Significance of serum adiponectin levels in patients with chronic liver disease

Balmer, Maria L.; Joneli, Jeannine; Schoepfer, A; Stickel, Felix; Thormann, Wolfgang; Dufour, Jean–François

doi:10.1042/cs20100008

Cited by 52 publications

(49 citation statements)

References 22 publications

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“…It is now well established that adiponectin is elevated in advanced liver disease and cirrhosis of any cause, although most evidence exists for viral, autoimmune, cholestatic, and alcohol‐related disease 15, 17, 18. A single report has directly linked NASH cirrhosis with elevated adiponectin,29 but others have included numerous patients with cryptogenic cirrhosis, in whom NASH is highly probable 5, 6…”

Section: Discussionmentioning

confidence: 99%

Hepatic fat loss in advanced nonalcoholic steatohepatitis: Are alterations in serum adiponectin the cause?

Samer²,

et al. 2013

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Advanced liver fibrosis in nonalcoholic steatohepatitis (NASH) is often accompanied by a reduction in hepatic fat to the point of complete fat loss (burnt-out NASH), but the mechanisms behind this phenomenon have not been elucidated. Adiponectin is raised in cirrhosis of any cause and has potent antisteatotic activity. In this study we examined 65 patients with advanced biopsy-proven NASH (fibrosis stage 3-4) and 54 with mild disease (fibrosis stage 0-1) to determine if disappearance of steatosis correlated with changes in serum adiponectin. All patents had fasting blood tests and anthropometric measures at the time of liver biopsy. Liver fat was accurately quantitated by morphometry. Serum adiponectin was measured by immunoassay. When compared to those with early disease, patients with advanced NASH were more insulin-resistant, viscerally obese, and older, but there was no difference in liver fat content or adiponectin levels. Adiponectin had a significant negative correlation with liver fat percentage in the whole cohort (r 5 20.28, P < 0.01), driven by patients with advanced NASH (r 5 20.40, P < 0.01). In advanced NASH, for each 4 lg/L increase in adiponectin there was an odds ratio OR of 2.0 (95% confidence interval [CI]: 1.3-3.0, P < 0.01) for a 5% reduction in hepatic fat. Adiponectin was highly and significantly associated with almost complete hepatic fat loss or burnt-out NASH (12.1 versus 7.4 lg/L, P 5 0.001) on multivariate analysis. A relationship between adiponectin, bile acids, and adipocyte fexaramine activation was demonstrated in vivo and in vitro, suggestive of hepatocyte-adipocyte crosstalk. Conclusion: Serum adiponectin levels in advanced NASH are independently associated with hepatic fat loss. Adiponectin may in part be responsible for the paradox of burnt-out NASH.

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Section: Discussionmentioning

confidence: 99%

Hepatic fat loss in advanced nonalcoholic steatohepatitis: Are alterations in serum adiponectin the cause?

Samer²,

et al. 2013

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“…However, blood adiponectin concentration was similar between patients with NASH-related cirrhosis and cirrhosis from other causes (24,37), indicating that the stage of the liver disease should also be taken into account when examining adiponectin in liver diseases, as liver could be one of the sites for adiponectin degradation. It was also found that adiponectin was positively correlated with surrogate markers of hepatic fibrosis, including transient elastography, fasting serum bile acids, and hyaluronate (37). A recent cross-sectional study showed that HBV-related HCC patients had higher adiponectin levels in comparison with healthy controls, patients with chronic hepatitis B, and cirrhosis patients (36).…”

Section: Discussionmentioning

confidence: 99%

“…Adiponectin was consistently shown to be lower in metabolic liver diseases, including NAFLD and NASH (35), but elevated in advanced liver disease like cirrhosis (24,36,37) and increases along with the severity of disease (23). However, blood adiponectin concentration was similar between patients with NASH-related cirrhosis and cirrhosis from other causes (24,37), indicating that the stage of the liver disease should also be taken into account when examining adiponectin in liver diseases, as liver could be one of the sites for adiponectin degradation. It was also found that adiponectin was positively correlated with surrogate markers of hepatic fibrosis, including transient elastography, fasting serum bile acids, and hyaluronate (37).…”

Section: Discussionmentioning

confidence: 99%

Plasma Adipokines and Risk of Hepatocellular Carcinoma in Chronic Hepatitis B Virus–Infected Carriers: A Prospective Study in Taiwan

