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Hu X, Xi Y, Bai W, Zhang Z, Qi J, Dong L, Liang H, Sun Z, Lei L, Fan G, Sun C, Huo C, Huang J, Wang T. Polymorphisms of adiponectin gene and gene–lipid interaction with hypertension risk in Chinese coal miners: A matched case-control study. PLoS One 2022; 17:e0268984. [PMID: 36094942 PMCID: PMC9467355 DOI: 10.1371/journal.pone.0268984] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/20/2020] [Accepted: 05/12/2022] [Indexed: 11/21/2022] Open
Abstract
Objective Low serum adiponectin level can predict hypertension development, and adiponectin gene (ADIPOQ) polymorphisms have been reported to be linked with hypertension risk. Whereas, the interaction between ADIPOQ polymorphisms and environmental factors on the susceptibility of hypertension remained unclear. The purpose of this study was to explore the relationship of ADIPOQ polymorphisms with hypertension risk and their interaction with lipid levels in coal miners. Methods A matched case-control study with 296 case-control pairs was performed in a large coal mining group located in North China. The participants were questioned by trained interviewers, and their ADIPOQ genotype and lipid levels were determined. Logistic regression, stratified analysis, and crossover analysis were applied to evaluate the effects of rs2241766, rs1501299, and rs266729 genotypes and gene–lipid interaction on hypertension risk. Results In this matched case-control study, the genotypes of rs2241766 TG+GG, rs1501299 GT+TT, and rs266729 CG+GG were marginally related to hypertension risk. Individuals with high total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) level were susceptible to hypertension (TC: odds ratio [OR] = 1.807, 95% confidence intervals [95%CI] = 1.266–2.581; LDL-C: OR = 1.981, 95%CI = 1.400–2.803; HDL-C: OR = 1.559, 95%CI = 1.093–2.223). Antagonistic interactions were detected between rs2241766 and TC, rs1501299 and TC, rs2241766 and LDL-C, and rs1501299 and HDL-C (rs2241766 and TC: OR = 0.393, 95%CI = 0.191–0.806; rs1501299 and TC: OR = 0.445, 95%CI = 0.216–0.918; rs2241766 and LDL-C: OR = 0.440, 95%CI = 0.221–0.877; rs1501299 and HDL-C: OR = 0.479, 95%CI = 0.237–0.967). Stratified analysis showed that hypertension risk was high for the subjects with rs2241766 TG+GG or rs1501299 GG under the low lipid level but low for those under the high lipid level. In the case group, the TC and LDL-C levels for rs2241766 TG+GG were lower than those for rs2241766 GG, and the TC and HDL-C levels for rs1501299 GT+TT were higher than those for rs1501299 GG. Conclusions Although the effects of ADIPOQ polymorphisms alone were not remarkable, an antagonistic interaction was observed between ADIPOQ polymorphisms and lipid levels.
