Table of Contents Author Guidelines Submit a Manuscript
PPAR Research
Volume 2009, Article ID 649286, 7 pages
http://dx.doi.org/10.1155/2009/649286
Research Article

The Role of the PGC1 Gly482Ser Polymorphism in Weight Gain due to Intensive Diabetes Therapy

1Division of Medical Genetics, Department of Medicine, University of Washington, Seattle, WA 98195-7720, USA
2Division of Metabolism, Endocrinology, and Nutrition, Department of Medicine, University of Washington, Seattle, WA 98195-7720, USA

Received 13 December 2008; Accepted 14 January 2009

Academic Editor: Marie-Claude Vohl

Copyright © 2009 Samir S. Deeb and John D. Brunzell. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Linked References

  1. A. S. Krolewski, E. J. Kosinski, J. H. Warram et al., “Magnitude and determinants of coronary artery disease in juvenile-onset, insulin-dependent diabetes mellitus,” The American Journal of Cardiology, vol. 59, no. 8, pp. 750–755, 1987. View at Publisher · View at Google Scholar
  2. The Diabetes Control and Complications Trial Research Group, “The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus,” The New England Journal of Medicine, vol. 329, no. 14, pp. 977–986, 1993. View at Publisher · View at Google Scholar
  3. J. Q. Purnell, J. E. Hokanson, S. M. Marcovina, M. W. Steffes, P. A. Cleary, and J. D. Brunzell, “Effect of excessive weight gain with intensive therapy of type 1 diabetes on lipid levels and blood pressure: results from the DCCT,” The Journal of the American Medical Association, vol. 280, no. 2, pp. 140–146, 1998. View at Publisher · View at Google Scholar
  4. J. Q. Purnell, R. K. Dev, M. W. Steffes et al., “Relationship of family history of type 2 diabetes, hypoglycemia, and autoantibodies to weight gain and lipids with intensive and conventional therapy in the diabetes control and complications trial,” Diabetes, vol. 52, no. 10, pp. 2623–2629, 2003. View at Publisher · View at Google Scholar
  5. M. C. Carr and J. D. Brunzell, “Abdominal obesity and dyslipidemia in the metabolic syndrome: importance of type 2 diabetes and familial combined hyperlipidemia in coronary artery disease risk,” The Journal of Clinical Endocrinology & Metabolism, vol. 89, no. 6, pp. 2601–2607, 2004. View at Publisher · View at Google Scholar
  6. S. S. Deeb, L. Fajas, M. Nemoto et al., “A Pro12Ala substitution in PPAR?2 associated with decreased receptor activity, lower body mass index and improved insulin sensitivity,” Nature Genetics, vol. 20, no. 3, pp. 284–287, 1998. View at Publisher · View at Google Scholar
  7. D. Altshuler, J. N. Hirschhorn, M. Klannemark et al., “The common PPAR? Pro12Ala polymorphism is associated with decreased risk of type 2 diabetes,” Nature Genetics, vol. 26, no. 1, pp. 76–80, 2000. View at Publisher · View at Google Scholar
  8. J. Ek, G. Andersen, S. A. Urhammer et al., “Mutation analysis of peroxisome proliferator-activated receptor-? coactivator-1 (PGC-1) and relationships of identified amino acid polymorphisms to type II diabetes mellitus,” Diabetologia, vol. 44, no. 12, pp. 2220–2226, 2001. View at Publisher · View at Google Scholar
  9. K. Hara, K. Tobe, T. Okada et al., “A genetic variation in the PGC-1 gene could confer insulin resistance and susceptibility to type II diabetes,” Diabetologia, vol. 45, no. 5, pp. 740–743, 2002. View at Publisher · View at Google Scholar
  10. H. Esterbauer, H. Oberkofler, V. Linnemayr et al., “Peroxisome proliferator-activated receptor-? coactivator-1 gene locus: associations with obesity indices in middle-aged women,” Diabetes, vol. 51, no. 4, pp. 1281–1286, 2002. View at Publisher · View at Google Scholar
  11. P. Puigserver and B. M. Spiegelman, “Peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α): transcriptional coactivator and metabolic regulator,” Endocrine Reviews, vol. 24, no. 1, pp. 78–90, 2003. View at Publisher · View at Google Scholar
