Figure 4 - uploaded by Jinqian Zhang
Content may be subject to copyright.
Source publication
HBV infection is a serious public health problem worldwide, which can contribute to the incidence of chronic hepatitis B (CHB), cirrhosis, and hepatocellular carcinoma (HCC).
In the present report, we assessed the association between adiponectin, its receptors and hepatic steatosis, fibrosis, and inflammation with hepatitis B virus.
Liver biopsies...
Contexts in source publication
Context 1
... there was no correla- tion between serum adiponectin, and hepatic adiponec- tin, adipoR1 or adipoR2 mRNA expression in any group, respectively. As shown in Figure 4, the adipoR1 mRNA ex- pression tended to be lower in liver biopsies of subjects with steatosis without reaching statistical significance (4.58 ±0.37 vs. 4.59 ± 0.47, P = 0.880) compared to sub- jects without steatosis. As shown in Figure 5, the adipoR2 mRNA expression was significantly decreased in liver bi- opsies of patients with steatosis compared to those with- out steatosis (3.57 ...
Context 2
... 0.33 vs. 7.12 ± 0.67; P = 0.000). AdipoR1/ GAPDH, and adipoR2/GAPDH cDNA ratios are shown in (Figures 4 and 5). The expression of adipoR1 mRNA normalized to GAPDH tended to be low- er in liver biopsies of subjects with steatosis without reaching statistical significance (4.58 ± 0.37 vs. 4.59 ± 0.47, P = 0.880) compared to the subjects without steatosis. ...
Similar publications
Objective
To assess the effect of a mixture of five herbal extracts (FT-5) on insulin resistance, glucose/lipid metabolism, hepatic steatosis, and to investigate whether the combination of FT-5 and pioglitazone would provide a robust effect on diabetes treatment, while may minimize undesirable side-effects of pioglitazone in diabetic Ay gene (KKAy)...
Citations
... This has also been found for human patients with simple steatosis and non-alcoholic steatohepatitis (NASH) [15]. The expression of ADIPOQ in the walls of liver vessels and in macrophages has already been shown in biopsies of chronic hepatitis B (CHB) patients with negatively stained hepatocytes [27]. Hepatocytes are found to be a source of ADIPOQ in liver diseases, while hepatic stellate cells (HSCs) in the quiescent and activated state are described to express ADIPOQ at the mRNA and protein levels [28,29]. ...
... ADIPOQ receptor2 (ADIPOR2) expression is already known to be liver-specific, but we also noted ADIPOR1 expression in hepatocytes, which is described as muscle-specific; however, it was also found in the liver tissue of humans and rodents [16,22,27,29]. ADIPOR1 with ADIPOR2 was previously described for HSCs in liver tissue [29]. ...
... The expression of ADIPOR1 is mainly found in the endothelium and KCs, but there is also some weak expression in hepatocytes. ADIPOR1 expression at the mRNA level in the liver has been detected in liver biopsies of CHB patients and tended to be higher in patients without steatosis [27]. These authors found the immunolocalization of ADIPOR2 on liver slides of the patients, but did not do the same for ADIPOR1, so it was impossible to establish the cellular localization of ADIPOR1 in liver tissue in this study [27]. ...
Background: The positive effects of prolonged every-other-day (EOD) feeding include decreased body weight and prolonged life span, but also changes in liver metabolism and functions. In the present paper, our aim was to examine the expression of adiponectin (ADIPOQ), leptin, and their receptors (ADIPOR1, ADIPOR2, and LEPR) in the liver tissue of EOD-fed mice in comparison to ad libitum (AL)-treated mice. Methods: After 9 months of EOD treatment, liver tissue was harvested and prepared for analysis. RT-PCR, protein semi-quantitative estimation, and cellular immunolocalization was performed. Results: We noted a decreased expression of leptin in the liver tissue of the EOD male mice in comparison to the AL mice on the protein level. ADIPOQ receptor R1 protein expression was decreased in the liver of EOD-fed male mice, while the expression of ADIPOR2 on the protein level was increased in the EOD animals. Conclusions: To the best of our knowledge, this is the first report showing ADIPOQ and leptin immunolocalization in the liver tissue in a dietary regime experiment. Decreases in leptin expression and IL-6 expression in liver tissue and increases in ADIPOR2 expression may be partly responsible for the beneficial effects of EOD treatment in the liver, including the decrease in inflammation. Further studies are needed to establish whether these changes depend on factors like the type of treatment, species, strain, gender, time of treatment, and others.
