Common polymorphisms (single-nucleotide polymorphisms SNP+45 and SNP+276) of the adiponectin gene regulate serum adiponectin concentrations and blood pressure in young Finnish men

Mousavinasab, Firoozeh; Tähtinen, Tuula; Jokelainen, Jari; Koskela, Pentti; Vanhala, Mauno; Oikarinen, Jarkko; Keinänen‐Kiukaanniemi, Sirkka; Laakso, Markku

doi:10.1016/j.ymgme.2005.08.010

Cited by 47 publications

(38 citation statements)

References 18 publications

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“…Diabetic subjects showed that plasma adiponectin levels are significantly higher in TT homozygous T2DM patients, in accord to similar findings in the literature [36]. In addition other studies dealt with 276 G/T allele, it was found that T allele of this variant was related with higher levels of serum adiponectin and was a protective factor fordiabetes, coronary heart disease, hypertension, or dyslipidemia in American [37], Fenland [38], Japanese, and Korean [39] populations. However, the conclusions in different populations are somehow controversial.…”

Section: Discussionsupporting

confidence: 86%

Adiponectin (+276 G/T), Tumor Necrosis Factor-alpha (-308 G/A) and Interleukin-6 (-174 C/G) Genes Polymorphisms in Egyptian Type 2 Diabetic Patients

Abd-Elbaky¹,

Matty²

2016

J Diabetes Metab

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Type 2 diabetes mellitus (T2DM) is a metabolic pro-inflammatory disorder characterized by chronic hyperglycemia and increased levels of circulating cytokines. Adiponectin, tumor necrosis factor-α (TNF-α), interleukin-6 (Il-6), are important cytokines mediators in the pathogenesis of T2DM. The single nucleotide polymorphisms (SNPs) present in the regulatory regions of cytokine genes often have an impact on their expression levels.Aim: Explore potential associations between SNP+276 G/T of adiponectin, SNP -308 G/A of TNF-α and SNP -174 C/G of IL-6 genes with T2DM and to assess its influence on their serum levels. Subjects and Methods:From the Egyptian population, we enrolled 95 T2DM patients and 85 non-diabetic controls. Serum adiponectin, TNF-α and IL-6 were measured. Genotyping for three SNPs of the adiponectin, TNF-α and IL-6 genes was performed by polymerase chain reaction-restriction fragment length polymorphism.Results: Subjects with the GT/TT genotype of SNP 276 were at increased risk for T2DM (OR=15.88, CI=7.56-33.31, P ≤ 0.01) and associated with hypoadiponectinemia compared with the GG genotype. Furthermore, the allelic frequency of the A allele of SNP 308 was significantly different between T2DM patients compared to controls (X 2 =30.54, P ≤ 0.0001). Moreover, Individuals with T2DM carrying the GA/AA genotypes had significantly higher serum TNF-α levels than those carrying GG genotype. In addition, Carriers of G allele of IL-6 were significantly more likely associated with T2DM.

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Section: Discussionsupporting

confidence: 86%

Adiponectin (+276 G/T), Tumor Necrosis Factor-alpha (-308 G/A) and Interleukin-6 (-174 C/G) Genes Polymorphisms in Egyptian Type 2 Diabetic Patients

Abd-Elbaky¹,

Matty²

2016

J Diabetes Metab

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“…38 With regard to the potential association between polymorphisms of the adiponectin gene and hypertension or carotid IMT, some of the 10 APM1 SNPs so far identified 39 have been associated with insulin resistance, DM2 or other features of the metabolic syndrome, 40 -42 and coronary artery disease. 43 In a case-control study, Iwashima et al 44 found the I164T polymorphism associated with hypertension in men only, whereas Mousavinasab et al 45 reported that the APM1 T276T genotype was associated with elevated diastolic BP in 252 Finnish men. The only study searching for an association between the 2 most common APM1 haplotypes (45 to 276) found no association with carotid IMT.…”

Section: Discussionmentioning

confidence: 99%

Carotid Intima-Media Thickness in Confirmed Prehypertensive Subjects

Femia¹,

Kozàkovà²,

Nannipieri³

et al. 2007

ATVB

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Objective-The purpose of this study was to test whether carotid intima-media thickness (IMT) is already increased in normotensive subjects who progress to hypertension (confirmed prehypertensives) independently of known determinants of vessel wall thickness. Methods and Results-Common carotid artery (CCA) far-wall IMT was measured (B-mode ultrasound) in 1536 subjects from the population-based Mexico City Diabetes Study at baseline and 3.5 years later. Key Words: blood pressure Ⅲ carotid arteries Ⅲ diabetes mellitus Ⅲ high-resolution B-mode ultrasonography I ntima-media thickness (IMT) of extracranial carotid arteries, as measured by high-resolution B-mode ultrasonography, marks advanced vascular disease in the peripheral and coronary circulation, 1 predicts cardiovascular (CVD) events 2,3 and response to therapy. 4 Several cross-sectional studies have demonstrated the association between carotid IMT and traditional CVD risk factors. 5 Hypertension is a major CVD risk factor that directly contributes to CVD, and carotid IMT is increased in hypertensive patients as compared with normotensive subjects. 6 -8 High blood pressure (BP) plays a direct pathogenic role in the initiation and progression of carotid wall hypertrophy as hemodynamic factors-such as local distending pressure, pulsatile load, and shear stress 9 -12 -can induce intrinsic alterations of the arterial wall resulting in intimal/medial thickening. Previous studies have demonstrated that carotid IMT is increased already in subjects with borderline hypertension. 13,14 This group of subjects is also characterized by concomitant metabolic abnormalities, such as obesityespecially visceral fat accumulation 15 -type 2 diabetes (DM2) or impaired glucose tolerance and dyslipidemia, which enhance CVD risk. Whether carotid IMT is increased also in normotensive subjects that will develop hypertension (ie, confirmed prehypertensives) has not been determined. Therefore, the main aim of this work was to test whether carotid IMT is increased in confirmed prehypertensives independently of known determinants of vessel wall thickness.Low circulating levels of adiponectin, an adipose tissuespecific collagen-like factor, have been reported in association with obesity, 16 DM2, 17 coronary artery disease, and hypertension. 18 Some studies have reported hypoadiponectinemia in subjects with high-normal BP, 19 whereas others have found that only hypertensive patients with insulin resistance 20 or renal dysfunction 21 had lower adiponectin levels. In studies measuring carotid IMT, 22,23 no significant association was detected between adiponectin levels and IMT when accounting for other relevant risk factors. Perhaps more Original

