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Blood Circulating Levels of Adipokines in Polycystic Ovary Syndrome Patients: A Systematic Review and Meta-analysis.
Mehrabani, S, Arab, A, Karimi, E, Nouri, M, Mansourian, M
Reproductive sciences (Thousand Oaks, Calif.). 2021;(11):3032-3050
Abstract
A body of studies has examined the circulating concentration of adipokines including apelin, vapin, resistin, and chemerin in polycystic ovary syndrome (PCOS) patients. However, their findings have been inconclusive. Therefore, we systematically reviewed available studies to illuminate the overall circulating concentration of adipokines in PCOS subjects. Cochrane's Library, PubMed, Scopus, and ISI Web of Science databases were searched from the earliest available date up to April 2021 for relevant articles. The quality of each study was assessed by the Newcastle-Ottawa Quality Assessment Scale. The pooled effect size was estimated based on the random effects model, and the standard mean differences (SMD) with a 95% confidence interval (CI) were reported. A total of 88 studies met the inclusion criteria and were included in the current systematic review and meta-analysis. The results of the analysis showed that serum levels of vaspin (SMD 0.69; 95% CI, 0.22 to 1.17; P = 0.004; I2 = 90.6%), chemerin (SMD 1.87; 95% CI, 1.35 to 2.40; P < 0.001; I2 = 94.4%), and resistin (SMD 0.66; 95% CI, 0.41 to 0.91; P < 0.001; I2 = 92.6%) were significantly higher in the PCOS group compared to controls. However, there was no significant difference between the PCOS and control groups in relation to apelin levels (SMD - 0.17; 95% CI, - 1.06 to 0.73; P = 0.714; I2 = 97.8%). We found that serum levels of vaspin, chemerin, and resistin were significantly higher in PCOS subjects compared with controls. It seems that these adipokines can be measured as a useful marker to predict the development of PCOS.
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The effect of meal frequency on biochemical cardiometabolic factors: A systematic review and meta-analysis of randomized controlled trials.
Abdollahi, S, Kazemi, A, de Souza, RJ, Clark, CCT, Soltani, S
Clinical nutrition (Edinburgh, Scotland). 2021;(5):3170-3181
Abstract
BACKGROUND Although several randomized controlled trials (RCTs) have supported the beneficial effects of higher meal frequency (MF) on cardiometabolic risk factors, the putative effects of higher MF on health remain inconclusive. This study systematically reviewed the evidence from RCTs of the effect of higher compared with lower MF on the blood lipid profile, glucose homeostasis, and adipokines. METHODS PubMed, Scopus, ISI Web of Science, and the Cochrane database were searched up to October 2020 to retrieve relevant RCTs. A DerSimonian and Laird random effects model was used to pool mean differences and 95% CI for each outcome. The quality of studies and evidence was assessed through standard methods. RESULTS Twenty-one RCTs (686 participants) were included in this meta-analysis. Overall results showed a significant improvement in total cholesterol [weighted mean difference (WMD) = -6.08 mg/dl; 95% CI: -10.68, -1.48; P = 0.01; I2 = 88%], and low-density cholesterol (LDL-C) (WMD = -6.82 mg/dl; 95% CI: -10.97, -1.60; P = 0.009; I2 = 85.7%), while LDL-C to high-density cholesterol ratio (LDL-C: HDL-C) increased (WMD = 0.22; 95% CI: 0.07, 0.36; P = 0.003; I2 = 0.0%) in higher MF vs. lower MF. No significant effects were found on measures of glycemic control, apolipoproteins-A1 and B, or leptin. In subgroup analyses, higher MF significantly reduced serum triglyceride (TG), and increased HDL-C, compared with lower MF in interventions > 12 weeks, and decreased serum TC and LDL-C in healthy participants. A significant reduction in LDL-C also was observed in studies where the same foods given both arms, simply divided into different feeding occasions, and in feeding studies, following higher MF compared to lower MF. CONCLUSION Our meta-analysis found that higher, compared with lower MF may improve total cholesterol, and LDL-C. The intervention does not affect measures of glycemic control, apolipoproteins-A1 and B, or leptin. However, the GRADE ratings of low credibility of the currently available evidence highlights the need for more high-quality studies in order to reach a firm conclusion.