... Patients with chronic HBV infection display a high level of adiponectin and this level decreases during interferon therapy along with HBV viral load (253,310). In these patients the level of adiponectin correlates with various stages of liver injury from liver inflammation and fibrosis to HCC (67,311). Current reports indicate that adiponectin may promote HBV polymerase activity and HBV DNA replication, while in turn HBV replication induces the expression of adiponectin (312). ...
... The level of adiponectin differs in patients with HBV compared with non-HBV/NAFLD patients where, for example, the level of adiponectin decreases with the development of MetS and NASH yet may increase in patients with cirrhosis regardless of metabolic factors (133,252,313). In other studies, however, liver histology indicates a correlation between adiponectin and steatosis but not between adiponectin and viral factors (311). ...
Non-alcoholic fatty liver disease (NAFLD) is strongly associated with the metabolic syndrome and is one of the most prevalent comorbidities in HIV and HBV infected patients. HIV plays an early and direct role in the development of metabolic syndrome by disrupting the mechanism of adipogenesis and synthesis of adipokines. Adipokines, molecules that regulate the lipid metabolism, also contribute to the progression of NAFLD either directly or via hepatic organokines (hepatokines). Most hepatokines play a direct role in lipid homeostasis and liver inflammation but their role in the evolution of NAFLD is not well defined. The role of HBV in the pathogenesis of NAFLD is controversial. HBV has been previously associated with a decreased level of triglycerides and with a protective role against the development of steatosis and metabolic syndrome. At the same time HBV displays a high fibrogenetic and oncogenetic potential. In the HIV/HBV co-infection, the metabolic changes are initiated by mitochondrial dysfunction as well as by the fatty overload of the liver, two interconnected mechanisms. The evolution of NAFLD is further perpetuated by the inflammatory response to these viral agents and by the variable toxicity of the antiretroviral therapy. The current article discusses the pathogenic changes and the contribution of the hepatokine/adipokine axis in the development of NAFLD as well as the implications of HIV and HBV infection in the breakdown of the hepatokine/adipokine axis and NAFLD progression.
... 26 The associations of adiponectin levels with HBV and HCV infections are quite different and associated with different clinical outcomes of liver diseases. [27][28][29][30][31][32] This comprehensive review summarises current knowledge of the associations of chronic HBV and HCV infection with metabolic derangements and extrahepatic diseases, including MetS, fatty liver, lipid metabolism, insulin resistance/T2DM, adiponectin and arteriosclerosis. ...
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.
... These results suggest that adiponectin may exert its biological effects by interacting with adipoR1 on the surface of ovarian cancer cells. In a previous study it was reported that 87.30 % of patients with epithelial ovarian cancer expressed adipoR1, an indication that adipoR1 is highly expressed in obesityrelated cancers [31]. Some authors have reported that the ratio of adipoR1 to R2 in follicular cells of patients with polycystic ovary was significantly higher than that in normal tissues [32]. ...
Purpose: To elucidate the effects and the underlying mechanism of adiponectin on human ovarian cancer cells. Methods: The level of adiponectin, adiponectin receptor-1, caspase-3 and bcl-2 in the serum and ascites of the patients were measured with enzyme-linked immunosorbent assay (ELISA), qPCR and Western blotting. The human ovarian cancer cell lines (Caov3 and SKOV3) were enumerated using 3-(4,5-dimethylthiazol-2-yl)-2,5-tetrazolium bromide (MTT) assay. Western blotting was also used to determine the levels of p-Akt, p-ERK and cyclin B. Results: Serum and ascite levels of adiponectin were significantly higher in ovarian cancer patients than in healthy patients (p < 0.05). Expression of adiponectin in the serum and ascites of patients in FIGO stage IV was remarkably higher than in earlier stages (p < 0.05). The proliferative effect of adiponectin on ovarian cells was dose-dependent. Adiponectin treatment significantly increased the expression of cyclin B in Caov3 and SKOV3, and reduced the levels of caspase-3 and bcl-2. Inhibitors of PI3K and MEK pathways significantly reduced the proliferation of attenuated Caov3 and SKOV3 by up-regulating cyclin B upon adiponectin treatment (p < 0.05), and thus alleviated the inhibitory effect of adiponectin on the expressions of caspase-3 and bcl-2. Conclusion: The findings demonstrate that adiponectin promotes proliferation of the cells via the PI3K/Akt and Raf/MEK/ERK pathways, and also provide new insights into ovarian cancer treatmment. © Pharmacotherapy Group, Faculty of Pharmacy, University of Benin, Benin City, 300001 Nigeria and 2018 The authors.
