Adiponectin levels and insulin resistance among patients with chronic hepatitis C

Carvalho, Raoni Freitas; Atta, Ajax Mercês; Oliveira, Ilka Regina Souza de; Santos, Taciana Pereira Sant'Ana; Santos, João Pedro Aguiar dos; Schinoni, María Isabel; Sousa-Atta, M.L.B.

doi:10.1016/j.actatropica.2017.12.004

Cited by 8 publications

(5 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Lower levels of adiponectin have been linked to steatosis, MetS, insulin resistance and poor responses to interferon therapy in CHC patients. [28][29][30][31] Although a study investigating the level of adiponectin in CHC patients shows controversial results compared to healthy controls, 173 lines of evidence from other studies conclusively demonstrate the negative correlation between adiponectin level and steatosis in CHC patients. [174][175][176] Of note, genotype 3 exhibits lower level of adiponectin than other HCV genotypes.…”

Section: Chroni C Hepatitis Vir Al Infec Ti On and Ad Ip Onec Tinmentioning

confidence: 99%

Systematic review: chronic viral hepatitis and metabolic derangement

Wang

Cheng

Kao

2019

Aliment Pharmacol Ther

View full text Add to dashboard Cite

Summary Background The liver has a critical role in the metabolism of glucose and lipids. Chronic hepatitis B virus (HBV) or hepatitis C virus (HCV) infection leads to a spectrum of liver disease including chronic hepatitis, cirrhosis and hepatocellular carcinoma. Metabolic syndrome (MetS) has a rising incidence owing to an epidemic of type 2 diabetes mellitus (T2DM) and obesity. Non‐alcoholic fatty liver disease is a liver manifestation of MetS and has become the most common cause of chronic liver disease worldwide. Aim To summarise the interplay among hepatitis viruses, MetS and its components. Methods We searched the literature about HBV, HCV infection, MetS, fatty liver and its components from PubMed. Results With respect to the viral replication cycle, lipids are important mediators between viral entry and hepatocyte in HCV infection, but not in HBV infection. Thus, HCV infection is inversely associated with hyperlipidaemia and lipid rebound occurs following sustained viral response induced by interferon‐based therapy or direct antiviral agents. In addition, HCV infection is positively associated with insulin resistance, hepatic steatosis, MetS and the risk of T2DM and atherosclerosis. In contrast, HBV infection may protect infected subjects from the development of MetS and hepatic steatosis. Accumulating evidence suggests that HBV infection is inversely associated with lipid metabolism, and exhibits no conclusive association with insulin resistance or the risk of T2DM and arteriosclerosis. Conclusions In patients with viral hepatitis and concurrent metabolic diseases, a multidisciplinary approach should be given rather than simply antiviral treatment.

show abstract

Section: Chroni C Hepatitis Vir Al Infec Ti On and Ad Ip Onec Tinmentioning

confidence: 99%

Systematic review: chronic viral hepatitis and metabolic derangement

Wang

Cheng

Kao

2019

Aliment Pharmacol Ther

View full text Add to dashboard Cite

show abstract

“…In addition to its significant involvement in the clinical outcome of BA with respect to the degree of liver fibrosis, a number of studies have reported the relationships between hyperadiponectinemia and the clinical parameters of liver fibrosis in cohorts with hepatitis viral infection. A more recent study by Carvalho et al[ 46 ] found that patients with HCV infection had significantly greater adiponectin levels than healthy controls. In 2013, Korah et al[ 47 ] examined serum adiponectin levels in patients with chronic HCV genotype 4 associated with steatosis and fibrosis.…”

Section: Anti-fibrotic Role Of Adiponectin In Clinical Practicementioning

confidence: 99%

Adiponectin as a novel biomarker for liver fibrosis

Udomsinprasert

Honsawek

Poovorawan

2018

WJH

View full text Add to dashboard Cite

Adiponectin is known to play primary roles in the regulation of systemic glucose homeostasis and lipid metabolism. Interestingly, emerging evidence indicates beneficial effects of adiponectin on liver fibrosis; however, the exact mechanisms of this action remain unclear. Herein, we aimed to summarize the recent findings regarding the role of adiponectin in liver fibrogenesis and update the current comprehensive knowledge regarding usefulness of adiponectin-based treatments in liver fibrosis. Adiponectin has been demonstrated to have an anti-fibrotic action in the liver by blocking the activation of hepatic stellate cell-mediated adenosine monophosphate-activated protein kinase and peroxisome proliferator-activated receptor-alpha pathways, which in turn diminish the expression of pro-fibrotic genes. In addition, hyperadiponectinemia was noted in patients with various chronic liver diseases (CLDs)-related liver fibrosis. An increase in circulating adiponectin levels was also found to be associated with the development of liver fibrosis, indicating a role of adiponectin as a non-invasive biomarker for predicting the progression of liver fibrosis. It is therefore reasonable to speculate that adiponectin may be developed as a new therapeutic candidate for the treatment of liver fibrosis. Nonetheless, future observations are still necessary to fully elucidate the extent of the effects of adiponectin on liver fibrotic outcomes, in order to modify adiponectin as an anti-fibrotic therapy that would speed up fibrosis reversal in patients with CLD.

show abstract

“…They suggested that follow up of hyperinsulinemia by serial assessment of HOMA-IR in non-diabetic HCV infected patients may be a biochemical indicator for progression of liver fibrosis [46]. On the other hand, some studies found no association between insulin resistance and liver fibrosis, like the one from Carvalho et al who concluded that patients with chronic hepatitis C have significant metabolic alterations (hyperadiponectinemia and high HOMA-IR values) that are independent of HCV viremia and liver fibrosis [47].…”

Section: Hcv Disease Progression In Patients With Metabolic Alterationsmentioning

confidence: 99%

Metabolic Factors and Their Influence on the Clinical Course and Response to HCV Treatment

Villar¹,

Villela-Nogueira²,

Silva³

et al. 2018

Hepatitis C - From Infection to Cure

View full text Add to dashboard Cite

Nowadays, direct-acting antivirals (DAA) have been used for hepatitis C virus (HCV) treatment leading to cure in 90-95% of non-cirrhotic patients depending on genotype, treatment experience, and regimen used. It was observed rates of antiviral response above 90% in compensated cirrhotic patients that should be treated for long time and/or ribavirin may be required. Metabolic syndrome, obesity, and insulin resistance are increasing worldwide and further contribute to hepatic steatosis and have long been recognized as a cause of lipid deposition in the liver. These factors affect the rate of antiviral response to interferon-based therapy, but it seems not impact DAA treatment. The effect of HCV eradication on hepatic steatosis and progression to fibrosis, cirrhosis, and hepatocellular carcinoma warrants further study in the era of direct-acting antivirals. Other factors that could be related to increase liver damage are vitamin D and associated polymorphisms. Patients with low concentration of total vitamin D [25(OH)D] presented high degree of fibrosis and high values of total cholesterol and triglycerides. In this chapter, we review the challenges and metabolic pathology associated with HCV infection and, discuss the influence of some metabolic factors which can cause liver damage.

show abstract

Adiponectin levels and insulin resistance among patients with chronic hepatitis C

Cited by 8 publications

References 31 publications

Systematic review: chronic viral hepatitis and metabolic derangement

Systematic review: chronic viral hepatitis and metabolic derangement

Adiponectin as a novel biomarker for liver fibrosis

Metabolic Factors and Their Influence on the Clinical Course and Response to HCV Treatment

Contact Info

Product

Resources

About