Effect of curcumin on visfatin and zinc-α2-glycoprotein in a rat model of non-alcoholic fatty liver disease

Li, Changping; Li, Juehong; Chen, Yun; Zhong, Xiaolin; Kang, Min Kyung

doi:10.1590/s0102-865020160110000001

Cited by 17 publications

(15 citation statements)

References 37 publications

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“…In addition, GLP-1RA administration decreased the serum visfatin levels, but the difference was not statistically significant. Our results were consistent with those of the previous studies [6][7][8]23,26]. We believe that GLP-1RAs ameliorate NAFLD by regulating adipokine levels, both systemically and locally, partly independent of weight loss.…”

Section: Discussionsupporting

confidence: 93%

“…Meanwhile, serum visfatin levels showed a tendency toward a positive correlation, but the difference was not statistically significant, which may be due to the insufficient sample size. Our results were consistent with those of the previous studies [6][7][8]23,26]. To further investigate the relationship of adipokines and NAFLD, we used the in-phase and outof-phase MRI techniques, which have been reported to have a significant correlation with histologic findings of fatty liver, and to have high value in diagnosing and judging the degree of steatosis of NAFLD.…”

Section: Discussionsupporting

confidence: 89%

“…However, our previous study demonstrated that serum resistin levels were positively correlated with serum lipids and not with insulin resistance in first-degree relatives of patients with T2DM [22]. Li et al demonstrated that serum visfatin levels were significantly higher in NAFLD rats than in rats in the control group, whereas decreasing visfatin level was therapeutically beneficial [23]. However, the study by Johannsen et al, which included 2,429 human subjects, demonstrated no association between visfatin levels and the presence or absence of NAFLD or the degree of hepatic fatty infiltration [24], whereas Qiu et al reported that decreased circulating levels of visfatin and adiponectin were independently associated with an increased risk of NAFLD in 372 adults [25].…”

Section: Discussionmentioning

confidence: 83%

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Effect of glucagon-like peptide-1 receptor agonists on adipokine level of nonalcoholic fatty liver disease in rats fed high-fat diet

et al. 2020

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BackgroundNonalcoholic fatty liver disease (NAFLD) is the leading cause of liver disease worldwide, and no effective treatment exists until now. Glucagon-like peptide-1 receptor agonists are becoming the preferred therapeutic option for the management of obesity and are becoming the preferred treatment options for the management of both NAFLD and type 2 diabetes mellitus, but the molecular mechanisms are still unclear.MethodsForty-five healthy male Wistar rats were divided into three groups: normal control, high-fat diet (HFD) group, HFD + liraglutide (100 mg/kg body weight) group. Biochemical parameters and adipokine levels were examined in the serum of rats. In order to judge the degree of steatosis of NAFLD, the magnetic resonance imaging and histopathology of the liver were also studied.Results and conclusionLiraglutide caused a significant decrease in the serum fasting glucose and improved the insulin resistance, dyslipidemia, and liver enzymes. It reduced the adipokine level, and alleviated the histopathology of liver of rats in the steatosis, ballooning, and lobular inflammation when compared to the HFD group. Thus, liraglutide demonstrated amelioration of NAFLD by decreasing the adipokine levels in this animal model and seems to be a promising molecule for the management of NAFLD.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 83%

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Effect of glucagon-like peptide-1 receptor agonists on adipokine level of nonalcoholic fatty liver disease in rats fed high-fat diet

et al. 2020

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“…Previous studies have shown that zinc-α-2-glycoprotein was a better predictor for IR than HOMA-IR index ( 156 – 158 ). Zinc-α-2-glycoprotein acts via interaction with p-ERK and TGF-β1, promoting proliferation of endothelial precursors, suppression of low-grade inflammation, regulation of metabolism of ketone bodies, and increased expression of visfatin in target cells ( 159 , 160 ). There is evidence that zinc-α-2-glycoprotein prevents cardiac hypertrophy and improves diastolic performances probably due to attenuation of cardiac fibrosis ( 161 ).…”

Section: Adipose Tissue Dysfunction and Heart Failurementioning

confidence: 99%

Emerging Role of Adipocyte Dysfunction in Inducing Heart Failure Among Obese Patients With Prediabetes and Known Diabetes Mellitus

Berezin

Lichtenauer

2020

Front. Cardiovasc. Med.

