of liver angiogenesis. On the other hand, it also presents the different strategies that have been used in experimental models to counteract excessive angiogenesis and the role of angiogenesis in the prevention and treatment of liver fibrosis.

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Significance of serum leptin and adiponectin levels in Egyptian patients with chronic hepatitis C virus associated hepatic steatosis and fibrosis

Abstract: AIM:To study serum levels of leptin and adiponectin in patients with chronic hepatitis C virus infection genotype-4 (HCV-4) related steatosis and fibrosis.

Cited by 20 publications

References 44 publications

The evolving relationship between adiponectin and insulin sensitivity in hepatitis C patients during viral clearance

The evolving relationship between adiponectin and insulin sensitivity in hepatitis C patients during viral clearance

HCV protein‐induced cytokine predicts treatment outcomes in chronic hepatitis C virus infection

Update on implications and mechanisms of angiogenesis in liver fibrosis

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