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C358A missense polymorphism of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH) and visfatin levels in obese females

International Journal of Obesity volume 34, pages 511–515 (2010)Cite this article

Subjects

Abstract

Background:

Recently, it has been shown that the polymorphism 385 C/A of FAAH (fatty acid amide hydrolase) was associated with overweight and obesity. Visfatin has been identified as a protein expressed in visceral adipose tissue with contradictory functions in glucose metabolism.

Objective:

The aim of our study was to investigate the relationship between polymorphism (cDNA 385 C->A) of the FAAH gene and visfatin levels in obese women.

Design:

A population of 143 females with obesity was analyzed. Indirect calorimetry, tetrapolar electrical bioimpedance, blood pressure and serial assessment of nutritional intake with 3-day written food records and biochemical analysis (lipid profile, visfatin, insulin, C-reactive protein and homeostasis model assessment for insulin sensitivity (HOMA)) were performed.

Results:

Ninety-four patients (65.7%) had the genotype C358C (wild-type group) and 49 (34.3%) patients had the genotype C358A (mutant type group). No differences were detected between groups in anthropometric parameters and dietary intakes. Insulin (15.6±7.6 vs 14.1±10.1 mUI l−1; P<0.05), glucose (101.2±21.9 vs 92.3±10.5 mg per 100 ml; P<0.05) and HOMA values (3.96±2.3 vs 3.15±2.8; P<0.05) were higher in the wild type-group than in the mutant type group. Visfatin levels were lower in the wild-type group than in the mutant type group (47.83±57.5 vs 65.71±55 ng ml−1; P<0.05).

Conclusion:

The novel finding of this study is the association of the mutant type group A358C of FAAH with lower glucose, insulin and HOMA levels than of the wild-type group with higher visfatin levels.

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References

  1. Fukuhara A, Matsuda M, Nishizawa M, Sagawa K, Tanaka M, Kishimoto K et al. Visfatin: a protein secreted by visceral fat that mimics the effects of insulin. Science 2005; 307: 426–430.

    Article  CAS  Google Scholar 

  2. Ognjanovic S . Genomic organization of the gene coding for human pre-B-cell colony enhancing factor and expression in human fetal membranes. J Mol Endocrinol 2001; 26: 107–117.

    Article  CAS  Google Scholar 

  3. Deustch DG, Ueda N, Yammamoto S . The fatty acid amide hydrolase (FAAH) 1. Prostaglandins Leukot Essent Fatty Acids 2002; 66: 201–210.

    Article  Google Scholar 

  4. Lichtman AH, Hawkins EG, Griffin G, Cravatt BF . Pharmacological activity of fatty acid amides is regulated, but not mediated, by fatty acid amide hydrolase in vivo. Pharmacol Exp Ther 2002; 302: 73–79.

    Article  CAS  Google Scholar 

  5. Matsuzawa Y . Adipocytokines: emerging therapeutic targets. Curr Atheros Rep 2005; 7: 58–62.

    Article  CAS  Google Scholar 

  6. Ameri A . The effects of cannabinnoids on the brain. Prog Neurobiol 1999; 58: 315–348.

    Article  CAS  Google Scholar 

  7. Fride E . Endocannabinoids in the central nervous system an overview. Prostaglandins Leukot Essent Fatty acids 2002; 66: 221–233.

    Article  CAS  Google Scholar 

  8. Sipe JC, Chiang K, Gerber AL, Beutler E, Cravatt BF . A Missense mutation in human fatty acid amide hydroxylase associated with problem drug abuse. Proc Natl Acad Sci USA 2002; 99: 8394–8399.

    Article  CAS  Google Scholar 

  9. Sipe JC, Waalen J, Gerber A, Beutler E . Overweight and obesity associated with a missense polymorphism in fatty acid amide hydrolase (FAAH). Int J of Obes 2005; 29: 755–759.

    Article  CAS  Google Scholar 

  10. Monteleone P, Tortorella A, Martiadis V, Filippo C, Canestrelli B, Maj M . The CDNA 385 C to A missense polymorphism of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH) os associated with overweight/obesity but not with binge eating disorder in overweight/obese women. Psychoneuroendocrinology 2008; 33: 546–550.

    Article  CAS  Google Scholar 

  11. Jensen D, Andreasen C, Andersen M, Hansen L, Eiberg H, Borch-Johnsen K et al. The functional pro129Thr variant of the FAAH gene is not associated with various fat accumulation phenotypes in a population-based cohort of 5801 whites. J Mol med 2007; 85: 445–449.