... Thirteen studies were carried out in patients with NAFLD and two studies in patients with CLD of different etiologies. Two studies among patients with CHB found no correlation between serum adiponectin and the stage of liver fibrosis [47,58]. The remaining two studies by Hui et al. and Liu et al. reported a significant association between the increased serum adiponectin and advanced liver fibrosis/cirrhosis using multivariate and univariate analyses, respectively [59,60]. ...
Chronic liver disease (CLD) is a major health problem worldwide. Non-alcoholic fatty liver disease (NAFLD), chronic hepatitis C (CHC), chronic hepatitis B (CHB), and alcoholic liver disease (ALD) are the most common etiologies of CLD. Liver biopsy is the gold standard for assessment of liver fibrosis, however, it is an invasive method. This review attempts to evaluate the usefulness of serum adiponectin, serum leptin, serum ferritin, serum transforming growth factor-β1 (TGF-β1), and serum platelet derived growth factor-BB (PDGF-BB) as non-invasive markers in the diagnosis of liver fibrosis/cirrhosis. A systematic search in MEDLINE, Web of Science, Scopus, and local databases was performed to identify articles published in English or Persian as of November 2017. Studies conducted among CLD patients, with biopsy proven fibrosis/cirrhosis, and providing sufficient details of patients’ clinicopathological characteristics were included. In the 95 studies included, there were a total of 15,548 CLD patients. More than 83% of studies were carried out in Asia and Europe. The relationship between liver fibrosis/cirrhosis and serum levels of ferritin, adiponectin, leptin, TGF-β1, and PDGF-BB was assessed in 42, 33, 27, nine, and three studies, respectively. Serum levels of the markers, particularly ferritin, could successfully predict liver fibrosis/cirrhosis, however, these data might not be clinically replicated and further studies are needed.
... HS has not been shown to have a negative impact on treatment and progression in CHB [21]. Wu et al. [22] found that adiponectin might be impaired in CHB with HS. In addition, they declared that reduced liver adiponectin expression may contribute to pathogenesis and the progression of CHB with HS [22]. ...
... Wu et al. [22] found that adiponectin might be impaired in CHB with HS. In addition, they declared that reduced liver adiponectin expression may contribute to pathogenesis and the progression of CHB with HS [22]. ...
Objectives: Our aim was to investigate the association of liver fibrosis and necroinflammation with HS in untreated young patients with chronic hepatitis B (CHB).
Materials and Methods: A retrospective study was conducted in a military hospital in Turkey. A total of 254 subjects with CHB were included in this study. These subjects were divided into two groups: group 1 consisted of patients with hepatic steatosis (HS) according to ultrasonography (USG) and group 2 consisted of non-HS subjects. Sociodemographic, biochemical, histopathological, virological and USG results were recorded for both groups retrospectively. Statistical analysis was performed using SPSS 22.0.
Results: The prevalence of HS was found to be 11.4 %. A significant statistical difference was found between group 1 and group 2 regarding the fibrosis degree (p=0.045). No statistically significant difference was noted between two groups for age, levels of ALT, AST, HBeAg, HBV-DNA levels, HAI scores, diagnosis age and duration of CHB. No difference was noted between the grade of HS and variables. A positive correlation was found between fibrosis groups and the grade of HS (p= 0.012, r= 0.158) and between HAI groups and the grade of HS (p=0.029, r= 0.137).
Conclusion: The prevalence of steatosis was not higher in patients with CHB. HS is associated with advanced hepatic fibrosis, but not viral liver disease.
