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      Effect of the Pro12Ala Polymorphism of the Peroxisome Proliferator-activated Receptor γ2 Gene on Lipid Profile and Adipokines Levels in Obese Subjects

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          Abstract

          Peroxisome proliferator-activated receptor γ (PPARγ) is a key regulator of metabolism, adipokines production and secretion. The aim of this study was to investigate the association between the PPARγ2 gene Pro12Ala polymorphism in obesity in terms of body mass index (BMI), lipid parameters, homeostasis model assessment of insulin resistance (HOMA-IR), serum lipid, leptin, adiponectin, resistin and chemerin levels. The study included 160 obese and 140 non obese subjects. The Pro12Ala polymorphism was determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Serum lipid, leptin, adiponectin, resistin and chemerin levels were measured. No association was found between the Pro12Ala polymorphism and BMI. Strikingly, in the study group, obese subjects with the AA genotype had significantly higher triglycerides ( p = 0.046) and resistin ( p <0.001) levels than those with the wild-type PP and heterozygous PA genotypes. Serum leptin and chemerin levels were significantly associated with Pro-12Ala poymorphism in the obese and non obese groups ( p <0.01). In the obese group, subjects with the homozygous AA genotype had significantly lower adiponectin ( p = 0.010) activity than the PP genotype. Our results suggest that the PPARγ2 gene Pro12Ala polymorphism has no direct association with obesity but does have significant influences on lipid profiles and adipokines levels.

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          A Pro12Ala substitution in PPARgamma2 associated with decreased receptor activity, lower body mass index and improved insulin sensitivity.

          The peroxisome proliferator-activated receptor-gamma (PPARgamma) is a transcription factor that has a pivotal role in adipocyte differentiation and expression of adipocyte-specific genes. The PPARgamma1 and gamma2 isoforms result from alternative splicing and have ligand-dependent and -independent activation domains. PPARgamma2 has an additional 28 amino acids at its amino terminus that renders its ligand-independent activation domain 5-10-fold more effective than that of PPARgamma1. Insulin stimulates the ligand-independent activation of PPARgamma1 and gamma2 (ref. 5), however, obesity and nutritional factors only influence the expression of PPARgamma2 in human adipocytes. Here, we report that a relatively common Pro12Ala substitution in PPARgamma2 is associated with lower body mass index (BMI; P=0.027; 0.015) and improved insulin sensitivity among middle-aged and elderly Finns. A significant odds ratio (4.35, P=0.028) for the association of the Pro/Pro genotype with type 2 diabetes was observed among Japanese Americans. The PPARgamma2 Ala allele showed decreased binding affinity to the cognate promoter element and reduced ability to transactivate responsive promoters. These findings suggest that the PPARgamma2 Pro12Ala variant may contribute to the observed variability in BMI and insulin sensitivity in the general population.
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            Molecular Regulation of Adipogenesis and Potential Anti-Adipogenic Bioactive Molecules

            Adipogenesis is the process by which precursor stem cells differentiate into lipid laden adipocytes. Adipogenesis is regulated by a complex and highly orchestrated gene expression program. In mammalian cells, the peroxisome proliferator-activated receptor γ (PPARγ), and the CCAAT/enhancer binding proteins (C/EBPs) such as C/EBPα, β and δ are considered the key early regulators of adipogenesis, while fatty acid binding protein 4 (FABP4), adiponectin, and fatty acid synthase (FAS) are responsible for the formation of mature adipocytes. Excess accumulation of lipids in the adipose tissue leads to obesity, which is associated with cardiovascular diseases, type II diabetes and other pathologies. Thus, investigating adipose tissue development and the underlying molecular mechanisms is vital to develop therapeutic agents capable of curbing the increasing incidence of obesity and related pathologies. In this review, we address the process of adipogenic differentiation, key transcription factors and proteins involved, adipogenic regulators and potential anti-adipogenic bioactive molecules.
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              From molecular action to physiological outputs: peroxisome proliferator-activated receptors are nuclear receptors at the crossroads of key cellular functions.

              Peroxisome proliferator-activated receptors (PPARs) compose a family of three nuclear receptors which act as lipid sensors to modulate gene expression. As such, PPARs are implicated in major metabolic and inflammatory regulations with far-reaching medical consequences, as well as in important processes controlling cellular fate. Throughout this review, we focus on the cellular functions of these receptors. The molecular mechanisms through which PPARs regulate transcription are thoroughly addressed with particular emphasis on the latest results on corepressor and coactivator action. Their implication in cellular metabolism and in the control of the balance between cell proliferation, differentiation and survival is then reviewed. Finally, we discuss how the integration of various intra-cellular signaling pathways allows PPARs to participate to whole-body homeostasis by mediating regulatory crosstalks between organs.
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                Author and article information

                Journal
                Balkan J Med Genet
                bjmg
                bjmg
                Balkan Journal of Medical Genetics : BJMG
                De Gruyter
                1311-0160
                2199-5761
                30 June 2017
                30 June 2017
                : 20
                : 1
                : 71-80
                Affiliations
                [1 ]deptDepartment of Biochemistry, Faculty of Pharmacy , universityNear East University , Nicosia, Mersin 10, Turkey
                [2 ]deptExperimental Health Science Research Center , universityNear East University , Nicosia, Mersin 10, Turkey
                [3 ]deptDepartment of Medical Biology, Cerrahpasa Faculty of Medicine ,universityIstanbul University , Istanbul, Turkey
                Author notes
                [* ] Eda Becer, Ph.D., M.Sc., Department of Biochemistry, Faculty of Pharmacy, Near East University, Nicosia, Mersin 10, Turkey. Tel: +90-392-680-2000, Ext: 128. Fax:+90-392-680-2038 edabecer@ 123456yahoo.com
                Article
                bjmg-2017-0007
                10.1515/bjmg-2017-0007
                5596824
                505a2b1e-558c-4b14-a1d2-0d3b16fcdd16
                © 2017 Walter de Gruyter GmbH, Berlin/Boston
                History
                Page count
                Pages: 10
                Categories
                Original Article

                adipokines,obesity,peroxisome proliferator-activated receptor γ(pparγ),polymorphism

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