Endocrine

, Volume 31, Issue 2, pp 93–99 | Cite as

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

  • Jie Hong
  • Wei-Qiong Gu
  • Yi-Fei Zhang
  • Yi-Sheng Yang
  • Chun-Fang Shen
  • Min Xu
  • Xiao-Ying Li
  • Wei-Qing Wang
  • Guang Ning
Original Paper

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.

Keywords

Insulin resistance Insulin secretion Obesity Impaired glucose tolerance Diabetes 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

Notes

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.

References

  1. 1.
    C. Weyer, C. Bogardus, P.A. Tataranni, R.E. Pratley, Diabetes Care 24, 89–94 (2001)CrossRefPubMedGoogle Scholar
  2. 2.
    C. Weyer, C. Bogardus, D.M. Mott, R.E. Pratley, J. Clin. Invest. 104, 787–794 (1999)CrossRefPubMedGoogle Scholar
  3. 3.
    G. Pillonetto, G. Sparacino, P. Magni, R. Bellazzi, C. Cobelli, Am. J. Physiol. Endocrinol. Metab. 282, E564–E573 (2002)PubMedGoogle Scholar
  4. 4.
    S.M. Haffner, R. D’Aqostino, M.F. Saad et al., Diabetes 45(6), 742–748 (l996)CrossRefGoogle Scholar
  5. 5.
    S.M. Haffner, G. Howard, E. Mayer et al., Diabetes 46(1), 63–69 (1997)CrossRefPubMedGoogle Scholar
  6. 6.
    F.B. Hu, T.Y. Li, G.A. Colditz, W.C. Willett, J.E. Manson, JAMA 14, 1785–1791 (2003)CrossRefGoogle Scholar
  7. 7.
    E. Ferrannini, S. Vichi, H. Beck-Nielsen, M. Laakso, G. Paolisso, U. Smith, Diabetes 45, 947–953 (1996)CrossRefPubMedGoogle Scholar
  8. 8.
    E.J. Mayer-Davis, T. Costacou, Curr. Diab. Rep. 2, 170–176 (2001)CrossRefGoogle Scholar
  9. 9.
    R.A. DeFronzo, Diabetes 28, 1095–1101 (1979)PubMedGoogle Scholar
  10. 10.
    M. Chen, R.N. Bergman, G. Pacini, D. Porte Jr., J. Clin. Endocrinol. Metab. 60, 13–20 (1985)CrossRefPubMedGoogle Scholar
  11. 11.
    M. Annette, J.B. Chang Halter, Am. J. Physiol. Endocrinol. Metab. 284, E7–E12 (2003)Google Scholar
  12. 12.
    A. Fritsche, A. Madaus, N. Stefan et al., Diabetes 51, S234–S239 (2002)CrossRefPubMedGoogle Scholar
  13. 13.
    W.Y. Fujimoto, S.L. Abbate, S.E. Kahn, J.E. Hokanson, J.D.␣Brunzell, Obes. Res. 2, 364–371 (1994)PubMedGoogle Scholar
  14. 14.
    K.M. Utzschneider, D.B. Carr, R.L. Hull et al., Diabetes 53, 2867–2872 (2004)CrossRefPubMedGoogle Scholar
  15. 15.
    T. Kuzuya, Br J Nutr. 84(Suppl 2), S177–181 (2000)Google Scholar
  16. 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, 2000Google Scholar
  17. 17.
    G.M. Steil, A. Volund, S.E. Kahn, R.N. Bergman, Diabetes 42, 250–256 (1993)Google Scholar
  18. 18.
    G. Pacini, G. Tonolo, M. Sambataro et al., Am J Physiol. 274(4 Pt 1), E592–599 (1998)Google Scholar
  19. 19.
    S.E. Kahn, D.L. Prigeon, D.K. McCulloch et al., Diabetes 42, 1663–1672 (1993)Google Scholar

Copyright information

© Humana Press Inc. 2007

Authors and Affiliations

  • Jie Hong
    • 1
  • Wei-Qiong Gu
    • 1
  • Yi-Fei Zhang
    • 1
  • Yi-Sheng Yang
    • 1
  • Chun-Fang Shen
    • 1
  • Min Xu
    • 1
  • Xiao-Ying Li
    • 1
    • 2
  • Wei-Qing Wang
    • 1
  • Guang Ning
    • 1
    • 2
  1. 1.Department of Endocrinology and Metabolism, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases, Rui-Jin HospitalShanghai Jiaotong University School of MedicineShanghaiPR China
  2. 2.The Endocrine and Metabolic DivisionE-Institute of Shanghai UniversitiesShanghaiPR China

Personalised recommendations