  12. A. R. Shuldiner and J. C. McLenithan, “Genes and pathophysiology of type 2 diabetes: more than just the Radle cycle all over again,” The Journal of Clinical Investigation, vol. 114, no. 10, pp. 1414–1417, 2004. View at Publisher · View at Google Scholar
  13. V. K. Mootha, C. M. Lindgren, K.-F. Eriksson et al., “PGC-1a-responsive genes involved in oxidative phosphorylation are coordinately downregulated in human diabetes,” Nature Genetics, vol. 34, no. 3, pp. 267–273, 2003. View at Publisher · View at Google Scholar
  14. M. E. Patti, A. J. Butte, K. Cusi et al., “Coordinated reduction of genes of oxidative metabolism in humans with insulin resistance and diabetes: potential role of PGC1 and NRF1,” Proceedings of the National Academy of Sciences of the United States of America, vol. 100, no. 14, pp. 8466–8471, 2003. View at Publisher · View at Google Scholar
  15. M. G. Dobson, C. P. F. Redfern, N. Unwin, and J. U. Weaver, “The N363S polymorphism of the glucocorticoid receptor: potential contribution to central obesity in men and lack of association with other risk factors for coronary heart disease and diabetes mellitus,” The Journal of Clinical Endocrinology & Metabolism, vol. 86, no. 5, pp. 2270–2274, 2001. View at Publisher · View at Google Scholar
  16. R. Rosmond, Y. C. Chagnon, G. Holm et al., “A glucocorticoid receptor gene marker is associated with abdominal obesity, leptin, and dysregulation of the hypothalamic-pituitary-adrenal axis,” Obesity Research, vol. 8, no. 3, pp. 211–218, 2000. View at Publisher · View at Google Scholar
  17. E. F. C. van Rossum and S. W. J. Lamberts, “Polymorphisms in the glucocorticoid receptor gene and their associations with metabolic parameters and body composition,” Recent Progress in Hormone Research, vol. 59, pp. 333–357, 2004. View at Publisher · View at Google Scholar
  18. E. Rask, T. Olsson, S. Soderberg et al., “Tissue-specific dysregulation of cortisol metabolism in human obesity,” The Journal of Clinical Endocrinology & Metabolism, vol. 86, no. 3, pp. 1418–1421, 2001. View at Publisher · View at Google Scholar
  19. H. Masuzaki, J. Paterson, H. Shinyama et al., “A transgenic model of visceral obesity and the metabolic syndrome,” Science, vol. 294, no. 5549, pp. 2166–2170, 2001. View at Publisher · View at Google Scholar
  20. J. R. Seckl and B. R. Walker, “Minireview: 11β-hydroxysteroid dehydrogenase type 1—a tissue-specific amplifier of glucocorticoid action,” Endocrinology, vol. 142, no. 4, pp. 1371–1376, 2001. View at Publisher · View at Google Scholar
  21. W. Siffert, “G protein β3 subunit 825T allele, hypertension, obesity, and diabetic nepropathy,” Nephrology Dialysis Transplantation, vol. 15, no. 9, pp. 1298–1306, 2000. View at Google Scholar
  22. M. Rydén, G. Faulds, J. Hoffstedt, A. Wennlund, and P. Arner, “Effect of the (C825T) Gβ3 polymorphism on adrenoceptor-mediated lipolysis in human fat cells,” Diabetes, vol. 51, no. 5, pp. 1601–1608, 2002. View at Publisher · View at Google Scholar
  23. N. Stefan, M. Stumvoll, F. Machicao, M. Koch, H. U. Häring, and A. Fritsche, “C825T polymorphism of the G protein β3 subunit is associated with obesity but not with insulin sensitivity,” Obesity Research, vol. 12, no. 4, pp. 679–683, 2004. View at Publisher · View at Google Scholar
  24. A. H. Kissebah, G. E. Sonnenberg, J. Myklebust et al., “Quantitative trait loci on chromosomes 3 and 17 influence phenotypes of the metabolic syndrome,” Proceedings of the National Academy of Sciences of the United States of America, vol. 97, no. 26, pp. 14478–14483, 2000. View at Publisher · View at Google Scholar
  25. C. Menzaghi, T. Ercolino, R. D. Paola et al., “A haplotype at the adiponectin locus is associated with obesity and other features of the insulin resistance syndrome,” Diabetes, vol. 51, no. 7, pp. 2306–2312, 2002. View at Publisher · View at Google Scholar
  26. K. Hara, P. Boutin, Y. Mori et al., “Genetic variation in the gene encoding adiponectin is associated with an increased risk of type 2 diabetes in the Japanese population,” Diabetes, vol. 51, no. 2, pp. 536–540, 2002. View at Google Scholar