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Zinc-alpha2-glycoprotein, dysglycaemia and insulin resistance: a systematic review and meta-analysis.
Pearsey, HM, Henson, J, Sargeant, JA, Davies, MJ, Khunti, K, Suzuki, T, Bowden-Davies, KA, Cuthbertson, DJ, Yates, TE
Reviews in endocrine & metabolic disorders. 2020;(4):569-575
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Abstract
To systematically review the current literature investigating associations between zinc-alpha2-glycoprotein (ZAG) and dysglycaemia (including type 2 diabetes (T2DM), poly-cystic-ovary syndrome (PCOS), pre-diabetes or insulin resistance). This included relationships between ZAG and continuous measures of insulin and glucose. Additionally, we performed a meta-analysis to estimate the extent that ZAG differs between individuals with or without dysglycaemia; whilst examining the potential influence of adiposity. A systematic search was performed on four databases for studies on circulating ZAG concentrations in adult human populations, comparing healthy controls to individuals with dysglycaemia. Key characteristics, including the mean ZAG concentrations (mg∙L-1), and any correlational statistics between ZAG and continuous measures of glucose, glycated haemoglobin (HbA1c) or insulin were extracted. Meta-analyses were performed to compare metabolically healthy controls to cases, and on studies that compared controls and cases considered overweight or obese (body mass index (BMI) ≥25 kg.m2). 1575 papers were identified and 14 studies (16 cohorts) were considered eligible for inclusion. Circulating ZAG was lower in individuals with dysglycaemia compared to metabolically healthy controls (-4.14 [-8.17, -0.11] mg.L-1; I2 = 98.5%; p < 0.001). When using data from only studies with overweight or obese groups with or without dysglycaemia (three studies (four cohorts); pooled n = 332), the difference in circulating ZAG was no longer significant (-0.30 [-3.67, 3.07] mg. L-1; I2 = 28.0%; p = 0.225). These data suggest that ZAG may be implicated in dysglycaemia, although there was significant heterogeneity across different studies and the mediating effect of adiposity cannot be excluded. Therefore, more research is needed before robust conclusions can be drawn.
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Circulating adipokines and risk of obesity related cancers: A systematic review and meta-analysis.
Yoon, YS, Kwon, AR, Lee, YK, Oh, SW
Obesity research & clinical practice. 2019;(4):329-339
Abstract
BACKGROUND Obesity can influence on carcinogenesis through alterations in adipokines and subsequent inflammatory changes. This meta-analysis was aimed to comprehensively assess the association between circulating adipokines and risk of obesity-related cancers. METHODS Pubmed and Embase were searched up to October 2017 for observational studies investigating the relationship between adipokines and cancers. Pooled odds ratio and the corresponding 95% confidence interval was estimated through the meta-analysis using a random-effects model. Findings A total of 93 observational studies (adiponectin = 60, high molecular weight adiponectin = 9, leptin = 39, IL-6 = 16, TNF-α = 10, and resistin = 17) were included. Adiponectin was significantly associated with decreased risk of cancer (pooled OR 0.70, 95% CI 0.60-0.80; I2 = 71.9%; Pheterogeneity <0.01). Leptin was significantly associated with increased risk of cancer (1.26, 1.05-1.51; I2 = 65.7%; Pheterogeneity <0.01). For each 5 μg/ml increase in adiponectin and 5 ng/ml increase in leptin, the pooled OR was 0.88 (0.83-0.93; I2 = 80.2%; Pheterogeneity <0.01) and 1.05 (1.01-1.09; I2 = 67.9%; Pheterogeneity<0.01)), respectively. There was nonlinear dose-response association (Pnonlinearity for adiponectin = 0.01; Pnonlinearity for leptin = 0.003).IL-6 (1.09, 0.94-1.25), TNF- α (1.65, 0.99-2.74), and resistin (1.28, 0.78-2.11) was not associated with risk of cancer. By cancer site and type, highest category of adiponectin was associated with decreased risk of breast (OR 0.74, 0.60-0.91), colorectal (0.74, 0.60-0.91), and endometrial cancer (0.49, 0.34-0.72). Higher leptin was associated with increased risk of endometrial (1.88, 1.24-2.87) and kidney cancer (2.07, 1.51-2.83). CONCLUSION Our study suggests that adiponectin and leptin may play a role in the etiology of cancer.
