Association of Serum Adipocytokines With Insulin Resistance and Liver Injury in Patients With Chronic Hepatitis C Genotype 4

Khattab, Mahmoud A.; Eslam, Mohammed; Aly, Mayada M.; Shatat, Mohammed; Hussen, Azaa; Moussa, Yossef I.; Elsaghir, Ghada; Abdalhalim, Hesham; Aly, Azza Ahmed; Gaber, Salwa; Harrison, Stephen A.

doi:10.1097/mcg.0b013e318256b68a

Cited by 8 publications

(12 citation statements)

References 37 publications

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“…However, when evaluated with respect to treatment outcomes, baseline adiponectin did not align with the absence of a SVR (Fig. a); a finding supported by some, but not all, previous reports .…”

Section: Discussionsupporting

confidence: 66%

“…Baseline serum cytokines have been cited as indicators of treatment outcomes . We observed a three‐fold increase in serum TNF‐α concentrations for patients for whom a SVR was not realized compared with those who achieved a SVR ( P = 0.124, Fig.…”

Section: Discussionmentioning

confidence: 86%

“…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%

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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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Section: Discussionsupporting

confidence: 66%

Section: Discussionmentioning

confidence: 86%

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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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“…Among adipocytokines, leptin and adiponectin are found to be associated with the insulin resistance and severity of hepatic damage [13]. For example, the correlation between these adipocytokines and liver injury, including liver steatosis, inflammation and fibrosis, has been studied in patients with NAFLD, HCV or HBV infection [14][15][16][17]. Recently, visfatin, a newly discovered proinflammatory and insulin-mimetic adipocytokine, was associated with fibrosis progression in NAFLD patients [18]; however, its role in chronic hepatitis B patients warrants further examinations.…”

Section: Introductionmentioning

confidence: 99%

Adipocytokines and liver fibrosis stages in patients with chronic hepatitis B virus infection

et al. 2015

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“…Notably, chronic hepatitis has been shown to cause changes in adiponectin levels56. However, there are very few studies on the change in adiponectin levels in patients with hepatogenic diabetes.…”

mentioning

confidence: 99%

Clinical implication of changes in serum adiponectin in patients with hepatogenic diabetes

Bao

Yuan

Duan

et al. 2014

Sci Rep

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Adiponectin is a protein hormone that modulates glucose metabolism and fatty acid oxidation. We explored the clinical implication of serum adiponectin in hepatogenic diabetes. Serum adiponectin levels were determined using enzyme–linked immunochemistry assay in 78 individuals including 19 hepatogenic diabetes, 20 type 2 diabetes (T2D), 20 chronic liver disease and 19 healthy controls. Cases and controls were matched by gender and body mass index (BMI). There is no difference in serum adiponectin levels among hepatogenic diabetic, T2D and healthy control groups. The levels of adiponectin are highest in chronic liver disease and lowest in T2D. Insulin levels are highest in hepatic diabetics and lowest in T2D. Hepatic diabetics have the lowest insulin sensitivity index (ISI). Serum adiponectin levels were negatively correlated with triglycerides and total cholesterol in T2D. Serum adiponectin is significantly increased in chronic liver disease, but lacks association with hepatogenic diabetes.

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Association of Serum Adipocytokines With Insulin Resistance and Liver Injury in Patients With Chronic Hepatitis C Genotype 4

Cited by 8 publications

References 37 publications

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

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

Adipocytokines and liver fibrosis stages in patients with chronic hepatitis B virus infection

Clinical implication of changes in serum adiponectin in patients with hepatogenic diabetes

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