Literature DB >> 23616186

Lack of association between C385A functional polymorphism of the fatty acid amide hydrolase gene and polycystic ovary syndrome.

V K Grolmusz1, B Stenczer, T Fekete, G Szendei, A Patócs, K Rácz, P Reismann.   

Abstract

The endocannabinoid system contributes to the regulation of appetite, food intake and energy balance. Fatty acid amide hydrolase is responsible for degradating anandamide, a key messenger of the endocannabinoid system. C385A is a common, functionally active genetic polymorphism of the gene encoding fatty acid amide hydrolase and has been associated with overweight and obesity. Our aim was to establish whether single nucleotide polymorphism C385A has an association with polycystic ovary syndrome or its clinical features.A monocentric pilot study was performed on 63 patients with polycystic ovary syndrome and 67 healthy control subjects. Anthropometric parameters and laboratory data were acquired from subjects. The alleles of the polymorphism were detected using polymerase chain reaction and subsequent cleavage by Eco130I (StyI) restriction endonuclease verified by direct DNA sequencing.No difference was found in minor allele frequency between patient and control groups. Those patients, carrying the C385A polymorphism were associated with higher free thyroxine hormone levels. In the control group, carriers of the polymorphism had significantly lower insulin levels.Our data indicate that the C385A polymorphism of the fatty acid amide hydrolase gene is not a genetic susceptibility factor for the development of polycystic ovary syndrome. However, the polymorphism might have a role in influencing the synthesis or metabolism of different hormones including thyroxin and insulin. © J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York.

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Year:  2013        PMID: 23616186     DOI: 10.1055/s-0033-1337941

Source DB:  PubMed          Journal:  Exp Clin Endocrinol Diabetes        ISSN: 0947-7349            Impact factor:   2.949


  4 in total

1.  MEN1 mutations and potentially MEN1-targeting miRNAs are responsible for menin deficiency in sporadic and MEN1 syndrome-associated primary hyperparathyroidism.

Authors:  Vince Kornél Grolmusz; Katalin Borka; Annamária Kövesdi; Kinga Németh; Katalin Balogh; Csaba Dékány; András Kiss; Anna Szentpéteri; Beatrix Sármán; Anikó Somogyi; Éva Csajbók; Zsuzsanna Valkusz; Miklós Tóth; Péter Igaz; Károly Rácz; Attila Patócs
Journal:  Virchows Arch       Date:  2017-06-08       Impact factor: 4.064

2.  Genetic variants of the HSD11B1 gene promoter may be protective against polycystic ovary syndrome.

Authors:  Vince Kornél Grolmusz; Orsolya Dóra Acs; Karolina Feldman-Kovács; Ágnes Szappanos; Balázs Stenczer; Tibor Fekete; György Szendei; Péter Reismann; Károly Rácz; Attila Patócs
Journal:  Mol Biol Rep       Date:  2014-06-27       Impact factor: 2.316

3.  True MEN1 or phenocopy? Evidence for geno-phenotypic correlations in MEN1 syndrome.

Authors:  Annamária Kövesdi; Miklós Tóth; Henriett Butz; Nikolette Szücs; Beatrix Sármán; Péter Pusztai; Judit Tőke; Péter Reismann; Mónika Fáklya; Géza Tóth; Anikó Somogyi; Katalin Borka; Annamária Erdei; Endre V Nagy; Veronika Deák; Zsuzsanna Valkusz; Péter Igaz; Attila Patócs; Vince Kornél Grolmusz
Journal:  Endocrine       Date:  2019-05-01       Impact factor: 3.633

Review 4.  Potential of Fatty Acid Amide Hydrolase (FAAH), Monoacylglycerol Lipase (MAGL), and Diacylglycerol Lipase (DAGL) Enzymes as Targets for Obesity Treatment: A Narrative Review.

Authors:  Justin Matheson; Xin Ming Matthew Zhou; Zoe Bourgault; Bernard Le Foll
Journal:  Pharmaceuticals (Basel)       Date:  2021-12-17
  4 in total

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