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. 2007 Mar 26;21(2):85–90. doi: 10.1002/jcla.20138

Insulin and C‐peptide levels, pancreatic beta cell function, and insulin resistance across glucose tolerance status in Thais

La‐or Chailurkit 1,✉, Wallaya Jongjaroenprasert 1, Suwannee Chanprasertyothin 2, Boonsong Ongphiphadhanakul 1
PMCID: PMC6649081  PMID: 17385686

Abstract

Impaired pancreatic beta cell function and insulin sensitivity are fundamental factors in the pathogenesis of type 2 diabetes; however, the predominant defect appears differ among ethnic groups. We conducted a cross‐sectional study to evaluate the contribution of impaired beta cell function and insulin sensitivity at different stages of the deterioration of glucose tolerance in Thais. The study involved 420 urban Thais of both sexes, 43–84 years old. A 75‐g oral glucose tolerance test was performed on all of the subjects. Indices of insulin resistance and beta cell function were calculated with the use of a homeostasis model assessment. The subjects were classified as having normal glucose tolerance (NGT), isolated impaired fasting glucose (IFG), isolated impaired glucose tolerance (IGT), combined IFG and IGT, or type 2 diabetes mellitus according to the American Diabetes Association (ADA) criteria. There were no differences between groups with regard to gender and age. The percentage of obesity was significantly greatest in the diabetic group. Fasting serum insulin and C‐peptide levels progressively increased from the NGT to the diabetic subjects. Serum C‐peptide was more strongly associated with newly diagnosed diabetes than insulin, and was an independent factor associated with newly diagnosed diabetic subjects. The insulin resistance index progressively increased when the glucose tolerance stage changed from NGT through diabetic subjects. Beta cell function did not change significantly in any other group compared to the NGT group. An increase in fasting serum C‐peptide may be a risk factor for type 2 diabetes. Obesity and insulin resistance are the predominant features in the deterioration of glucose tolerance in Thais. J. Clin. Lab. Anal. 21:85–90, 2007. 2007 Wiley‐Liss, Inc.

Keywords: diabetes, obesity, homeostasis model assessment, beta cell function, insulin resistance