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Association Between Peripheral Adipokines and Inflammation Markers: A Systematic Review and Meta-Analysis.
Graßmann, S, Wirsching, J, Eichelmann, F, Aleksandrova, K
Obesity (Silver Spring, Md.). 2017;(10):1776-1785
Abstract
OBJECTIVE Obesity-induced inflammation potentially promotes a variety of chronic conditions. This study aimed to summarize cross-sectional associations between adipose tissue-derived hormones (leptin and adiponectin) and inflammatory biomarkers (C-reactive protein [CRP], interleukin [IL]-6, and tumor necrosis factor [TNF]-α) by means of meta-analysis. METHODS A systematic search of the databases EMBASE and MEDLINE (PubMed) up to January 2017 was conducted. Data were independently extracted and evaluated by two reviewers. Pooled effect sizes and 95% confidence intervals were calculated using random-effects models. RESULTS After the initial search, 5,907 publications were retrieved; of these, an overall 60 studies with 45,210 participants were deemed eligible for inclusion in the meta-analysis. Positive correlations with inflammatory biomarkers were observed for leptin (pooled Rho = 0.35, 0.20, and 0.20 for CRP, IL-6, and TNF-α, respectively), whereas the respective correlations with adiponectin were negative (pooled Rho = -0.18, -0.14, and -0.12 for CRP, IL-6, and TNF-α, respectively). Stratification by age showed that the observed correlations tended to be weaker with the increasing age of participants. No apparent differences were observed by sex and adiposity status. CONCLUSIONS This is the first quantitative synthesis of human studies on the association between circulating adipokines and inflammation biomarkers. Potential influence of age on these associations requires further evaluation.
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Association between circulating adipocytokine concentrations and microvascular complications in patients with type 2 diabetes mellitus: A systematic review and meta-analysis of controlled cross-sectional studies.
Rodríguez, AJ, Nunes, Vdos S, Mastronardi, CA, Neeman, T, Paz-Filho, GJ
Journal of diabetes and its complications. 2016;(2):357-67
Abstract
BACKGROUND The adipocytokines leptin and adiponectin have been variously associated with diabetic microvascular complications. No comprehensive clinical data exist examining the association between adipocytokines and the presence of these complications. METHODS This is a systematic review of cross-sectional studies comparing circulating adipocytokines in patients with type 2 diabetes mellitus (T2DM), with and without microvascular complications. Studies were retrieved from MEDLINE, EMBASE, Scopus and Cochrane databases. Study quality was evaluated using a modified Newcastle-Ottawa Scale. Meta-analysis was performed using an inverse-variance model, providing standardised mean differences (SMD) and 95% confidence intervals (CI). Heterogeneity was determined by I(2) statistic. RESULTS Amongst 554 identified studies, 28 were included in the review. Study quality range was 3.5-9 (maximum 11). Higher leptin levels were associated with microalbuminuria (SMD=0.41; 95% CI=0.14-0.67; n=901; p=0.0003), macroalbuminuria (SMD=0.68; 95% CI=0.30-1.06; n=406; p=0.0004), and neuropathy (SMD=0.26; 95% CI=0.07-0.44; n=609; p=0.008). Higher adiponectin levels were associated with microalbuminuria (SMD=0.55; 95% CI=0.29-0.81, n=274; p<0.001), macroalbuminuria (SMD=1.37; 95% CI=0.78-1.97, n=246; p<0.00001), neuropathy (SMD=0.25; 95% CI=0.14-0.36; n=1516; p<0.00001), and retinopathy (SMD=0.38; 95% CI=0.25-0.51; n=1306; p<0.00001). Meta-regression suggested no influence of body mass index and duration of diabetes on effect size, and a weak trend in terms of age on effect size. DISCUSSION Our meta-analysis suggests leptin and adiponectin levels are higher in T2DM patients with microvascular complications. Studies were limited by cross-sectional design. Large prospective analyses are required to validate these findings.