... Both AdipoR1 and AdipoR2 are expressed on the surface of peripheral blood mononuclear cells (PBMCs) [10]. The expression of adiponectin receptors on PBMCs is modulated by clinical conditions such as being overweight with coronary artery disease [11], severe obesity [12][13], T2DM [14] and patients with end-stage kidney disease [15]. These observations indicate a possible link between adiponectin signalling and metabolic diseases. ...
... Exercise training has an insulin sensitizing effect like adiponectin in that exercise training also promotes glucose uptake into skeletal muscle and stimulates fatty acid oxidation [6]. Although changes in metabolic conditions are known to alter adiponectin receptor expression levels in PBMCs [11][12][13][14][15], little is known regarding whether lifestyle interventions, including exercise and/or exercise training, modulate the expression of AdipoR1 and AdipoR2 genes in PBMCs. ...
Little is known about the effect of exercise training on the expression of adiponectin receptor genes in peripheral blood mononuclear cells (PBMCs). In this study, we investigated the effects of aerobic training on the expression of AdipoR1 and AidpoR2 mRNAs in PBMCs, whole body insulin sensitivity, and circulating adiponectins in men. Thirty young men were randomly assigned to either a control (n=15) or an exercise (n=15) group. Subjects assigned to the exercise group underwent a 12-week jogging and/or running programme on a motor-driven treadmill at an intensity of 60%-75% of the age-based maximum heart rate with duration of 40 minutes per session and a frequency of 5 days per week. Two-way mixed ANOVA with repeated measures was used to test any significant time-by-group interaction effects for the measured variables at p=0.05. We found significant time-by-group interaction effects for waist circumference (p=0.001), VO2max (p<0.001), fasting insulin (p=0.016), homeostasis model assessment for insulin resistance (HOMA-IR) (p=0.010), area under the curve (AUC) for insulin response during the 75-g oral glucose tolerance test (p=0.002), high-molecular weight (HMW) adiponectin (p=0.016), and the PBMC mRNA levels of AdipoR1 (p<0.001) and AdipoR2 (p=0.001). The exercise group had significantly increased mRNA levels of AdipoR1 and AdipoR2 in PBMCs, along with increased whole body insulin sensitivity and HMW adiponectin, decreased waist circumference, and increased VO2max compared with the control group. In summary, the current findings suggest that exercise training modulates the expression of AdipoR1 and AdipoR2 mRNAs in PBMCs, implying that manipulation of the expression of these genes could be a potential surrogate for lifestyle intervention-mediated improvements of whole body insulin sensitivity and glucose homeostasis.
... Several studies reported the association between serum adipocytokine levels and liver histology in CHB patients. One study explored the association of serum adiponectin levels and liver histology in 89 CHB patients [55]. Although the authors did not identify any association between serum adiponectin levels and liver fibrosis stage, the immunohistochemistry of liver biopsies showed a significant association between hepatic adiponectin immunoreactivity and liver fibrosis stage. ...
Adipocytokines play an important role in lipid metabolism and liver disease progression. However, the interactions between hepatitis B virus (HBV) infection and adipocytokines remain largely unknown.
To investigate the association of HBV infection with adipocytokines in HBV-infected and noninfected subjects. In addition, the impact of adipocytokines on serum HBV DNA, HBsAg levels and liver fibrosis stage was also examined.
A case-control analysis of patients with and without chronic HBV infection was performed. The HBV group consisted of 187 patients with chronic HBV infection, and the control group consisted of 184 age-, gender- and body mass index-matched subjects without HBV infection. Fasting blood glucose, lipid profiles, adiponectin, leptin and visfatin levels were compared between the two groups. APRI and FIB-4 were calculated to estimate the severity of liver fibrosis.
Most of the enrolled subjects had lower ALT levels [228 (57.7 %) ALT < ULN] and milder hepatic fibrosis [381 (96.5 %) APRI < 0.7; 307 (77.7 %) FIB4 < 1.45]. The HBV group had significantly higher serum adiponectin and visfatin but lower leptin levels than the control group. This difference remained significant after adjustment for age, sex, BMI and ALT levels (p < 0.05). Serum adiponectin, leptin and visfatin levels were significantly associated with serum HBsAg and HBV DNA levels (p < 0.05). In addition, a higher serum adiponectin level was associated with advanced liver fibrosis in elder male HBeAg-negative patients.
