Adiponectin Levels in Graves' Disease – Systematic Review and Meta-Analysis
Abdulrahman IsmaielA L AbunahlehAdam ElSayedDaniel-Corneliu LeucuțaStefan‐Lucian PopaMohamed IsmaielDan L. Dumitraşcu
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Abstract:
Graves' disease is the most prevalent cause of hyperthyroidism worldwide. Adiponectin, the most abundant adipokine, plays a significant role in a cluster of prevalent diseases connected to metabolic disorders.Although the association between adiponectin and Graves' disease has been studied, the existing data is inconsistent. Therefore, we conducted this systematic review and meta-analysis to evaluate the relationship between adiponectin levels and Graves' disease.We performed a systematic electronic search on PubMed, EMBASE, Scopus and Cochrane Library using predefined keywords. We used the NHLBI quality assessment tools to assess the included studies.There were 11 studies involving 781 subjects included in our qualitative synthesis, while 6 studies were included in our quantitative synthesis. We observed significantly increased adiponectin levels in Graves' disease patients compared to controls (MD 2.983 [95% CI 0.138-5.828]) and hypothyroidism patients (MD 3.389 [95% CI 1.332-5.446]). Nevertheless, no significant MD was observed when comparing Graves' disease patients with and without Graves' ophthalmopathy (MD -27.124 [95% CI -88.893 - 34.645]).Adiponectin levels were significantly higher in patients with Graves' disease compared to controls and hypothyroidism patients. However, patients with and without Graves' ophthalmopathy did not present a significant mean difference in adiponectin levels.Keywords:
Graves' ophthalmopathy
The aim of this study was to investigate whether recurrent pregnancy loss (RPL) is associated with adipokine gene polymorphisms (namely the leptin -2548 (G/A), adiponectin 276 (G/T), and adiponectin 45 (T/G) polymorphisms) and/or adipokine serum levels.A total of 145 women participated in the study. For the analysis of serum adipokine levels, 19 healthy fertile women (control group) and 60 women suffering from RPL were included. For the polymorphism analysis, 126 women suffering from RPL were included. Serum adipokine levels were determined using a commercial radioimmunoassay kit. Adipokine polymorphisms were analyzed using an allele-specific polymerase chain reaction (PCR).Our immunoassays revealed that serum leptin levels were similar in control and RPL groups (17.34 and 20.16 ng/mL, respectively). In contrast, serum adiponectin levels were significantly higher in women with RPL than in controls (9.83 and 6.89 μg/mL, respectively; P < 0.05). Unfortunately, our allele-specific PCR experiments did not reveal any significant differences in allele frequency between women with RPL and NCBI allele frequencies.This study demonstrates that adiponectinemia is increased in patients suffering from RPL. However, association of adiponectin with adverse pregnancy outcomes remains to be elucidated.
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Adipose tissue has been identified as an endocrine organ secreting adipokines involved in metabolic and inflammatory pathways. Adiponectin, an anti-inflammatory adipokine, is reduced in sepsis. High Molecular Weight (HMW) adiponectin, the biologically most relevant molecule, has been investigated very little in human sepsis. Zinc-alpha2-glycoprotein (ZAG) is a novel adipokine and its expression in adipose tissue is positively correlated with adiponectin expression. It is not yet known whether ZAG has a role in sepsis. In this study we assessed levels of HMW adiponectin and ZAG during different stages of sepsis. A prospective observational pilot study was carried out on 21 septic patients. Serum samples were taken on day 1 and 2 post ICU admission and on day of discharge. Samples were analysed for total and HMW adiponectin, HMW/total adiponectin ratio, and ZAG. Results were correlated with clinical and metabolic data. There were no differences in total adiponectin, HMW adiponectin and ZAG plasma concentrations between day 1 (admission) and day 2 of the sepsis episode. Compared to admission, a significant increase in total and HMW adiponectin and ZAG was observed on the day of discharge when clinical improvement had been achieved. There was also an increase in the HMW/total adiponectin ratio at that time. Our data demonstrate an increase in both HMW adiponectin and total adiponectin in patients who had clinically recovered from sepsis. The increase in HMW/total adiponectin ratio with improvement of the clinical condition suggests that HMW adiponectin may have a greater role in the inflammatory process and insulin resistance seen in sepsis. In this pilot study, we have also demonstrated a significant increase in ZAG in critically ill patients temporally related to recovery from sepsis.
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Metabolic syndrome(MS) may be caused by atypical antipsychotics(AAPs),and the possible mechanisms have not been fully revealed.Adipocytes regulate energy metabolism through release of adipocytokines.Studies have demonstrated that the impact of AAPs on adipokines is one of the potential mechanisms of drug-induced MS,and adiponectin is an important adipocytokine closely related to MS.The association between AAPs-induced MS and adiponectin is reviewed in this paper.
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Background: Adipose tissue dysfunction has been implicated in the pathophysiology of Alzheimer’s disease. However, the involvement of adipokines, particularly adiponectin, remains unclear. Objective: To compare serum and cerebrospinal fluid (CSF) levels of adiponectin, leptin and leptin-to-adiponectin ratio in patients within the spectrum of Alzheimer’s disease and evaluate their relationship with classical biomarkers and their value as markers of progression. Methods: Amnestic mild cognitive impairment (MCI, n = 71) and Alzheimer’s dementia (AD, n = 53) subjects were consecutively recruited for serum and CSF adiponectin and leptin determination using an analytically validated commercial enzyme-linked immunosorbent assay (ELISA). Correlations were explored using adjusted Spearman’s correlation coefficients. A logistic regression model and ROC analysis were performed to evaluate the staging predictive value of adipokines. Results: Serum adiponectin was 33% higher in AD when compared to MCI patients. Adiponectin CSF levels, similar in both groups, were positively correlated with A β 42 and cognitive function, though only in women. The area under the ROC curve was 0.673 (95% CI:0.57-0.78) for serum adiponectin as predictor of dementia stage and the cut-off 10.85 μg/ml maximized the sum of specificity (87%) and sensitivity (44%). Conclusion: Although longitudinal studies are required, we hypothesize that higher serum adiponectin in AD patients constitutes a strategy to compensate possible central signaling defects. In addition, adiponectin might be specifically assigned to neuroprotective functions in women and eventually involved in the female-biased incidence of Alzheimer’s disease.