    Article  CAS  Google Scholar 

  12. Duart MJ, Arroyo CO, Moreno JL . Validation of a insulin model for the reactions in RIA. Clin Chem Lab Med 2002; 40: 1161–1167.

    Article  Google Scholar 

  13. Mathews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF . Homesotasis model assessment: insulin resistance and beta cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985; 28: 412–414.

    Article  Google Scholar 

  14. Friedewald WT, Levy RI, Fredrickson DS . Estimation of the concentration of low-density lipoprotein holesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem 1972; 18: 499–502.

    CAS  Google Scholar 

  15. Feurer ID, Mullen JL . Bedside measurement of resting energy expenditure and respiratory quotient via indirect calorimetry. Nutr Clin Pract 1986; 1: 43–49.

    Article  Google Scholar 

  16. Pichard C, Slosman D, Hirschel B, Kyle U . Bioimpedance analysis: an improved method for nutritional follow up. Clin Res 1993; 41: 53.

    Google Scholar 

  17. Mataix J, Mañas M . Tablas de composición de alimentos españoles. University of Granada: Granada, 2003.

  18. Chiang KP, Gerber AL, Sipe JC, Cravatt BF . Reduced cellular expression and activity of the P129T mutant fatty acid amide hydrolase: evidence for a link between defects in the endocannabinoid system and problem drug use. Hum Mol Genet 2004; 13: 2113–2119.

    Article  CAS  Google Scholar 

  19. Papazoglou D, Panagopoulos I, Papanas N, Gioka T, Papadopoulos T, Papathanasiou P et al. The FAAH Pro129Thr polymorphism is not associated with severe obesity in Greek Subjects. Horm Metab Res 2008; 40: 907–910.

    Article  CAS  Google Scholar 

  20. Aberle J, Fedderwitz I, Klages N, George E, Beil FU . Genetic variation in two proteins of the endocannabinoid system and their influence on body mass index and metabolism under low fat diet. Horm Metab Res 2007; 39: 395–397.

    Article  CAS  Google Scholar 

  21. Egertova M, Cravatt BF, Elphick MR . Comparative analysis of FAAH and CB1 canabinoid receptor expression in the mouse brain: evidence of a widespread role for fatty acid amide hydrolase in regulation of endocannabinoid signalling. Neuroscience 2003; 119: 481–496.

    Article  CAS  Google Scholar 

  22. Cota D, Marsicano G, Lutz B, Vicennati V, Stalla GK, Pasqualli R et al. endogenous cannabinoid system as a modulator of food intake. Int J Obes Relat Metab Disor 2003; 27: 289–301.

    Article  CAS  Google Scholar 

  23. Brendt J, Klöting N, Kralisch S, Kovacs P, Fasshauer M, Schön M et al. Plasma visfatin concentrations and fat depot specific RNA expresión in humans. Diabetes 2005; 54: 2911–2916.

    Article  Google Scholar 

  24. Sethi JK, Vidal Puig A . Visfatin: the missing link between intra-abdominal obesity and diabetes? Trends Mol Med 2005; 11: 344–350.

    Article  CAS  Google Scholar 

  25. Haider DG, Schaller G, Kapiotis S, Maier C, Luger A, Woltz M . The release of the adipocytokine visfatin is regulated by glucose and insulin. Diabetologia 2006; 49: 1909–1914.

    Article  CAS  Google Scholar 

  26. Perwitz N, Fasshauer M, Klein J . Cannabinoid receptor signaling directly inhibits thermogenesis and alters expression of adiponectin and vsifatin. Horm Metab Res 2006; 38: 356–358.

    Article  CAS  Google Scholar 

  27. Reimann M, Ziemssen T, Huisman HW, Schutte R, Malan L, Van Rooyen JM et al. Ethnic-specific correlations of visfatin with circulating markers of endothelial inflammation and function. Obesity (Silver Spring) 2009; 17: 2210–2215.

    Article  Google Scholar 

Download references

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Authors and Affiliations

  1. Institute of Endocrinology and Nutrition, Medicine School and Unit of Investigation, Hospital Rio Hortega, University of Valladolid, Valladolid, Spain

    D A de Luis, M Gonzalez Sagrado, R Aller, O Izaola, R Conde & E Romero

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  1. D A de Luis
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  2. M Gonzalez Sagrado
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  3. R Aller
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  4. O Izaola
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  5. R Conde
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  6. E Romero
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Correspondence to D A de Luis.

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de Luis, D., Gonzalez Sagrado, M., Aller, R. et al. C358A missense polymorphism of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH) and visfatin levels in obese females. Int J Obes 34, 511–515 (2010). https://doi.org/10.1038/ijo.2009.283

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