REFERENCES

  • 1. Aekplakorn W, Stolk RP, Neal B, et al. The prevalence and management of diabetes in Thai adults: the International Collaborative Study of Cardiovascular Disease in Asia. Diabetes Care 2003;26:2758–2763. [DOI] [PubMed] [Google Scholar]
  • 2. King H, Aubert RE, Herman WH. Global burden of diabetes, 1995–2025: prevalence, numerical estimates, and projections. Diabetes Care 1998;21:1414–1431. [DOI] [PubMed] [Google Scholar]
  • 3. Jensen CC, Cnop M, Hull RL, Fujimoto WY, Kahn SE. Beta‐cell function is a major contributor to oral glucose tolerance in high‐risk relatives of four ethnic groups in the U.S. Diabetes 2002;51:2170–2178. [DOI] [PubMed] [Google Scholar]
  • 4. Chiu KC, Cohan P, Lee NP, Chuang LM. Insulin sensitivity differs among ethnic groups with a compensatory response in beta‐cell function. Diabetes Care 2000;23:1353–1358. [DOI] [PubMed] [Google Scholar]
  • 5. Haffner SM, D'Agostino R, Saad MF, et al. Increased insulin resistance and insulin secretion in nondiabetic African‐Americans and Hispanics compared with non‐Hispanic whites. The Insulin Resistance Atherosclerosis Study. Diabetes 1996;45:742–748. [DOI] [PubMed] [Google Scholar]
  • 6. Jones CN, Pei D, Staris P, Polonsky KS, Chen YD, Reaven GM. Alterations in the glucose‐stimulated insulin secretory dose‐response curve and in insulin clearance in nondiabetic insulin‐resistant individuals. J Clin Endocrinol Metab 1997;82:1834–1838. [DOI] [PubMed] [Google Scholar]
  • 7. Kahn BB, Flier JS. Obesity and insulin resistance. J Clin Invest 2000;106:473–481. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8. Wannamethee SG, Shaper AG, Durrington PN, Perry IJ. Hypertension, serum insulin, obesity and the metabolic syndrome. J Hum Hypertens 1998;12:735–741. [DOI] [PubMed] [Google Scholar]
  • 9. Tan CE, Ma S, Wai D, Chew SK, Tai ES. Can we apply the National Cholesterol Education Program Adult Treatment Panel definition of the metabolic syndrome to Asians? Diabetes Care 2004;27:1182–1186. [DOI] [PubMed] [Google Scholar]
  • 10. Janus ED, Watt NM, Lam KS, et al. The prevalence of diabetes, association with cardiovascular risk factors and implications of diagnostic criteria (ADA 1997 and WHO 1998) in a 1996 community‐based population study in Hong Kong Chinese. Hong Kong Cardiovascular Risk Factor Steering Committee. American Diabetes Association. Diabetic Med 2000;17:741–745. [DOI] [PubMed] [Google Scholar]
  • 11. Cockram CS. Diabetes mellitus: perspective from the Asia‐Pacific region. Diabetes Res Clin Pract 2000;50(Suppl 2):S3–S7. [DOI] [PubMed] [Google Scholar]
  • 12. Polonsky KS, Rubenstein AH. C‐peptide as a measure of the secretion and hepatic extraction of insulin. Pitfalls and limitations. Diabetes 1984;33:486–494. [DOI] [PubMed] [Google Scholar]
  • 13. American Diabetes Association . Diagnosis and classification of diabetes mellitus. Diabetes Care 2004;27(Suppl 1):S5–S10. [DOI] [PubMed] [Google Scholar]
  • 14. World Health Organization . The Asia‐Pacific perspective: redefining obesity and its treatment. World Health Organization, Western Pacific Region: World Health Organization; 2000. [Google Scholar]
  • 15. Wallace TM, Levy JC, Matthews DR. Use and abuse of HOMA modeling. Diabetes Care 2004;27:1487–1495. [DOI] [PubMed] [Google Scholar]
  • 16. Efrat S. Prospects for treatment of type 2 diabetes by expansion of the beta‐cell mass. Diabetes 2001;50(Suppl 1):S189–S190. [DOI] [PubMed] [Google Scholar]
  • 17. Porte D Jr. Clinical importance of insulin secretion and its interaction with insulin resistance in the treatment of type 2 diabetes mellitus and its complications. Diabetes Metab Res Rev 2001;17:181–188. [DOI] [PubMed] [Google Scholar]
  • 18. Fukushima M, Usami M, Ikeda M, et al. Insulin secretion and insulin sensitivity at different stages of glucose tolerance: a cross‐sectional study of Japanese type 2 diabetes. Metabolism 2004;53:831–835. [DOI] [PubMed] [Google Scholar]
  • 19. Tripathy D, Carlsson M, Almgren P, et al. Insulin secretion and insulin sensitivity in relation to glucose tolerance: lessons from the Botnia study. Diabetes 2000;49:975–980. [DOI] [PubMed] [Google Scholar]
  • 20. Haffner SM, Howard G, Mayer E, et al. Insulin sensitivity and acute insulin response in African‐Americans, non‐Hispanic whites, and Hispanics with NIDDM: the Insulin Resistance Atherosclerosis Study. Diabetes 1997;46:63–69. [DOI] [PubMed] [Google Scholar]
  • 21. Yeni‐Komshian H, Carantoni M, Abbasi F, Reaven GM. Relationship between several surrogate estimates of insulin resistance and quantification of insulin‐mediated glucose disposal in 490 healthy nondiabetic volunteers. Diabetes Care 2000;23:171–175. [DOI] [PubMed] [Google Scholar]
  • 22. Bonora E, Targher G, Alberiche M, et al. Homeostasis model assessment closely mirrors the glucose clamp technique in the assessment of insulin sensitivity: studies in subjects with various degrees of glucose tolerance and insulin sensitivity. Diabetes Care 2000;23:57–63. [DOI] [PubMed] [Google Scholar]
  • 23. Chen KW, Boyko EJ, Bergstrom RW, et al. Earlier appearance of impaired insulin secretion than of visceral adiposity in the pathogenesis of NIDDM. 5‐Year follow‐up of initially nondiabetic Japanese‐American men. Diabetes Care 1995;18:747–753. [DOI] [PubMed] [Google Scholar]
  • 24. Mokdad AH, Bowman BA, Ford ES, Vinicor F, Marks JS, Koplan JP. The continuing epidemics of obesity and diabetes in the United States. JAMA 2001;286:1195–1200. [DOI] [PubMed] [Google Scholar]
  • 25. Martin BC, Warram JH, Krolewski AS, Bergman RN, Soeldner JS, Kahn CR. Role of glucose and insulin resistance in development of type 2 diabetes mellitus: results of a 25‐year follow‐up study. Lancet 1992;340:925–929. [DOI] [PubMed] [Google Scholar]
  • 26. DeFronzo RA, Bonadonna RC, Ferrannini E. Pathogenesis of NIDDM. A balanced overview. Diabetes Care 1992;15:318–368. [DOI] [PubMed] [Google Scholar]
  • 27. Lee TH. Prevalence of obesity in Korean non‐insulin‐dependent diabetic patients. Diabetes Res Clin Pract 1996;32:71–80. [DOI] [PubMed] [Google Scholar]
  • 28. Chan WB, Tong PC, Chow CC, et al. The associations of body mass index, C‐peptide and metabolic status in Chinese Type 2 diabetic patients. Diabetic Med 2004;21:349–353. [DOI] [PubMed] [Google Scholar]
  • 29. Nagaya T, Yoshida H, Takahashi H, Kawai M. Increases in body mass index, even within non‐obese levels, raise the risk for type 2 diabetes mellitus: a follow‐up study in a Japanese population. Diabetic Med 2005;22:1107–1111. [DOI] [PubMed] [Google Scholar]
  • 30. Del Prato S, Marchetti P, Bonadonna RC. Phasic insulin release and metabolic regulation in type 2 diabetes. Diabetes 2002;51(Suppl 1):S109–S116. [DOI] [PubMed] [Google Scholar]
  • 31. Kahn SE. The relative contributions of insulin resistance and beta‐cell dysfunction to the pathophysiology of type 2 diabetes. Diabetologia 2003;46:3–19. [DOI] [PubMed] [Google Scholar]
  • 32. Davies MJ, Rayman G, Grenfell A, Gray IP, Day JL, Hales CN. Loss of the first phase insulin response to intravenous glucose in subjects with persistent impaired glucose tolerance. Diabetic Med 1994;11:432–436. [DOI] [PubMed] [Google Scholar]
  • 33. Prando R, Cheli V, Melga P, Giusti R, Ciuchi E, Odetti P. Is type 2 diabetes a different disease in obese and nonobese patients? Diabetes Care 1998;21:1680–1685. [DOI] [PubMed] [Google Scholar]
  • 34. Lee WR. The changing demography of diabetes mellitus in Singapore. Diabetes Res Clin Pract 2000;50(Suppl 2):S35–S39. [DOI] [PubMed] [Google Scholar]

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