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Adiponectin is a most abundant secretory protein produced by adipocytes of white adipose tissue. Adiponectin circulates in blood as three different (high-molecular, middle-molecular, and low-molecular weight) isoforms, gives its effects through AdipoR1 and AdipoR2 receptor. Primary data suggesting that adiponectin has insulin-sensitizing, anti-atherogenic, and anti-inflammatory effects. High serum level of adiponectin is positively associated with inflammation severity and pathological progression in chronic kidney disease, liver disease and inflammatory bowel disease. It has emerged as a valuable biomarker for insulin sensitivity, cardiovascular risk and inflammation. Adiponectin is gaining attention for its therapeutic role in Alzheimer’s disease. Adiponectin appears to play a crucial role not only in glucose and lipid metabolism but also the development and progression of different cancers. Adiponectin also produced locally in the retinas participate in defense of various eye diseases. This review summarizes the role of adiponectin as benevolent adipokine in different disorders.
Adiponectin receptor 1
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Adipose tissue is a major site for energy storage.Increasingly,however,it has been recognized as an important endocrine organ that secretes a number of biologically active adipokines.Of these adipokines,adiponectin has attracted much attention.Many studies have showed protective effects of adiponectin on metabolic syndrome and cardiovascular diseases.Promoting the secretion of adiponectin is expected to be a novel therapeutic tool for metabolic syndrome and cardiovascular disease.
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Adipocytokines, such as adiponectin, TNF-alpha, and leptin, are cytokines secreted by visceral adipocytes, and they are associated with metabolic syndrome. Adiponectin is one of the adipocytokines, and is a protein comprised of 244 amino acids. It is known as ACRP30, GBP28, and AdipoQ. Adiponectin is secreted by adipocytes, has three different isoforms, including trimers (low-molecular weight: LMW), hexamers (middle-molecular-weight: MMW), and higher-order oligomeric (high-molecular-weight: HMW) structures, and affects the biological activity. Adiponectin is a clinically relevant parameter measured routinely in subjects at risk of type 2 diabetes and metabolic syndrome. We investigated the adiponectin levels using a number of ELISA assay kits.
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Adiponectin (also known as APM1, Acrp 30, AdipoQ or GBP28) is a 30kD circulating plasma protein and is the most abundant adipokine secreted by adipose tissue. In humans, adiponectin accounts for approximately 0.01% of circulating plasma proteins.1 It is thought to have a unique spectrum of properties for an adipokine, many of which are anti-atherosclerotic, and is downregulated in the presence of increasing central adiposity.
Intravascular Ultrasound
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Adipose tissue is an active metabolic tissue that secretes multiple metabolically important proteins, known as adipokines. Adiponectin is an important adipokine because of its beneficial effects on glucose and lipid metabolism. Low levels of adiponectin are associated with disease states such as diabetes and cardiovascular disease. Direct administration of adiponectin has been shown to be beneficial in animal models of diabetes, obesity and atherosclerosis. Adiponectin levels in humans can be increased through indirect methods such as weight loss or treatment with thiazolidinediones. This article will review the epidemiology and therapeutic options with adiponectin.
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Adipokines secreted by adipose tissue exert powerful regulatory effects on metabolism and energy balance. The contribution of various fat depots to circulating adipokine concentrations has not been clarified. Moreover, it is unknown whether these adipokines play a role in hepatic steatosis (ST) or progression to portal fibrosis and non-alcoholic steatohepatitis (PT/NASH). The purpose of this study was to explore the relationship between adipokines produced in omental (OM) and subcutaneous (SQ) fat with circulating concentrations, and to examine whether adipokines determine which patients with ST develop PT/NASH. We studied 20 females undergoing bariatric surgery (BMI 48 ± 7 kg/m2; age 40 ± 4 yr) categorized as ST or PF/NASH by liver biopsy. In serum and in OM and SQ fat samples, we quantified the adipokines leptin, resistin, MCP-1, and adiponectin by ELISA. In serum, we also measured high molecular weight (HMW) and low MW (LMW) adiponectin multimers by immunoblot, since we reported that HMW adiponectin was correlated with insulin sensitivity and reduced risk of Metabolic Syndrome. In comparing ST and PT/NASH, there were no differences in serum leptin, resistin, MCP-1, total adiponectin, and HMW and LMW adiponectin. In adipose tissues, OM adiponectin was higher in PF/NASH compared with ST (102.1 ± 8.7 vs. 82.5 ± 19.7 ng/mL; P < 0.05), while SQ adiponectin and tissue leptin levels did not differ between subgroups. OM adiponectin was also correlated with serum HMW adiponectin (r = 0.67, P < 0.05) but not LMW; in contrast, SQ adiponectin did not correlate with either serum HMW or LMW. In conclusion: 1) Serum levels of leptin, resistin, MCP-1, adiponectin, and adiponectin multimers were similar in ST and PT/NASH patients. 2) PT/NASH patients had higher OM adiponectin. 3) OM but not SQ adiponectin was highly correlated with serum HMW, the multimer associated with insulin sensitivity. The data suggest that factors intrinsic to liver, rather than secreted adipokines, determine which patients with hepatic steatosis progress to PT/NASH.
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