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“…Reports on children and on adults undergoing treatments that could possibly interfere with adiponectin levels were excluded. Three SNPs (g.Ϫ11391G3 A, g.ϩ45T3 G, and g.ϩ276G3 T) fulfilled these criteria (33,34,36,41,43,44,46,49,50,55,(62)(63)(64)(65)(66). For each of these variants, a multivariate, random-effect metaanalysis was performed to estimate the weighted mean differences (WMDs) in adiponectin levels between genotypes along with their 95% CIs.…”

Section: Adiponectin: a Salutary Adipokinementioning

confidence: 99%

Genetic Influences of Adiponectin on Insulin Resistance, Type 2 Diabetes, and Cardiovascular Disease

2007

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Recent evidence points to molecules secreted by the adipose tissue, or adipokines, as possible links between increased adipose mass and metabolic abnormalities. Among these molecules, adiponectin has drawn much attention because of its insulin-sensitizing and antiatherogenic actions, suggesting that genetic deficits in its production or action may contribute to insulin resistance and coronary artery disease (CAD). A meta-analysis of the data published to date supports this hypothesis. Two independent effects, corresponding to the two linkage disequilibrium blocks that can be identified at the adiponectin locus, appear to be present. In the 5 block, the g.؊11391G3 A variant has a modest but significant effect on adiponectinemia, with a mean difference between genotypes of 1.64 ng/ml (95% CI 0.88 -2.41). In the 3 block, the g. O ur view of adipose tissue has undergone dramatic changes over the past 15 years. Previously believed to be a mere energy depot, adipose tissue is now considered a major endocrine organ regulating whole-body metabolism as well as inflammatory and immune responses (1,2). These actions are mediated by a number of molecules-collectively known as adipokines-that are secreted by adipocytes and act in an autocrine, paracrine, or endocrine fashion, adapting metabolic fluxes to the amount of stored energy (1,2). The discovery of such endocrine function of the adipose tissue has prompted the hypothesis that a genetic dysregulation of the adipokine network may contribute to the pathogenesis of insulin resistance and related disorders such as type 2 diabetes and cardiovascular disease. Of all the molecules that have been shown to be produced by the adipose tissue, adiponectin has drawn special attention, largely due to its effects on both insulin sensitivity and inflammation, and the fact that its expression and serum levels can be modulated by peroxisome proliferatoractivated receptor (PPAR)-␥ agonists drugs (Fig. 1). In this article, we will review the evidence that has been thus far gathered on the role of genetic variants in the adiponectin and adiponectin receptors genes as modulators of adiponectin-circulating levels and susceptibility to insulin resistance traits. We will also discuss the directions in which research on this topic is heading. ADIPONECTIN: A SALUTARY ADIPOKINEAdiponectin, also known as adipocyte complement-related protein 30 (Acrp30), gelatin-binding protein 28 (Gbp28), adipose most abundant transcript 1(apM1), or AdipoQ, is exclusively produced by adipocytes (3-6). It is abundantly present in serum, where it circulates in two higher-order forms: a low-molecular weight dimer of trimers and a larger high-molecular weight complex of 12-18 subunits (7). Serum levels are 15% higher in women than in men (8). Data from both animal and human studies indicate that adiponectin has insulin-enhancing as well as anti-inflammatory actions (rev. in 9). Adiponectin levels are markedly reduced in obese/diabetic mice, and injection of the adiponectin globular domain to these animals ameliorates ...

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Common polymorphisms (single-nucleotide polymorphisms SNP+45 and SNP+276) of the adiponectin gene regulate serum adiponectin concentrations and blood pressure in young Finnish men

Cited by 47 publications

References 18 publications

Adiponectin (+276 G/T), Tumor Necrosis Factor-alpha (-308 G/A) and Interleukin-6 (-174 C/G) Genes Polymorphisms in Egyptian Type 2 Diabetic Patients

Adiponectin (+276 G/T), Tumor Necrosis Factor-alpha (-308 G/A) and Interleukin-6 (-174 C/G) Genes Polymorphisms in Egyptian Type 2 Diabetic Patients

Carotid Intima-Media Thickness in Confirmed Prehypertensive Subjects

Genetic Influences of Adiponectin on Insulin Resistance, Type 2 Diabetes, and Cardiovascular Disease

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