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Affiliation(s)
- Xiaoqin Hu
- Cancer Hospital Affiliated to Shanxi Medical University/Shanxi Hospital Affiliated to Cancer Hospital, Chinese Academy of Medical Sciences/Shanxi Province Cancer Hospital, School of Public Health, Shanxi Medical University, Taiyuan, China
- * E-mail: (TW); (XH)
| | - Yanfeng Xi
- Cancer Hospital Affiliated to Shanxi Medical University/Shanxi Hospital Affiliated to Cancer Hospital, Chinese Academy of Medical Sciences/Shanxi Province Cancer Hospital, Taiyuan, China
| | - Wenqi Bai
- Cancer Hospital Affiliated to Shanxi Medical University/Shanxi Hospital Affiliated to Cancer Hospital, Chinese Academy of Medical Sciences/Shanxi Province Cancer Hospital, Taiyuan, China
| | - Zhenjun Zhang
- Cancer Hospital Affiliated to Shanxi Medical University/Shanxi Hospital Affiliated to Cancer Hospital, Chinese Academy of Medical Sciences/Shanxi Province Cancer Hospital, Taiyuan, China
| | - Jiahao Qi
- School of Public Health, Shanxi Medical University, Taiyuan, China
| | - Liang Dong
- School of Public Health, Shanxi Medical University, Taiyuan, China
| | - Huiting Liang
- School of Public Health, Shanxi Medical University, Taiyuan, China
| | - Zeyu Sun
- School of Public Health, Shanxi Medical University, Taiyuan, China
| | - Lijian Lei
- School of Public Health, Shanxi Medical University, Taiyuan, China
| | - Guoquan Fan
- School of Public Health, Shanxi Medical University, Taiyuan, China
| | - Chenming Sun
- Sinopharm Tongmei General Hospital, Datong, China
| | - Cheng Huo
- Sinopharm Tongmei General Hospital, Datong, China
| | | | - Tong Wang
- School of Public Health, Shanxi Medical University, Taiyuan, China
- * E-mail: (TW); (XH)
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Wu J, Xu G, Cai W, Huang Y, Xie N, Shen Y, Xie L. The association of two polymorphisms in adiponectin-encoding gene with hypertension risk and the changes of circulating adiponectin and blood pressure: A meta-analysis. Oncotarget 2017; 8:14636-14645. [PMID: 28099908 PMCID: PMC5362431 DOI: 10.18632/oncotarget.14680] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/10/2016] [Accepted: 01/09/2017] [Indexed: 12/12/2022] Open
Abstract
Objectives This meta-analysis was prepared to synthesize published data on the association of two polymorphisms (T45G and G276T) in adiponectin-encoding gene (ADIPOQ) with hypertension risk and the changes of circulating adiponectin and blood pressure. Methodology and Major Findings Data were collected and corrected by two authors, and were managed with Stata software. In total, 12 articles were synthesized, including 12 studies (3358 cases and 5121 controls) for the association of two study polymorphisms with hypertension risk and 11 studies (3053 subjects) for the between-genotype changes of adiponectin and/or blood pressure. Based on all qualified studies, the risk prediction for hypertension was nonsignificant for both polymorphisms, with significant heterogeneity for G276T polymorphism (I2 = 53.8%). Overall changes in adiponectin and blood pressure were also nonsignificant for T45G, while contrastingly 276GT genotype was associated with significantly higher levels of adiponectin (weighted mean difference [WMD] = 0.72 μg/mL, 95% confidence interval [CI]: 0.04 to 1.41, P = 0.038), systolic (WMD = 5.15 mm Hg, 95% CI: 0.98 to 9.32, P = 0.016) and diastolic (WMD = 3.45 mm Hg, 95% CI: 0.37 to 6.53, P = 0.028) blood pressure with evident heterogeneity (I2 = 72.0%, 78.3% and 80.0%, respectively), and these associations were more obvious in hypertensive patients. Publication bias was a low probability event for overall comparisons. Conclusions Our findings suggested that in spite of the nonsignificant association between ADIPOQ T45G or G276T polymorphism and hypertension, the heterozygous mutation of G276T was observed to account for increased levels of circulating adiponectin and blood pressure, especially in hypertensive patients.
