Apelin and <scp>G212A</scp> apelin receptor gene polymorphism in obese and diabese youth

Kotanidou, Eleni P; Kalinderi, Kallirhoe; Kyrgios, Ioannis; Efraimidou, S.; Fidani, Liana; Papadopoulou‐Alataki, Efimia; Eboriadou-Petikopoulou, Maria; Galli-Tsinopoulou, Assimina

doi:10.1111/ijpo.251

“…APLNR encodes a family member of the G protein-coupled receptors. Several studies have investigated polymorphisms of APLNR and the susceptibility of DCM (37)(38)(39). In addition, the 212A allele of the APLNR G212A polymorphism is considered to be significantly associated with reduced risk of idiopathic DCM (39), suggesting that alteration of this gene may influence the DCM.…”

Section: Itga11 Col6a1 Lamc2mentioning

confidence: 99%

“…Several studies have investigated polymorphisms of APLNR and the susceptibility of DCM (37)(38)(39). In addition, the 212A allele of the APLNR G212A polymorphism is considered to be significantly associated with reduced risk of idiopathic DCM (39), suggesting that alteration of this gene may influence the DCM. In the present study, PENK and APLNR were identified as two crucial genes in module 2, suggesting that they may exert more important functions in DCM than other genes.…”

Section: Itga11 Col6a1 Lamc2mentioning

confidence: 99%

Bioinformatics method identifies potential biomarkers of dilated cardiomyopathy in a human induced pluripotent stem cell-derived cardiomyocyte model

Yu

¹

,

Gong

²

,

Zhong

³

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Dilated cardiomyopathy (DCM) is the most common type of cardiomyopathy that account for the majority of heart failure cases. The present study aimed to reveal the underlying molecular mechanisms of DCM and provide potential biomarkers for detection of this condition. The public dataset of GSE35108 was downloaded, and 4 normal induced pluripotent stem cell (iPSC)-derived cardiomyocytes (N samples) and 4 DCM iPSC-derived cardiomyocytes (DCM samples) were utilized. Raw data were preprocessed, followed by identification of differentially expressed genes (DEGs) between N and DCM samples. Crucial functions and pathway enrichment analysis of DEGs were investigated, and protein-protein interaction (PPI) network analysis was conducted. Furthermore, a module network was extracted from the PPI network, followed by enrichment analysis. A set of 363 DEGs were identified, including 253 upregulated and 110 downregulated genes. Several biological processes (BPs), such as blood vessel development and vasculature development (FLT1 and MMP2), cell adhesion (CDH1, ITGB6, COL6A3, COL6A1 and LAMC2) and extracellular matrix (ECM)-receptor interaction pathway (CDH1, ITGB6, COL6A3, COL6A1 and LAMC2), were significantly enriched by these DEGs. Among them, MMP2, CDH1 and FLT1 were hub nodes in the PPI network, while COL6A3, COL6A1, LAMC2 and ITGB6 were highlighted in module 3 network. In addition, PENK and APLNR were two crucial nodes in module 2, which were linked to each other. In conclusion, several potential biomarkers for DCM were identified, such as MMP2, FLT1, CDH1, ITGB6, COL6A3, COL6A1, LAMC2, PENK and APLNR. These genes may serve significant roles in DCM via involvement of various BPs, such as blood vessel and vasculature development and cell adhesion, and the ECM-receptor interaction pathway.

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“…Interestingly, obese subjects with impaired glucose metabolism only had lower apelin levels than controls. In the obese subgroup, carriers of the major G-allele had lower apelin levels [174]. However, the investigated sample size and so the statistical power was low (90 obese vs. 90 controls).…”

Section: Complement Component 3a Receptor 1 (C3ar1) Apelin Receptor mentioning

confidence: 91%

Genetic Determination of Serum Levels of Diabetes-Associated Adipokines

Schleinitz

¹

2015

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■ AbstractAdipose tissue secretes an abundance of proteins. Some of these proteins are known as adipokines and adipose-derived hormones which have been linked with metabolic disorders, including type 2 diabetes, and even with cancer. Variance in serum adipokine concentration is often closely associated with an increase (obesity) or decrease (lipodystrophy) in fat tissue mass, and it is affected by age, gender, and localization of the adipose tissue. However, there may be genetic variants which, in consequence, influence the serum concentration of a certain adipokine, and thereby promote metabolic disturbances or, with regard to the "protective" allele, exert beneficial effects. This review focuses on the genetic determination of serum levels of the following adipokines: adiponectin, chemerin, leptin, progranulin, resistin, retinol binding protein 4, vaspin, adipsin, apelin, and omentin. The article reports on the latest findings from genome-wide association studies (GWAS) and candidate gene studies, showing variants located in/nearby the adipokine genes and other (non-receptor) genes. An extra chapter highlights adipokine-receptor variants. Epigenetic studies on adipokines are also addressed.

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“…However, the relationship between the receptor SNP and serum apelin levels was not investigated [173]. To date, the rs11544374 G/A APJ polymorphism only was found to exert an effect on circulating apelin levels in childhood obesity ( Table 2) [174]. Interestingly, obese subjects with impaired glucose metabolism only had lower apelin levels than controls.…”

Section: Complement Component 3a Receptor 1 (C3ar1) Apelin Receptor mentioning

confidence: 99%

Genetic Determination of Serum Levels of Diabetes-Associated Adipokines

Schleinitz¹

2016

Rev Diabet Stud

0

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■ AbstractAdipose tissue secretes an abundance of proteins. Some of these proteins are known as adipokines and adipose-derived hormones which have been linked with metabolic disorders, including type 2 diabetes, and even with cancer. Variance in serum adipokine concentration is often closely associated with an increase (obesity) or decrease (lipodystrophy) in fat tissue mass, and it is affected by age, gender, and localization of the adipose tissue. However, there may be genetic variants which, in consequence, influence the serum concentration of a certain adipokine, and thereby promote metabolic disturbances or, with regard to the "protective" allele, exert beneficial effects. This review focuses on the genetic determination of serum levels of the following adipokines: adiponectin, chemerin, leptin, progranulin, resistin, retinol binding protein 4, vaspin, adipsin, apelin, and omentin. The article reports on the latest findings from genome-wide association studies (GWAS) and candidate gene studies, showing variants located in/nearby the adipokine genes and other (non-receptor) genes. An extra chapter highlights adipokine-receptor variants. Epigenetic studies on adipokines are also addressed.

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Apelin and G212A apelin receptor gene polymorphism in obese and diabese youth

Abstract: Obese (especially diabese) youngsters demonstrated lower serum apelin levels; the G212A polymorphism of the APLNR gene was found to exert a favourable effect on circulating apelin levels in childhood obesity.

Cited by 25 publications

References 30 publications

Bioinformatics method identifies potential biomarkers of dilated cardiomyopathy in a human induced pluripotent stem cell-derived cardiomyocyte model

Bioinformatics method identifies potential biomarkers of dilated cardiomyopathy in a human induced pluripotent stem cell-derived cardiomyocyte model

Genetic Determination of Serum Levels of Diabetes-Associated Adipokines

Genetic Determination of Serum Levels of Diabetes-Associated Adipokines

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