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Does vitamin D supplementation alter plasma adipokines concentrations? A systematic review and meta-analysis of randomized controlled trials.
Dinca, M, Serban, MC, Sahebkar, A, Mikhailidis, DP, Toth, PP, Martin, SS, Blaha, MJ, Blüher, M, Gurban, C, Penson, P, et al
Pharmacological research. 2016;:360-371
Abstract
We aimed to elucidate the role of vitamin D supplementation on adipokines through a systematic review and a meta-analysis of randomized placebo-controlled trials (RCTs). The search included PUBMED, Scopus, Web of Science and Google Scholar through July 1st, 2015. Finally we identified 9 RCTs and 484 participants. Meta-analysis of data from 7 studies did not find a significant change in plasma adiponectin concentrations following vitamin D supplementation (mean difference [MD]: 4.45%, 95%CI: -3.04, 11.93, p=0.244; Q=2.18, I(2)=0%). In meta-regression, changes in plasma adiponectin concentrations following vitamin D supplementation were found to be independent of treatment duration (slope: 0.25; 95%CI: -0.69, 1.19; p=0.603) and changes in serum 25-hydroxy vitamin D [25(OH)D] levels (slope: -0.02; 95%CI: -0.15, 0.12; p=0.780). Meta-analysis of data from 6 studies did not find a significant change in plasma leptin concentrations following vitamin D supplementation (MD: -4.51%, 95%CI: -25.13, 16.11, p=0.668; Q=6.41, I(2)=21.97%). Sensitivity analysis showed that this effect size is sensitive to one of the studies; removing it resulted in a significant reduction in plasma leptin levels (MD: -12.81%, 95%CI: -24.33, -1.30, p=0.029). In meta-regression, changes in plasma leptin concentrations following vitamin D supplementation were found to be independent of treatment duration (slope: -1.93; 95%CI: -4.08, 0.23; p=0.080). However, changes in serum 25(OH)D were found to be significantly associated with changes in plasma leptin levels following vitamin D supplementation (slope: 1.05; 95%CI: 0.08, 2.02; p=0.033). In conclusion, current data did not indicate a significant effect of vitamin D supplementation on adiponectin and leptin levels.
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Adipokine levels during the first or early second trimester of pregnancy and subsequent risk of gestational diabetes mellitus: A systematic review.
Bao, W, Baecker, A, Song, Y, Kiely, M, Liu, S, Zhang, C
Metabolism: clinical and experimental. 2015;(6):756-64
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Abstract
OBJECTIVE We aimed to systematically review available literature linking adipokines to gestational diabetes mellitus (GDM) for a comprehensive understanding of the roles of adipokines in the development of GDM. METHODS We searched PubMed/MEDLINE and EMBASE databases for published studies on adipokines and GDM through October 21, 2014. We included articles if they had a prospective study design (i.e., blood samples for adipokines measurement were collected before GDM diagnosis). Random-effects models were used to pool the weighted mean differences comparing levels of adipokines between GDM cases and non-GDM controls. RESULTS Of 1523 potentially relevant articles, we included 25 prospective studies relating adipokines to incident GDM. Our meta-analysis of nine prospective studies on adiponectin and eight prospective studies on leptin indicated that adiponectin levels in the first or early second trimester of pregnancy were 2.25 μg/ml lower (95% CI: 1.75-2.75), whereas leptin levels were 7.25 ng/ml higher (95% CI 3.27-11.22), among women who later developed GDM than women who did not. Prospective data were sparse and findings were inconsistent for visfatin, retinol binding protein (RBP-4), resistin, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and vaspin. We did not identify prospective studies for several novel adipokines, including chemerin, apelin, omentin, or adipocyte fatty acid-binding protein. Moreover, no published prospective studies with longitudinal assessment of adipokines and incident GDM were identified. CONCLUSION Adiponectin levels in the first or second trimester of pregnancy are lower among pregnant women who later develop GDM than non-GDM women, whereas leptin levels are higher. Well-designed prospective studies with longitudinal assessment of adipokines during pregnancy are needed to understand the trajectories and dynamic associations of adipokines with GDM risk.