  27. T. M. Frayling, N. J. Timpson, M. N. Weedon et al., “A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity,” Science, vol. 316, no. 5826, pp. 889–894, 2007. View at Publisher · View at Google Scholar
  28. C. Dina, “New insights into the genetics of body weight,” Current Opinion in Clinical Nutrition and Metabolic Care, vol. 11, no. 4, pp. 378–384, 2008. View at Publisher · View at Google Scholar
  29. Y. L. Muller, C. Bogardus, O. Pedersen, and L. Baier, “A Gly482Ser missense mutation in the peroxisome proliferator-activated receptor γ coactivator-1 is associated with altered lipid oxidation and early insulin secretion in Pima Indians,” Diabetes, vol. 52, no. 3, pp. 895–898, 2003. View at Publisher · View at Google Scholar
  30. H. Esterbauer, H. Oberkofler, F. Krempler, and W. Patsch, “Human peroxisome proliferator activated receptor gamma coactivator 1 (PPARGC1) gene: cDNA sequence, genomic organization, chromosomal localization, and tissue expression,” Genomics, vol. 62, no. 1, pp. 98–102, 1999. View at Publisher · View at Google Scholar
  31. C. Ling, P. Poulsen, E. Carlsson et al., “Multiple environmental and genetic factors influence skeletal muscle PGC-1a and PGC-1ß gene expression in twins,” The Journal of Clinical Investigation, vol. 114, no. 10, pp. 1518–1526, 2004. View at Publisher · View at Google Scholar
  32. C. Handschin, J. Rhee, J. Lin, P. T. Tarr, and B. M. Spiegelman, “An autoregulatory loop controls peroxisome proliferator-activated receptor γ coactivator 1α expression in muscle,” Proceedings of the National Academy of Sciences of the United States of America, vol. 100, no. 12, pp. 7111–7116, 2003. View at Publisher · View at Google Scholar
  33. M. Ridderstråle, L. E. Johansson, L. Rastam, and U. Lindblad, “Increased risk of obesity associated with the variant allele of the PPARGC1A Gly482Ser polymorphism in physically inactive elderly men,” Diabetologia, vol. 49, no. 3, pp. 496–500, 2006. View at Publisher · View at Google Scholar
  34. L. Sun, Z. Yang, F. Jin et al., “The Gly482Ser variant of the PPARGC1 gene is associated with type 2 diabetes mellitus in northern Chinese, especially men,” Diabetic Medicine, vol. 23, no. 10, pp. 1085–1092, 2006. View at Publisher · View at Google Scholar
  35. I. Barroso, J. Luan, M. S. Sandhu et al., “Meta-analysis of the Gly482Ser variant in PPARGC1A in type 2 diabetes and related phenotypes,” Diabetologia, vol. 49, no. 3, pp. 501–505, 2006. View at Publisher · View at Google Scholar
  36. L. Pérusse, T. Rice, Y. C. Chagnon et al., “A genome-wide scan for abdominal fat assessed by computed tomography in the Québec Family Study,” Diabetes, vol. 50, no. 3, pp. 614–621, 2001. View at Publisher · View at Google Scholar
  37. R. E. Pratley, D. B. Thompson, M. Prochazka et al., “An autosomal genomic scan for loci linked to prediabetic phenotypes in pima indians,” The Journal of Clinical Investigation, vol. 101, no. 8, pp. 1757–1764, 1998. View at Publisher · View at Google Scholar
  38. L. Andrulionytè, J. Zacharova, J.-L. Chiasson, and M. Laakso, “Common polymorphisms of the PPAR-γ2 (Pro12Ala) and PGC-1α (Gly482Ser) genes are associated with the conversion from impaired glucose tolerance to type 2 diabetes in the STOP-NIDDM trial,” Diabetologia, vol. 47, no. 12, pp. 2176–2184, 2004. View at Publisher · View at Google Scholar
  39. L. J. Scott, K. L. Mohlke, L. L. Bonnycastle et al., “A genome-wide association study of type 2 diabetes in finns detects multiple susceptibility variants,” Science, vol. 316, no. 5829, pp. 1341–1345, 2007. View at Publisher · View at Google Scholar
  40. L. F. Michael, Z. Wu, R. B. Cheatham et al., “Restoration of insulin-sensitive glucose transporter (GLUT4) gene expression in muscle cells by the transcriptional coactivator PGC-1,” Proceedings of the National Academy of Sciences of the United States of America, vol. 98, no. 7, pp. 3820–3825, 2001. View at Publisher · View at Google Scholar