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The interplay of insulin resistance and β-cell dysfunction involves the development of type 2 diabetes in Chinese obeses

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Abstract

Type 2 diabetes mellitus (T2DM) is a heterogeneous disorder characterized by defects in insulin secretion and action and obesity plays an important role in the deterioration of glucose metabolism. In the present study we evaluated the degree of insulin resistance and first-phase insulin secretion of β-cell in obese subjects with normal glucose tolerance (NGT), impaired glucose tolerance (IGT), and T2DM in Chinese. A total of 220 subjects underwent standard 75 g oral glucose tolerance test (OGTT) and insulin-modified frequently sampled intravenous glucose tolerance test (FSIGT). Insulin sensitivity index (S I) was assessed by the reduced sample number (n = 12) of Bergman’s minimal model method with FSIGT. Insulin secretion capacities were determined by the insulinogenic index (I 30 min − I 0 min)/(G 30 min − G 0 min) in OGTT and the acute insulin response to glucose (AIR) in FSIGT. The disposition index (DI), the product of AIR and S I was used to determine whether AIR was adequate to compensate for insulin resistance. The S I in healthy lean control group was significantly higher than that in NGT, IGT, and T2DM group, but there was no significant difference among NGT, IGT, and T2DM group. The AIR in NGT group was significantly greater than that in control group, but then it was progressively decreased in IGT and T2DM group. The value of DI in control group was significantly higher than that in those three abnormal groups, and was decreased from NGT to IGT and T2DM group with significant difference. It indicates that obese subjects with different glucose tolerances have a similar degree of insulin resistance but differ in insulin secretion in Chinese Han population.

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References

  1. C. Weyer, C. Bogardus, P.A. Tataranni, R.E. Pratley, Diabetes Care 24, 89–94 (2001)

    Article  CAS  PubMed  Google Scholar 

  2. C. Weyer, C. Bogardus, D.M. Mott, R.E. Pratley, J. Clin. Invest. 104, 787–794 (1999)

    Article  CAS  PubMed  Google Scholar 

  3. G. Pillonetto, G. Sparacino, P. Magni, R. Bellazzi, C. Cobelli, Am. J. Physiol. Endocrinol. Metab. 282, E564–E573 (2002)

    CAS  PubMed  Google Scholar 

  4. S.M. Haffner, R. D’Aqostino, M.F. Saad et al., Diabetes 45(6), 742–748 (l996)

    Article  Google Scholar 

  5. S.M. Haffner, G. Howard, E. Mayer et al., Diabetes 46(1), 63–69 (1997)

    Article  CAS  PubMed  Google Scholar 

  6. F.B. Hu, T.Y. Li, G.A. Colditz, W.C. Willett, J.E. Manson, JAMA 14, 1785–1791 (2003)

    Article  Google Scholar 

  7. E. Ferrannini, S. Vichi, H. Beck-Nielsen, M. Laakso, G. Paolisso, U. Smith, Diabetes 45, 947–953 (1996)

    Article  CAS  PubMed  Google Scholar 

  8. E.J. Mayer-Davis, T. Costacou, Curr. Diab. Rep. 2, 170–176 (2001)

    Article  Google Scholar 

  9. R.A. DeFronzo, Diabetes 28, 1095–1101 (1979)

    CAS  PubMed  Google Scholar 

  10. M. Chen, R.N. Bergman, G. Pacini, D. Porte Jr., J. Clin. Endocrinol. Metab. 60, 13–20 (1985)

    Article  CAS  PubMed  Google Scholar 

  11. M. Annette, J.B. Chang Halter, Am. J. Physiol. Endocrinol. Metab. 284, E7–E12 (2003)

    Google Scholar 

  12. A. Fritsche, A. Madaus, N. Stefan et al., Diabetes 51, S234–S239 (2002)

    Article  CAS  PubMed  Google Scholar 

  13. W.Y. Fujimoto, S.L. Abbate, S.E. Kahn, J.E. Hokanson, J.D.␣Brunzell, Obes. Res. 2, 364–371 (1994)

    CAS  PubMed  Google Scholar 

  14. K.M. Utzschneider, D.B. Carr, R.L. Hull et al., Diabetes 53, 2867–2872 (2004)

    Article  CAS  PubMed  Google Scholar 

  15. T. Kuzuya, Br J Nutr. 84(Suppl 2), S177–181 (2000)

    Google Scholar 

  16. Steering Committee of the Western Pacific Region of the World Health Organization, the International Association for the Study of Obesity, and the International Obesity Task Force. Melbourne, Australia: Health Communications Australia Pty Ltd, 2000

  17. G.M. Steil, A. Volund, S.E. Kahn, R.N. Bergman, Diabetes 42, 250–256 (1993)

    Google Scholar 

  18. G. Pacini, G. Tonolo, M. Sambataro et al., Am J Physiol. 274(4 Pt 1), E592–599 (1998)

  19. S.E. Kahn, D.L. Prigeon, D.K. McCulloch et al., Diabetes 42, 1663–1672 (1993)

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Acknowledgments

This study was supported by grants from National Natural Science Foundation of China (No. 30570880). The authors would like to thank Professor Bergman RN for his generous support in providing the minimal model software for our clinical center.

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Correspondence to Guang Ning.

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Hong, J., Gu, WQ., Zhang, YF. et al. The interplay of insulin resistance and β-cell dysfunction involves the development of type 2 diabetes in Chinese obeses. Endocr 31, 93–99 (2007). https://doi.org/10.1007/s12020-007-0002-2

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  • DOI: https://doi.org/10.1007/s12020-007-0002-2

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