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Affiliation(s)
- Jianmin Wu
- Department of Cadre's Ward, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China
| | - Guoyan Xu
- Department of Cadre's Ward, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China
| | - Wenqin Cai
- Department of Cadre's Ward, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China
| | - Yun Huang
- Department of Cadre's Ward, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China
| | - Ningyu Xie
- Department of Cadre's Ward, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China
| | - Yihua Shen
- Department of Cadre's Ward, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China
| | - Liangdi Xie
- Department of Cadre's Ward, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China
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de Faria APC, Modolo R, Sabbatini AR, Barbaro NR, Corrêa NB, Brunelli V, Tanus-Santos JE, Fontana V, Moreno H. Adiponectin -11377C/G and +276G/T polymorphisms affect adiponectin levels but do not modify responsiveness to therapy in resistant hypertension. Basic Clin Pharmacol Toxicol 2014; 117:65-72. [PMID: 25546819 DOI: 10.1111/bcpt.12368] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/12/2014] [Accepted: 12/11/2014] [Indexed: 01/03/2023]
Abstract
Resistant hypertension (RHTN) is a multifactorial and polygenic disease, frequently associated with obesity. Low plasma adiponectin levels, a hormone produced by the adipose tissue, were associated with RHTN. Single nucleotide polymorphisms (SNPs) -11377C/G (rs266729) and +276G/T (rs1501299) in ADIPOQ (adiponectin gene) were associated with hypertension. This study evaluated the association between two SNPs (-11377C/G and +276G/T) and adiponectin levels in RHTN. This study comprised 109 patients with RHTN genotyped for both polymorphisms. A cross-sectional study was designed to compare features of CC homozygous versus G allele carriers for -11377C/G and GG homozygous versus T allele carriers for +276G/T. Office and ambulatory BP measurements were similar among genotypes subgroups in both SNPs as well as the markers of target organ damage (arterial stiffness, left ventricular mass index and microalbuminuria). Adiponectin concentrations were significantly higher in CC compared to G carrier for -11377C/G (CC:7.0 (4.0-10.2) versus G allele:5.5 (2.5-7.9), p = 0.04) and lower in GG compared to T carrier for +276G/T (GG:5.3 (2.3-7.7) versus T allele:7.1 (3.6-10.5), p = 0.04). Adjusting for systolic ambulatory BP, body mass index, age, gender, race and presence of type 2 diabetes, multiple linear regression analyses revealed that the minor alleles G (β-coefficient= -0.14, SE=0.07, p = 0.03) and T (β-coefficient=0.12, SE=0.06, p = 0.04) were independent predictors of adiponectin. The -11377C/G and +276G/T SNPs in ADIPOQ were associated with adiponectin levels in RHTN individuals.
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Affiliation(s)
- Ana Paula C de Faria
- Laboratory of Cardiovascular Pharmacology, Faculty of Medical Sciences, University of Campinas, Campinas, SP, Brazil
| | - Rodrigo Modolo
- Laboratory of Cardiovascular Pharmacology, Faculty of Medical Sciences, University of Campinas, Campinas, SP, Brazil
| | - Andréa R Sabbatini
- Laboratory of Cardiovascular Pharmacology, Faculty of Medical Sciences, University of Campinas, Campinas, SP, Brazil
| | - Natália R Barbaro
- Laboratory of Cardiovascular Pharmacology, Faculty of Medical Sciences, University of Campinas, Campinas, SP, Brazil
| | - Nathália B Corrêa
- Laboratory of Cardiovascular Pharmacology, Faculty of Medical Sciences, University of Campinas, Campinas, SP, Brazil
| | - Veridiana Brunelli
- Laboratory of Cardiovascular Pharmacology, Faculty of Medical Sciences, University of Campinas, Campinas, SP, Brazil
| | - José E Tanus-Santos
- Department of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto, SP, Brazil
| | - Vanessa Fontana
- Brazilian Biosciences National Laboratory, Brazilian Center for Research in Energy and Materials, Campinas, SP, Brazil
| | - Heitor Moreno
- Laboratory of Cardiovascular Pharmacology, Faculty of Medical Sciences, University of Campinas, Campinas, SP, Brazil