Chen

Yang

et al. 2014

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background: Obesity is considered a risk factor for hepatocellular carcinoma (HCC). The relationship between adipocytokine and HCC in hepatitis B virus (HBV) carriers remains unclear. We prospectively investigated the association of adiponectin, leptin, and visfatin levels with HCC.Methods: We conducted a nested case-control study in a community-based cohort with 187 incident HCC and 374 HCC-free HBV carriers. Unconditional logistic regression was conducted to estimate the ORs and 95% confidence intervals (CI).Results: Adiponectin, but not leptin and visfatin, levels were associated with an increased risk of HCC after adjustment for other metabolic factors and HBV-related factors. The risk was increased [OR ¼ 0.51; 95% CI, 0.12-2.11; OR ¼ 4.88 (1.46-16.3); OR ¼ 3.79 (1.10-13.0); OR ¼ 4.13 (1.13-15.1) with each additional quintiles, respectively] with a significant dose-response trend (P trend ¼ 0.003). HCC risk associated with higher adiponectin level was higher in HBV carriers with ultrasonographic fatty liver, genotype C infection, higher viral load, and with elevated alanine aminotransferase. Longitudinally, participants with higher adiponectin were less likely to achieve surface antigen of hepatitis B virus (HBsAg) seroclearance and more likely to have persistently higher HBV DNA. Eventually, they were more likely to develop liver cirrhosis [OR ¼ 1.65 (0.62-4.39); OR ¼ 3.85 (1.47-10.1); OR ¼ 2.56 (0.96-6.84); OR ¼ 3.76 (1.33-10.7) for the second, third, fourth, and fifth quintiles, respectively; P trend ¼ 0.017] before HCC.Conclusions: Elevated adiponectin levels were independently associated with an increased risk of HCC. Impact: Adiponectin may play different roles in the virus-induced and metabolic-related liver diseases, but the underlying mechanism remains unknown. Cancer Epidemiol Biomarkers Prev; 23(8); 1659-71. Ó2014 AACR.

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“…Adiponectin is believed to be negatively regulated by BAs, as patients with NASH had high levels of BAs but low levels of adiponectin (Bechmann et al, 2013). One study found increased levels of adiponectin in patients with cirrhosis possibly indicating that adiponectin levels begin to increase again after NASH progression into fibrosis and cirrhosis (Balmer et al, 2010). Adiponectin also activates ceramidase, which has recently been implicated in the progression of NAFLD to NASH (Dasarathy et al, 2011; Holland et al, 2013; Silva et al, 2014).…”

Section: Bas and Glucose Cholesterol And Lipid Metabolism Pathwaysmentioning

confidence: 99%

The role of bile acids in nonalcoholic fatty liver disease and nonalcoholic steatohepatitis

Chow

Lee

Guo

2017

Molecular Aspects of Medicine

121

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Nonalcoholic fatty liver disease is growing in prevalence worldwide. It is started by the presence of macrosteatosis on liver histology but is often clinically asymptomatic. However, it can progress into nonalcoholic steatohepatitis which is a more severe form of liver disease characterized by inflammation and fibrosis. Further progression leads to cirrhosis, which predisposes patients to hepatocellular carcinoma or liver failure. The mechanism by which simple steatosis progresses to steatohepatitis is not entirely clear. However, multiple pathways have been proposed. A common link amongst many of these pathways is disruption of the homeostasis of bile acids. Other than aiding in the absorption of lipids and lipid-soluble vitamins, bile acids act as ligands. For example, they bind to farnesoid X receptor, which is critically involved in many of the pathways responsible for maintaining bile acid, glucose, and lipid homeostasis. Alterations to these pathways can lead to deregulation in energy balance and increased inflammation and fibrosis. Repeated insults over time may be the key to development of steatohepatitis. For this reason, current drugs target aspects of these pathways to try to reduce and halt inflammation and fibrosis. This review will focus on the role of bile acids in these various pathways and how changes in these pathways may result in steatohepatitis. While there is no approved pharmaceutical treatment for either hepatic steatosis or steatohepatitis, this review will also touch upon the multitude of potential therapies.

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Significance of serum adiponectin levels in patients with chronic liver disease

Cited by 52 publications

References 22 publications

Hepatic fat loss in advanced nonalcoholic steatohepatitis: Are alterations in serum adiponectin the cause?

Hepatic fat loss in advanced nonalcoholic steatohepatitis: Are alterations in serum adiponectin the cause?

Plasma Adipokines and Risk of Hepatocellular Carcinoma in Chronic Hepatitis B Virus–Infected Carriers: A Prospective Study in Taiwan

The role of bile acids in nonalcoholic fatty liver disease and nonalcoholic steatohepatitis

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