Diabetes Research and Clinical Practice
Volume 88, Issue 1 , Pages 76-80 , April 2010

C358A missense polymorphism of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH) and insulin resistance in patients with diabetes mellitus type 2

Received 11 November 2009 ,Revised 7 December 2009 ,Accepted 14 December 2009.

References 

  1. Aranceta J, Perez Rodrigo C, Serra Majem L. Prevalencia de la obesidad en España: estudio SEEDO 97. Med. Clin. (Barc.). 1998;111:441–445
  2. Matsuzawa Y, Adipocytokines: . Emerging therapeutic targets. Curr. Atheroscler. Rep. 2005;7:58–62
  3. Ameri A. The effects of cannabinnoids on the brain. Prog. Neurobiol. 1999;58:315–348
  4. Brown SM, Warger-Miller J, Mackie K. Cloning and molecular characterization of the rat CB2 cannabinoid receptor. Biochim. Biophys. Acta. 2002;1576:255–264
  5. Deustch DG, Ueda N, Yammamoto S. The fatty acid amide hydrolase (FAAH) 1. Prostaglandins Leukot. Essent. Fatty Acids. 2002;66:201–210
  6. 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
  7. 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. U.S.A. 2002;99:8394–8399
  8. Sipe JC, Waalen J, Gerber A, Beutler E. Overweight and obesity associated with a missense polymorphism in fatty acid amide hydrolase (FAAH). Int. J. Obes. 2005;29:755–759
  9. 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) is associated with overweight/obesity but not with binge eating disorder in overweight/obese women. Psychoneuroendocrinology. 2008;33:546–550
  10. 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
  11. Duart MJ, Arroyo CO, Moreno JL. Validation of an insulin model for the reactions in RIA. Clin. Chem. Lab. Med. 2002;40:1161–1167
  12. Mathews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher Df. Homeostasis model assessment: insulin resistance and beta cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985;28:412–414
  13. Pfutzner A, Langefeld M, Kunt T, Lobig M. Evaluation of human resistin assays with serum from patients with type 2 diabetes and different degrees of insulin resistance. Clin. Lab. 2003;49:571–576
  14. Meier U, Gressner M. Endocrine regulation of energy metabolism: review of pathobiochemical and clinical chemical aspects of leptin, ghrelin, adiponectin, and resistin. Clin. Chem. 2004;50:1511–1525
  15. Suominen P. evaluation of an enzyme immunometric assay to measure serum adiponectin concentrations. Clin. Chem. 2004;50:219–221
  16. Lubrano V, Cocci F, Battaglia D, Papa A. Usefulness of high-sensitivity IL6 measurement for clinical characterization of patients with coronary artery disease. J. Clin. Lab. Anal. 2005;19:110–114
  17. Khan SS, Smith MS, Reda D, Suffredini AF, Mc Coy JP. Multiplex bead array assays for detection of soluble cytokines: comparisons of sensitivity and quantitative values among kits from multiple manufactures. Cytometry B: Clin. Cytom. 2004;61:35–39
  18. Feurer ID, Mullen JL. Bedside measurement of resting energy expenditure and respiratory quotient via indirect calorimetry. Nutr. Clin. Pract. 1986;1:43–49
  19. Pichard C, Slosman D, Hirschel B, Kyle U. Bioimpedance analysis: an improved method for nutritional follow up. Clin. Res. 1993;41:53
  20. Mataix J, Mañas M. Tablas de composición de alimentos españoles. University of Granada; 2003;
  21. 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
  22. 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
  23. 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
  24. Egertova M, Cravatt BF, Elphick MR. Comparative analysis of FAAH and CB1 cannabinoid 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
  25. Cota D, Marsicano G, Lutz B, Vicennatu V, Stalla GK, Pasqualli R, et al. endogenous cannabinoid system as a modulator of food intake. Int. J. Obes. Relat. Metab. Disord. 2003;27:289–301
  26. Salmennienmi U, Zacharova J, Ruotsalainen E, Vauhkonen I, Pihlajamaki J, Kainulainen S. Association of adiponectin level and variants in the adiponectin gene with glucose metabolism, energy expenditure and cytokines in offspring of type 2 diabetic patients. J. Clin. Endocrinol. Metab. 2005;Epub ahead of print
  27. Mantzmoros CS, Manson JE, Meigs J, Hu FB. Circulating adiponectin levels are associated with better glycemic control, more favourable lipid profile and reduced inflammation in women with type 2 diabetes. J. Clin. Endocrinol. Metab. 2005;90(8):4542–4548

PII: S0168-8227(09)00544-0

doi: 10.1016/j.diabres.2009.12.019

Diabetes Research and Clinical Practice
Volume 88, Issue 1 , Pages 76-80 , April 2010

Article Tools