Patients with chronic HBV infection have significantly higher serum adiponectin and visfatin but lower leptin levels than healthy controls. Serum adipocytokine levels independently correlate with HBV viremia, HBsAg levels and liver fibrosis stages.
... In the past decade, an increasing number of studies have demonstrated the involvement of various adipokines in the process of liver cirrhosis, of which the most important are leptin (1), adiponectin (2), tumor necrosis factor-α, resistin and interleukin-6 (3,4). Visfatin, a novel adipokine which has insulin-like effects, regulates inflammatory and immunomodulatory processes (5,6) and catalyzes the rate-limiting step in the production of nicotinamide adenine dinucleotide from nicotinamide. ...
The present study was conducted to investigate the effects of visfatin on the activation of hepatic stellate cells (HSC) and the possible underlying mechanism. HSC were isolated from the livers of Sprague‑Dawley rats by in situ perfusion of collagenase and pronase and a single‑step density Nycodenz gradient. The culture‑activated cells were serum‑starved and incubated with different concentrations of recombinant visfatin (0, 25, 50, 100 or 200 ng/ml) for 24 h. The expression of α‑smooth muscle actin (α‑SMA), collagen types I and III and connective tissue growth factor (CTGF) were then measured by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blot analysis. The results demonstrated that 100 and 200 ng/ml concentrations of visfatin induced the expression of α‑SMA in culture‑activated rat HSC, which was accompanied by a significant increase in collagen types I and III, as confirmed by western blot and RT‑qPCR analyses. In addition, treatment of the HSC with certain concentrations of visfatin upregulated the expression of CTGF. These findings suggested that visfatin activated HSC and induced the production of collagen types I and III.
... Moreover, our results indicate that insulin resistance and adipokines are involved in the pathogenesis of liver injury in patients with HCV infection. The results of the present study confirm those of others insofar that hepatic steatosis was positively related to HOMA-IR index and hypoadiponectinemia [13,14] . Interestingly, the reduced hepatic expression of adiponectin was also demonstrated in chronic hepatitis B patients with hepatic steatosis [13] . ...
... The results of the present study confirm those of others insofar that hepatic steatosis was positively related to HOMA-IR index and hypoadiponectinemia [13,14] . Interestingly, the reduced hepatic expression of adiponectin was also demonstrated in chronic hepatitis B patients with hepatic steatosis [13] . Numerous studies have indicated that adiponectin stimulates matrix metalloproteinase complexes [14,15] . ...
Aim:
To analyze adipokine concentrations, insulin resistance and hepatic expression of suppressor of cytokine signaling 3 (SOCS-3) in patients with chronic hepatitis C genotype 1 with normal body weight, glucose and lipid profile.
Methods:
The study group consisted of 31 patients with chronic hepatitis C and 9 healthy subjects. Total levels of adiponectin, leptin, resistin, visfatin, omentin, osteopontin and insulin were measured using an ELISA kit. The hepatic expression of SOCS-3 was determined by the use of the reverse transcription polymerase chain reaction method.
Results:
Homeostasis model assessment for insulin resistance (HOMA-IR) values were significantly higher in hepatitis C virus (HCV) infected patients without metabolic disorders compared to healthy controls (2.24 vs 0.59, P = 0.0003). Hepatic steatosis was observed in 32.2% of patients with HCV infection and was found in patients with increased HOMA-IR index (2.81 vs 1.99, P = 0.05) and reduced adiponectin level (5.96 vs 8.37, P = 0.04). Inflammatory activity (G ≥ 2) was related to increased osteopontin concentration (34.04 vs 23.35, P = 0.03). Advanced liver fibrosis (S ≥ 2) was associated with increased levels of omentin and osteopontin (436.94 vs 360.09, P = 0.03 and 32.84 vs 20.29, P = 0.03) and reduced resistin concentration (1.40 vs 1.74, P = 0.047). No correlations were reported between adipokine profile, HOMA-IR values and hepatic expression of the SOCS-3 gene.
Conclusion:
We speculated that no relationship between adipokines and HOMA-IR values may indicate that HCV can induce insulin resistance itself. Some adipokines appear to be biochemical markers of steatosis, inflammation and fibrosis in patients with chronic HCV infection. © 2014 Baishideng Publishing Group Inc. All rights reserved.
