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Associations between TRPV4 genotypes and body mass index in Taiwanese subjects

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Abstract

Body weight regulation is influenced neuronally via the hypothalamus, which strongly expresses TRPV4. TRPV4 deficiency in mice confers resistance against diet-induced obesity. We investigated the association between TRPV4 gene variants and body mass index (BMI) in Taiwanese subjects. A sample population of 617 Taiwanese subjects was enrolled, and ten TRPV4 gene polymorphisms were selected and genotyped. After adjusting for clinical covariates, significant associations were observed between three studied polymorphisms and BMI using a dominant model (P = 4.83 × 10−4, P = 1.17 × 10−4, and P = 3.37 × 10−4 for rs3742037, rs10735104, and rs3742035, respectively). Obesity as defined according to both the Asian and National Institutes of Health (NIH) criteria was significantly associated with rs10735104 (P = 0.003 and P = 0.037, respectively) in a dominant model. Genotypes at the TRPV4 locus independently affect BMI and obesity status in Taiwanese subjects. This association may broaden our understanding of the role of neuronal influence on body weight regulation. The regulation of TRPV4 channels in skeletal muscle and adipose tissue could also be a new therapeutic target for preventing the development of obesity.

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Abbreviations

SNPs:

Single nucleotide polymorphisms

BMI:

Body mass index

GWAS:

Genome-wide association studies

TRP:

Transient receptor potential

TRPV4:

Transient receptor potential vanilloid subtype 4

NIH:

National Institutes of Health

ELISA:

Enzyme-linked immunosorbent assay

HDL:

High-density lipoprotein

LDL:

Low-density lipoprotein

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Acknowledgments

This study was supported by a grant from the National Science Council, Taiwan (NSC101-2314-B-303-023-MY3), and a grant from the Buddhist Tzu Chi General Hospital (TCRD-I100-01-01) to YL Ko.

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None.

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Correspondence to Yu-Lin Ko.

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Communicated by S. Hohmann.

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Duan, DM., Wu, S., Hsu, LA. et al. Associations between TRPV4 genotypes and body mass index in Taiwanese subjects. Mol Genet Genomics 290, 1357–1365 (2015). https://doi.org/10.1007/s00438-015-0996-8

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  • DOI: https://doi.org/10.1007/s00438-015-0996-8

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