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Lim JW, Dillon J, Miller M. Proteomic and genomic studies of non-alcoholic fatty liver disease - clues in the pathogenesis. World J Gastroenterol 2014; 20:8325-8340. [PMID: 25024592 PMCID: PMC4093687 DOI: 10.3748/wjg.v20.i26.8325] [Citation(s) in RCA: 29] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/24/2013] [Revised: 01/14/2014] [Accepted: 04/03/2014] [Indexed: 02/06/2023] Open
Abstract
Non-alcoholic fatty liver disease (NAFLD) is a widely prevalent hepatic disorder that covers wide spectrum of liver pathology. NAFLD is strongly associated with liver inflammation, metabolic hyperlipidaemia and insulin resistance. Frequently, NAFLD has been considered as the hepatic manifestation of metabolic syndrome. The pathophysiology of NAFLD has not been fully elucidated. Some patients can remain in the stage of simple steatosis, which generally is a benign condition; whereas others can develop liver inflammation and progress into non-alcoholic steatohepatitis, fibrosis, cirrhosis and hepatocellular carcinoma. The mechanism behind the progression is still not fully understood. Much ongoing proteomic researches have focused on discovering the unbiased circulating biochemical markers to allow early detection and treatment of NAFLD. Comprehensive genomic studies have also begun to provide new insights into the gene polymorphism to understand patient-disease variations. Therefore, NAFLD is considered a complex and mutifactorial disease phenotype resulting from environmental exposures acting on a susceptible polygenic background. This paper reviewed the current status of proteomic and genomic studies that have contributed to the understanding of NAFLD pathogenesis. For proteomics section, this review highlighted functional proteins that involved in: (1) transportation; (2) metabolic pathway; (3) acute phase reaction; (4) anti-inflammatory; (5) extracellular matrix; and (6) immune system. In the genomic studies, this review will discuss genes which involved in: (1) lipolysis; (2) adipokines; and (3) cytokines production.
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Wang J, Guo XF, Yu SJ, Song J, Zhang JX, Cao Z, Wang J, Ji MY, Dong WG. Adiponectin polymorphisms and non-alcoholic fatty liver disease risk: a meta-analysis. J Gastroenterol Hepatol 2014; 29:1396-405. [PMID: 24548122 DOI: 10.1111/jgh.12562] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Accepted: 01/30/2014] [Indexed: 02/06/2023]
Abstract
BACKGROUND AND AIM The adiponectin polymorphism has been implicated in susceptibility to non-alcoholic fatty liver disease (NAFLD), but the results remain inconclusive. The aim of this meta-analysis is to investigate the association between adiponectin polymorphisms and NAFLD risk. METHODS All eligible case-control studies published up to September 2013 were identified by searching PubMed, Web of Science, and CNKI. Effect sizes of odds ratio (OR) and 95% confidence interval (95% CI) were calculated by using a fixed- or random-effect model. RESULTS A total of 10 case-control studies were included; of those, there were nine studies (1223 cases and 1580 controls) for +45T>G polymorphism, seven studies (876 cases and 989 controls) for +276G>T polymorphism, and three studies (299 cases and 383 controls) for -11337C>G polymorphism. Overall, a significantly increased risk was found for +45T>G and -11377C>G polymorphism (+45T>G: OR = 1.45, 95% CI: 1.06-2.00 for recessive model, OR = 1.48, 95% CI: 1.07-2.06 for GG vs TT; -11377C>G: OR = 1.52, 95% CI: 1.10-2.09 for dominant model, OR = 3.88, 95% CI: 1.29-11.68 for GG vs CC), while for +276G>T polymorphism, we found a significantly decreased risk between them (OR = 0.65, 95% CI: 0.45-0.94 for recessive model, OR = 0.58, 95% CI: 0.40-0.84 for TT vs GG). In subgroup analysis by ethnicity, significant association was detected among Asians for +276G>T polymorphism, but not for +45T>G polymorphism. Besides, none of the three adiponectin polymorphisms was associated with the serum adiponectin levels. CONCLUSION This meta-analysis suggests that adiponectin +45T>G and -11377C>G polymorphisms might be a risk factor for NAFLD, while +276G>T polymorphism may be a protective factor for NAFLD among Asians.
