Association of inflammatory and anti‐inflammatory cytokines with insulin resistance in chronic hepatitis C

Hung, Chao‐Hung; Lee, Chuan–Mo; Chen, Chien‐Hung; Hu, Tsung–Hui; Jiang, Shengjie; Wang, Jing‐Houng; Lu, Sheng‐Nan; Wang, Peiwei

doi:10.1111/j.1478-3231.2009.01991.x

Cited by 39 publications

(39 citation statements)

References 46 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%

“…[14][15][16] Because both HCV infection and adiponectin are critically involved in metabolism, their precise relationship might aid to probe the therapeutic targets for HCV-associated cardiometabolic complications but remains inconclusive. For example, compared with controls, serum adiponectin levels have been reported to be higher, [17][18][19] lower 20 or not different 21 in chronic hepatitis C (CHC) patients. All studies 17,[22][23] but one 24 failed to correlate HCV viral load with adiponectin levels.…”

Section: Introductionmentioning

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: Introductionmentioning

confidence: 99%

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

et al. 2017

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“…Since the HCV cohort was overweight, we suspect that the observed differences in adiponectin level cannot be explained solely by a larger mass of adipose. Moreover, in one of the previous studies, adiponectin level correlated with TNF-α levels and higher degree of hepatic necroinflammation [26]. Since adiponectin is metabolized by the liver, and probably excreted in the biliary tract [27], an increase of adiponectin levels in chronic hepatitis C might reflect a secondary response to HCV-induced chronic liver disease.…”

Section: Discussionmentioning

confidence: 99%

Association of Serum Adipocytokines with Hepatic Steatosis and Fibrosis in Patients with Chronic Hepatitis C

Baranova¹,

Jarrar

Stepanova

et al. 2010

Digestion

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Background: The pathogenic mechanisms of hepatic steatosis in hepatitis C (HCV) remain unclear. Aim: To assess the potential role of cytokines and adipokines in HCV-related steatosis and fibrosis. Methods: We profiled several adipokines, cytokines, and related soluble molecules in 99 HCV patients and analyzed their potential associations with hepatic steatosis and fibrosis. Results: Serum leptin and IL-1RA were significantly higher in HCV genotype 1 as compared to genotype 3. On the other hand, serum resistin, IL-8, IL-1B and sIL-6R, were significantly higher in HCV genotype 3. No differences were observed for adiponectin, visfatin, IL-6 and TNF-α. Regardless of HCV genotype, steatosis could be predicted by a combination of IL-8, IL-6, and sIL-6R/IL-6. When analysis was repeated for each of the genotypes, the reliability of models improved. Regardless of HCV genotype, moderate to severe fibrosis (Metavir score >F2), was predicted by IL-8 and resistin levels. Conclusions: Analysis of adipocytokines associated with steatosis supports the hypothesis that steatogenic pathways differ in HCV genotype 3 from those infected with non-genotype 3 infections.

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“…It is also important to keep in mind that fat is not only a source of free fatty acids, but also a source of proinflammatory and anti-inflammatory cytokines which are able to modulate the circulation of free fatty acids from fat tissue to liver and again from liver to peripheral tissues [76] . These cytokines are also involved in some key steps of the progressive liver damage observed in individuals affected by steatohepatitis.…”

Section: Fat As An Endocrine Organ: Cytokinesmentioning

confidence: 99%

Liver steatosis in hepatitis C patients

González‐Reimers¹

2015

WJH

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would affect HCV patients who are also obese or diabetics. In fact, several genotypes exert metabolic effects which overlap with some of those observed in the metabolic syndrome. In this review we will analyse the pathogenic pathways involved in the development of steatosis in HCV patients. Several cytokines and adipokines also become activated and are involved in "pure" steatosic effects, in addition to inflammation. They are probably responsible for the evolution of simple steatosis to steatohepatitis, making it difficult to explain why such alterations only affect a proportion of steatosic patients. Core tip: Chronic hepatitis C virus (HCV) infection can lead to steatosis and steatohepatitis. Increased liver triglyceride synthesis is mediated by several transcription factors such as sterol regulatory elementbinding protein (SREBP) whose expression is enhanced, in turn, by HCV core protein. Chronic HCV infection is also associated with insulin resistance that seems to be selective because although it activates systemic lipolysis, it increases triglyceride synthesis within the liver. This is due to the stimulatory effect of insulin on SREBP. It remains to be answered why not all patients with HCV infection and steatosis develop steatohepatitis despite early cytokine activation and metabolic derangements. AbstractThere is controversy regarding some aspects of hepatitis C virus (HCV) infection-associated liver steatosis, and their relationship with body fat stores. It has classically been found that HCV, especially genotype 3, exerts direct metabolic effects which lead to liver steatosis. This supports the existence of a so called viral steatosis and a metabolic steatosis, which REVIEWSubmit a

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Association of inflammatory and anti‐inflammatory cytokines with insulin resistance in chronic hepatitis C

Abstract: Our data suggest that chronic HCV infection is associated with increased IR, which is correlated inversely with the serum adiponectin level. The complex role of adiponectin in the pathogenesis of IR and hepatic necroinflammation in chronic HCV infection merit further investigation.

Cited by 39 publications

References 46 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

Association of Serum Adipocytokines with Hepatic Steatosis and Fibrosis in Patients with Chronic Hepatitis C

Liver steatosis in hepatitis C patients

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