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Adipose tissue dysfunction is a predictor for cardiovascular (CV) events and heart failure (HF) in patient population with obesity, metabolic syndrome, and known type 2 diabetes mellitus. Previous preclinical and clinical studies have yielded controversial findings regarding the role of accumulation of adipose tissue various types in CV risk and HF-related clinical outcomes in obese patients. There is evidence for direct impact of infiltration of epicardial adipocytes into the underlying myocardium to induce adverse cardiac remodeling and mediate HF development and atrial fibrillation. Additionally, perivascular adipocytes accumulation is responsible for release of proinflammatory adipocytokines (adiponectin, leptin, resistin), stimulation of oxidative stress, macrophage phenotype switching, and worsening vascular reparation, which all lead to microvascular inflammation, endothelial dysfunction, atherosclerosis acceleration, and finally to increase in CV mortality. However, systemic effects of white and brown adipose tissue can be different, and adipogenesis including browning of adipose tissue and deficiency of anti-inflammatory adipocytokines (visfatin, omentin, zinc-α2-glycoprotein, glypican-4) was frequently associated with adipose triglyceride lipase augmentation, altered glucose homeostasis, resistance to insulin of skeletal muscles, increased cardiomyocyte apoptosis, lowered survival, and weak function of progenitor endothelial cells, which could significantly influence on HF development, as well as end-organ fibrosis and multiple comorbidities. The exact underlying mechanisms for these effects are not fully understood, while they are essential to help develop improved treatment strategies. The aim of the review is to summarize the evidence showing that adipocyte dysfunction may induce the onset of HF and support advance of HF through different biological mechanisms involving inflammation, pericardial, and perivascular adipose tissue accumulation, adverse and electrical cardiac remodeling, and skeletal muscle dysfunction. The unbalancing effects of natriuretic peptides, neprilysin, and components of renin-angiotensin system, as exacerbating cause of altered adipocytokine signaling Berezin et al. Adipocyte Dysfunction in Heart Failure on myocardium and vasculature, in obesity patients at high risk of HF are disputed. The profile of proinflammatory and anti-inflammatory adipocytokines as promising biomarker for HF risk stratification is discussed in the review.

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“…Turmeric (active ingredient curcumin), also known as the Siam tulip, is a plant most notably cultivated in India as a spice recognized by its yellow color. Turmeric has been studied to be a therapeutic agent for NAFLD patients [ 64 , 65 , 66 , 67 , 68 , 69 , 70 , 71 , 72 , 73 , 74 , 75 , 76 , 77 , 78 ]. Curcumin is acknowledged as powerful antioxidant and anti-inflammatory agent, in addition to its many other beneficial features [ 74 ].…”

Section: Household Herbsmentioning

confidence: 99%

Potential Therapeutic Benefits of Herbs and Supplements in Patients with NAFLD

Perumpail

Iqbal

et al. 2018

Diseases

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Our aim is to review the efficacy of various herbs and supplements as a possible therapeutic option in the treatment and/or prevention of nonalcoholic fatty liver disease (NAFLD). We performed a systematic review of medical literature using the PubMed Database by searching the chemical names of many common herbs and supplements with “AND (NAFLD or NASH)”. Studies and medical literature that discussed the roles and usage of herbs and supplements in NAFLD and nonalcoholic steatohepatitis (NASH) from inception until 20 June 2018 were reviewed. Many studies have claimed that the use of various herbs and supplements may improve disease endpoints and outcomes related to NAFLD and/or NASH. Improvement in liver function tests were noted. Amelioration or reduction of lobular inflammation, hepatic steatosis, and fibrosis were also noted. However, well-designed studies demonstrating improved clinical outcomes are lacking. Furthermore, experts remain concerned about the lack of regulation of herbs/supplements and the need for further research on potential adverse effects and herb–drug interactions. In conclusion, preliminary data on several herbs have demonstrated promising antioxidant, anti-inflammatory, anti-apoptotic, and anti-adipogenic properties that may help curtail the progression of NAFLD/NASH. Clinical trials testing the safety and efficacy must be completed before widespread use can be recommended.

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Effect of curcumin on visfatin and zinc-α2-glycoprotein in a rat model of non-alcoholic fatty liver disease

Cited by 17 publications

References 37 publications

Effect of glucagon-like peptide-1 receptor agonists on adipokine level of nonalcoholic fatty liver disease in rats fed high-fat diet

Effect of glucagon-like peptide-1 receptor agonists on adipokine level of nonalcoholic fatty liver disease in rats fed high-fat diet

Emerging Role of Adipocyte Dysfunction in Inducing Heart Failure Among Obese Patients With Prediabetes and Known Diabetes Mellitus

Potential Therapeutic Benefits of Herbs and Supplements in Patients with NAFLD

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