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Affiliation(s)
- Jun Wang
- Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China
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Association of four insulin resistance genes with type 2 diabetes mellitus and hypertension in the Chinese Han population. Mol Biol Rep 2014; 41:925-33. [PMID: 24414038 PMCID: PMC3929032 DOI: 10.1007/s11033-013-2937-0] [Citation(s) in RCA: 27] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/02/2013] [Accepted: 12/20/2013] [Indexed: 12/18/2022]
Abstract
Insulin resistance plays an important role in the development of type 2 diabetes mellitus (T2DM) and hypertension. The purpose of the present study was to evaluate the association between four insulin resistance genes (ADIPOQ, LEPR, RETN, and TRIB3) and both T2DM and hypertension. A total of 768 Han Chinese subjects were recruited into this study, including 188 cases who had T2DM alone, 223 cases who had hypertension alone, 181 cases with both T2DM and hypertension, and 176 control subjects with neither T2DM nor hypertension. Twenty-three tag SNPs in four insulin resistance genes were genotyped and analyzed for association with T2DM and hypertension. One intron SNP (rs13306519) in LEPR and one 3′UTR SNP (rs1063537) in ADIPOQ demonstrated a significant association with T2DM (P = 0.024 and 0.014 respectively). Another intron SNP (rs12037879) in LEPR and a promoter region SNP (rs266729) in ADIPOQ were significantly associated with hypertension (P = 0.041 and 0.042, respectively). These associations survived the permutation test (P = 0.023, 0.018, 0.026, and 0.035, respectively). These associations were still found to be significant in the additive model after adjusting for potential confounding factors including age, sex, BMI, HDL, LDL, total cholesterol, and triglyceride levels (P = 0.024, 0.016, 0.04, and 0.043, respectively). No other gene variants were found to be significantly associated with T2DM or hypertension (P > 0.05). None of the studied gene variants were found to be significantly associated with T2DM+ hypertension (P > 0.05). A significant interaction was observed between two SNPs rs13306519 in LEPR and rs266729 in ADIPOQ for T2DM (P_int = 0.012, OR_int = 2.67) and hypertension (P_int = 0.0041, OR_int = 2.23). These findings suggest that variants in ADIPOQ and LEPR are risk factors for T2DM and hypertension in the Chinese population and that variants in RETN and TRIB3 are not major risk factors for these diseases.
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Xi B, Shen Y, Zhao X, Chandak GR, Cheng H, Hou D, Li Y, Ott J, Zhang Y, Wang X, Mi J. Association of common variants in/near six genes (ATP2B1, CSK, MTHFR, CYP17A1, STK39 and FGF5) with blood pressure/hypertension risk in Chinese children. J Hum Hypertens 2014; 28:32-36. [PMID: 23759979 DOI: 10.1038/jhh.2013.50] [Citation(s) in RCA: 37] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/06/2012] [Revised: 03/18/2013] [Accepted: 03/20/2013] [Indexed: 01/11/2023]
Abstract
Recent genome-wide association studies have identified several single-nucleotide polymorphisms (SNPs) that are associated with blood pressure (BP)/hypertension. In this study, we aimed to examine the established associations amongst Chinese children. We genotyped six SNPs (ATP2B1 rs17249754, CSK rs1378942, MTHFR rs1801133, CYP17A1 rs1004467, STK39 rs3754777 and FGF5 rs16998073) in Chinese children (N=3077, age range, 6-18 years). Based on the Chinese age- and sex-specific BP standards, 619 hypertensive cases and 2458 controls with normal BP were identified. Of the six SNPs, only ATP2B1 rs17249754 SNP was significantly associated with the risk of hypertension (allelic odds ratio (OR)=1.25, 95% confidence interval (CI): 1.08-1.44, P=0.003). Although all other SNPs showed a trend towards increasing the BP values and risk of hypertension, there was no statistically significant association after false discovery rate analysis. We calculated the weighted risk score using six SNPs, for systolic BP (SBP), diastolic BP (DBP) and hypertension. Each additional weighted risk score was associated with SBP by 1.18 mm Hg (95% CI=0.62-1.73, P<0.001), but not with the DBP (β=0.28, 95% CI=(-0.15)-0.74), and overall increased the risk of hypertension by 1.19-fold (95% CI=1.04-1.35, P=0.01). The present study confirmed the significant association of ATP2B1 rs17249754 with risk of hypertension among Chinese children, but failed to replicate the association of CSK rs1378942, MTHFR rs1801133, CYP17A1 rs1004467, STK39 rs3754777 and FGF5 rs16998073 with BP/risk of hypertension.
