Increased circulating adiponectin in males with chronic HCV hepatitis

Canavesi, Elena; Porzio, Marianna; Ruscica, Massimiliano; Rametta, Raffaela; Macchi, Chiara; Pelusi, Serena; Dongiovanni, Paola; Magni, Paolo; Valenti, Luca

doi:10.1016/j.ejim.2015.08.001

Cited by 7 publications

(9 citation statements)

References 35 publications

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“…Based on HCV genotype-stratified analyses, increased PAI-1 after SVR was significant only in patients with G1 HCV infection, whereas altered patterns in leptin (unchanged) [25] and adiponectin (decreased) levels [26] did not change after HCV genotype stratification. The decrease in adiponectin levels observed in CHC patients after SVR was consistent with a previous case-control study showing that CHC is associated with increased serum adiponectin [33]. Our previous studies confirmed the non-hepatic origin of increases in PAI-1 observed after SVR [24] and revealed that the high PAI-1 level is linked to a poor metabolic profile [5].…”

Section: Discussionsupporting

confidence: 89%

The Evolving Interplay among Abundant Adipokines in Patients with Hepatitis C during Viral Clearance

et al. 2017

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How hepatatitis C virus (HCV) infection affects the interplay among abundant adipokines in the host remains unclear. A prospective study was conducted with 450 consecutive genotype 1 (G1) and G2 HCV patients who completed a course of anti-HCV therapy and underwent pre-therapy and 24-week post-therapy surveys to assess various profiles and levels of abundant adipokines, including leptin, adiponectin, and plasminogen activator inhibitor-1 (PAI-1). Before anti-HCV therapy, multivariate analyses showed gender to be associated with leptin and adiponectin levels, and BMI with leptin and PAI-1 levels. Among patients with a sustained virological response (SVR, n = 372), associations at 24 weeks post-therapy were as follows: gender and BMI with all adipokine levels; hepatic steatosis and aspartate aminotransferase to platelet ratio index with adiponectin levels; and HOMA-IR and HCV genotype with PAI-1 levels. Paired t-tests revealed increased post-therapeutic PAI-1 levels in G1 SVR patients and decreased adiponectin levels in all SVR patients compared to pre-therapeutic levels. HCV infection may obscure associations between abundant adipokines and metabolic/hepatic profiles. In SVR patients, a higher hierarchical status of PAI-1 versus adiponectin in affecting glucose metabolism was noted at 24 weeks post-therapy. Such genotype-non-specific adiponectin decreases and G1-specific PAI-1 increases warrant careful follow-up of HCV patients after SVR according to viral genotype.

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Section: Discussionsupporting

confidence: 89%

The Evolving Interplay among Abundant Adipokines in Patients with Hepatitis C during Viral Clearance

et al. 2017

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“…In addition, before anti-HCV therapy, adiponectin levels were not associated with HCV RNA levels, consistent with the results of most studies. 2,17,[22][23] Combined, these results indicate that the impact of HCV infection on adiponectin levels, if any, does not occur directly through viral RNA modulation but through alterations subsequent to HCV infection, probably in metabolic or hepatic aspects. 2 The high correlation noted between HMW adiponectin and adiponectin (total) confirmed the representativeness of adiponectin in surveying insulin sensitivity.…”

Section: Discussionmentioning

confidence: 79%

“…[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%

“…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. Low adiponectin levels in CHC patients have been linked to poor anti-HCV immune and therapeutic responses as well as hepatic steatosis, metabolic syndrome and IR.…”

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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“…Increased adiponectin levels were noted in HCV-infected patients [74][75][76][77], especially those with severe fibrosis [78], compared with controls, suggesting a pattern of adiponectin resistance [67,76], although one study found similar adiponectin levels between HCV-infected patients and controls [67]. Studies involving various HCV genotypes have reported diverse findings regarding adiponectin alteration and its correlation with HCV viral load or disease progression.…”

Section: Adiponectinmentioning

confidence: 99%

Roles of Adipokines in Digestive Diseases: Markers of Inflammation, Metabolic Alteration and Disease Progression

Chang

Yang

2020

IJMS

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Adipose tissue is a highly dynamic endocrine tissue and constitutes a central node in the interorgan crosstalk network through adipokines, which cause pleiotropic effects, including the modulation of angiogenesis, metabolism, and inflammation. Specifically, digestive cancers grow anatomically near adipose tissue. During their interaction with cancer cells, adipocytes are reprogrammed into cancer-associated adipocytes and secrete adipokines to affect tumor cells. Moreover, the liver is the central metabolic hub. Adipose tissue and the liver cooperatively regulate whole-body energy homeostasis via adipokines. Obesity, the excessive accumulation of adipose tissue due to hyperplasia and hypertrophy, is currently considered a global epidemic and is related to low-grade systemic inflammation characterized by altered adipokine regulation. Obesity-related digestive diseases, including gastroesophageal reflux disease, Barrett’s esophagus, esophageal cancer, colon polyps and cancer, non-alcoholic fatty liver disease, viral hepatitis-related diseases, cholelithiasis, gallbladder cancer, cholangiocarcinoma, pancreatic cancer, and diabetes, might cause specific alterations in adipokine profiles. These patterns and associated bases potentially contribute to the identification of prognostic biomarkers and therapeutic approaches for the associated digestive diseases. This review highlights important findings about altered adipokine profiles relevant to digestive diseases, including hepatic, pancreatic, gastrointestinal, and biliary tract diseases, with a perspective on clinical implications and mechanistic explorations.

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Increased circulating adiponectin in males with chronic HCV hepatitis

Cited by 7 publications

References 35 publications

The Evolving Interplay among Abundant Adipokines in Patients with Hepatitis C during Viral Clearance

The Evolving Interplay among Abundant Adipokines in Patients with Hepatitis C during Viral Clearance

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

Roles of Adipokines in Digestive Diseases: Markers of Inflammation, Metabolic Alteration and Disease Progression

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