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Affiliation(s)
- B Xi
- 1] Department of Epidemiology, Capital Institute of Pediatrics, Beijing, China [2] Department of Maternal and Child Health Care, School of Public Health, Shandong University, Jinan, China
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Kim DH, Kim C, Ding EL, Townsend MK, Lipsitz LA. Adiponectin levels and the risk of hypertension: a systematic review and meta-analysis. Hypertension 2013; 62:27-32. [PMID: 23716587 DOI: 10.1161/hypertensionaha.113.01453] [Citation(s) in RCA: 116] [Impact Index Per Article: 9.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/14/2022]
Abstract
Animal studies and small controlled studies in humans suggest that adiponectin may regulate blood pressure via brain-mediated and endothelium-mediated mechanisms. We performed a systematic review and meta-analysis to evaluate the epidemiological evidence on plasma adiponectin levels and hypertension in free-living adult population. A systematic search of MEDLINE and EMBASE, up to February 2013, identified 43 nonprospective and 5 prospective studies that included 17 598 adults (8220 with hypertension; mean age 19-69 years; and mean body mass index 22-38 kg/m(2)). Two investigators independently extracted data on adiponectin levels by hypertension status and dose-response relationship. We used a random-effects model to compute the weighted mean difference in adiponectin levels between adults with hypertension and normotensive adults and a 2-stage generalized least-square trend methods to compute the odds ratio of hypertension per 1 µg/mL increase in adiponectin. Adults with hypertension had 1.64 µg/mL (95% confidence interval, -2.07, -1.21) lower adiponectin levels than normotensive adults. Every 1 µg/mL increase in adiponectin levels was associated with 6% reduced risk of hypertension (95% confidence interval, 0.92, 0.97). These findings were consistent across study design and characteristics, including age, sex, and body mass index (P>0.05). However, our meta-analysis was limited by unexplained large between-study heterogeneity, a small number of prospective studies, and selective reporting of dose-response data. In conclusion, epidemiological evidence suggests that plasma adiponectin level is a biomarker and possible mediator in the development of adiposity-related hypertension. The question remains as to adiponectin as a potential therapeutic target and its relationship with other adipokines in blood pressure regulation.
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Affiliation(s)
- Dae Hyun Kim
- Division of Gerontology, Beth Israel Deaconess Medical Center, Boston, MA, USA.
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Gao M, Ding D, Huang J, Qu Y, Wang Y, Huang Q. Association of genetic variants in the adiponectin gene with metabolic syndrome: a case-control study and a systematic meta-analysis in the Chinese population. PLoS One 2013; 8:e58412. [PMID: 23593121 PMCID: PMC3617191 DOI: 10.1371/journal.pone.0058412] [Citation(s) in RCA: 20] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/18/2012] [Accepted: 02/04/2013] [Indexed: 12/13/2022] Open
Abstract
Background The prevalence of metabolic syndrome has been rising worldwide, including in China, but knowledge on specific genetic determinants of metabolic syndrome is very limited. A number of studies have reported that polymorphisms in the ADIPOQ gene are associated with metabolic syndrome in Chinese Han populations. However, data is still conflicting. The objective of this study was to examine the associations of the adiponectin genetic variants with metabolic syndrome by a case-control study and meta-analyses in Chinese. Methods We first investigated the association of ADIPOQ rs2241766 (+45T>G in exon 2), rs266729 (−11377C>G in promoter) and rs1501299 (+276G>T in intron 2) polymorphisms with metabolic syndrome in a Hubei Han Chinese population with 322 metabolic syndrome patients and 161 normal controls recruited from the Yichang, Hubei. Then we comprehensively reviewed the association between ADIPOQ rs2241766/rs266729/rs1501299 and metabolic syndrome in the Chinese populations via a meta-analysis. The strength of association was assessed by odds ratios (ORs) with 95% confidence intervals (CI). Results The G allele frequency of rs2241766 in metabolic syndrome patients was significantly higher than those of controls group (29.8% vs 23.3%, OR = 1.40, P = 0.033). The logistic regression analysis adjusted by gender and age showed a nominally significant association for rs2241766 GG+GT genotype (P = 0.065, OR = 1.55) and rs1501299 GG genotype in recessive model (OR = 1.54, P = 0.066). However, no association was observed for rs266729 in our sample. We identified thirteen studies for rs2241766 (2,684 metabolic syndrome patients and 2,864 controls), three studies for rs266729, and eleven studies for rs1501299 (2,889 metabolic syndrome patients and 3,304 controls) in Chinese. Meta-analysis indicated significant associations for the rs2241766 G allele (OR = 1.14, 95%CI = 1.05–1.24, P = 0.003), rs266729 GG+GT genotypes (OR = 0.80, 95%CI = 0.68–0.92, P = 0.003) and rs1501299 GG+TG genotypes (OR = 1.42, 95%CI 1.16–1.75, P = 0.001). Conclusions Our results demonstrated ADIPOQ as a pleiotropic locus for metabolic syndrome and its components in the Han Chinese population.
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Affiliation(s)
- Meng Gao
- Hubei Key Lab of Genetic Regulation and Integrative Biology, College of Life Sciences, Central China Normal University, Wuhan, China
| | - Daxia Ding
- Hubei Key Lab of Genetic Regulation and Integrative Biology, College of Life Sciences, Central China Normal University, Wuhan, China
| | - Jinghua Huang
- Hubei Key Lab of Genetic Regulation and Integrative Biology, College of Life Sciences, Central China Normal University, Wuhan, China
| | - Yali Qu
- Wuhan Center of Medical Therapeutics, Wuhan, China
| | - Yu Wang
- Department of Pharmacology and Pharmacy, the University of Hong Kong, Hong Kong, China
| | - Qingyang Huang
- Hubei Key Lab of Genetic Regulation and Integrative Biology, College of Life Sciences, Central China Normal University, Wuhan, China
- * E-mail:
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Xi B, Zhang M, Wang C, Shen Y, Zhao X, Wang X, Mi J. The common SNP (rs9939609) in the FTO gene modifies the association between obesity and high blood pressure in Chinese children. Mol Biol Rep 2012; 40:773-8. [PMID: 23111453 DOI: 10.1007/s11033-012-2113-y] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/25/2012] [Accepted: 10/03/2012] [Indexed: 02/02/2023]
Abstract
Previous studies have suggested that common variants in fat mass- and obesity-associated (FTO) gene are associated with body mass index (BMI) and the risk of obesity. Since obesity plays an important role in the etiology of high blood pressure (HBP), we aim to investigate the association between obesity and HBP in a population with different variants of the FTO gene. A total of 3,494 children (1,775 boys, 50.8 %) aged 6-18 years were recruited for measuring pubertal status, BMI and systolic and diastolic blood pressure. The single nucleotide polymorphism rs9939609 of the FTO gene was genotyped. The blood pressure levels increased by 1.4, 1.5 and 1.8 mmHg for systolic blood pressure and 0.8, 0.9 and 1.2 mmHg for diastolic blood pressure per 1-unit BMI increase in subjects carrying TT, TA and AA genotypes, respectively. After stratifying for FTO rs9939609 genotypes (TT, TA and AA), the odds ratios (95 % confidence intervals) of HBP in obese versus non-obese children were 4.26 (3.18-5.71), 5.13 (2.96-8.90) and 10.37 (1.59-67.43), respectively, with adjustment for age, gender and pubertal status. The FTO rs9939609 SNP modifies the effect of obesity on HBP in Chinese children, with obese ones carrying the AA homozygous genotype of the FTO rs9939609 having the highest risk of developing HBP.
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Affiliation(s)
- Bo Xi
- Department of Maternal and Child Health Care, School of Public Health, Shandong University, Jinan, 250012, China
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