Journal List > Korean Diabetes J > v.32(6) > 1002258

Choi, Rhee, Kim, Won, Park, Lee, Oh, Park, and Kim: Insulin Sensitivity and Insulin Secretion Determined by Homeostasis Model Assessment and Future Risk of Diabetes Mellitus in Korean Men

Abstract

Background

Insulin resistance and progressive pancreatic beta cell dysfunction have been identified as the two fundamental features in the type 2 diabetes. Homeostasis model assessment (HOMA), based on plasma levels of fasting glucose and insulin, has been widely validated and applied for quantifying insulin resistance and secretion. This study was performed to assess the predictive value of HOMA indices for future diabetes risk.

Methods

In 14,976 Korean men, in which medical check-up was performed both in 2002 and 2006 in a university hospital health promotion center in Seoul, Korea, prospective assessment for diabetes risk was assessed. At baseline, anthropometric measurements were done and fasting glucose, insulin, lipid profiles were measured. HOMA-insulin resistance (HOMA-IR) and beta cell function (HOMA β-cell) were calculated from fasting glucose and insulin levels.

Results

After 4 years, 286 subjects (1.9%) were newly diagnosed as diabetes mellitus. These patients (mean age 40.3 years) were age-matched with 632 control subjects (mean age 39.8 years) and diabetes risk was assessed with HOMA indices. Among the parameters, body mass index, fasting glucose and HOMA β-cell were the significant determinants for future diabetes risk. When the subjects were divided into two groups according to the baseline median values of HOMA-IR and HOMA β-cell, and assessed jointly, those with the low HOMA β-cell and high HOMA-IR showed the highest risk for future diabetes (RR 39.065, 95% CI 11.736~130.035, P < 0.01). The subjects with low baseline HOMA β-cell showed higher RR for diabetes than those with high baseline HOMA-IR (4.413 vs. 3.379, P = 0.018, P = 0.051).

Conclusion

High HOMA-IR and low HOMA β-cell were associated with the highest risk for future diabetes in this prospective study of Korean male subjects. These data suggest the value of HOMA indices for diabetes risk in epidemiologic studies in Asian subjects.

Figures and Tables

Fig. 1
Selection and entry of study subjects in this study.
kdj-32-498-g001
Table 1
Baseline characteristics of diabetic case and control subjects
kdj-32-498-i001

BMI, body mass index; DBP, diastolic blood pressure; HOMA-IR, homeostasis model assessment of insulin resistance; SBP, systolic blood pressure.

Table 2
Multiple logistic regression analysis with newly diagnosed diabetes mellitus as the dependent variable
kdj-32-498-i002

BMI, body mass index; HOMA-IR, homeostasis model assessment of insulin resistance.

Table 3
Relative risk for future diabetes according to different levels of HOMA-IR and HOMA β-cell
kdj-32-498-i003

Logistic regression analyses were performed with age, body mass index and smoking included in the model. HOMA-IR, homeostasis model assessmentof insulin resistance.

References

1. Fonseca VA. Identification and treatment of prediabetes to prevent progression to type 2 diabetes. Clinical cornerstone. 2007. 8:10–20.
crossref
2. Ministry for Health. Korea Centers for Disease Control and Prevention: Third Korea National Health and Nutrition Examination Survey (KNHANES III). Welfare and Family Affairs. 2005. Seoul:
3. Yoon KH, Lee JH, Kim JW, Cho JH, Choi YH, Ko SH, Zimmet P, Son HY. Epidemic obesity and type 2 diabetes in Asia. Lancet. 2006. 368:1681–1688.
crossref
4. Albright A. What is public health practice telling us about diabetes. J Am Diet Assoc. 2008. 108:S12–S18.
crossref
5. Kahn SE. The relative contributions of insulin resistance and beta-cell dysfunction to the pathophy- siology of type 2 diabetes. Diabetologia. 2003. 46:3–19.
6. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentration in man. Diabetologia. 1985. 28:412–419.
7. Matsumoto K, Miyake S, Yano M, Ueki Y, Yamaguchi Y, Akazawa S, Tominaga Y. Glucose tolerance, insulin secretion, and insulin sensitivity in nonobese and obese Japanese subjects. Diabetes Care. 1997. 20:1562–1568.
crossref
8. Haffner SM, Miettinen H, Stern MP. The homeostasis model in the San Antonio Heart Study. Diabetes Care. 1997. 20:1087–1092.
crossref
9. Song Y, Manson JE, Tinker L, Howard BV, Kuller LH, Nathan L, Rifai N, Liu S. Insulin sensitivity and insulin secretion determined by homeostasis model assessment and risk of diabetes in a multiethinic cohort of women. Diabetes Care. 2007. 30:1747–1752.
10. Bonora E, Kiechl S, Willeit J, Oberhollenzer F, Egger G, Meigs JB, Bonadonna RC, Muggeo M. Population-based incidence rates and risk factors for type 2 diabetes in white individuals: the Bruneck study. Diabetes. 2004. 53:1782–1789.
crossref
11. Haffner SM, Gonzalez C, Miettinen H, Kenedy E, Stern MP. A prospective analysis of the HOMA model. Diabetes Care. 1996. 19:1138–1141.
12. Osei K, Rhinesmith S, Gaillard T, Schuster D. Impaired insulin sensitivity, insulin secretion, and glucose effectiveness predict future development of impaired glucose tolerance and type 2 diabetes in pre-diabetic African Americans. Diabetes Care. 2004. 27:1439–1446.
13. Li CL, Tsai ST, Chou P. Relative role of insulin resistance and β-cell dysfunction in the Progression to type 2 diabetes-The Kinmen Study. Diabetes Research and Clinical Practice. 2003. 59:225–232.
crossref
14. Hanley AJ, Williams K, Gonzalez C, D'Agostino RB Jr, Wagenknecht LE, Stern MP, Haffner SM. San Antonio Heart Study. Mexico City Diabetes Study. Insulin Resistance Atherosclerosis Study. Prediction of type 2 diabetes using simple measures of insulin resistance: combined results from the San Antonio Heart Study, the Mexico City Diabetes Study, and the Insulin Resistance Atherosclerosis Study. Diabetes. 2003. 52:463–469.
crossref
15. Hayashi T, Boyko E, Leonetti D, McNeely M, Newell-Morris L, Kahn SE, Fujimoto WY. Visceral adiposity and the risk of impaired glucose tolerance. Diabetes Care. 2003. 26:650–655.
16. DeFronzo RA, Tobin JD, Andres R. Glucose clamp technique: a method for quantifying insulin secretion and resistance. Am J Physiol. 1979. 237:E214–E223.
crossref
17. Seltzer HS, Allen EW, Herron AL Jr, Brennan MT. Insulin secretion in response to glycemic stimulus: Relation of delayed initial release to carbohydrate intolerance in mild diabetes mellitus. J Clin Invest. 1967. 46:323–335.
crossref
18. Seino Y, Ikeda M, Yawata M. The insulinogenic index in secondary diabetes. Horm Metab Res. 1975. 7:107–115.
crossref
19. Yalow RS, Berson SA. Plasma insulin concentrations in nondiabetic and early diabetic subjects: determinations by a new sensitive immunoassay technic. Diabetes. 1960. 9:254–260.
crossref
20. Bonora E, Targher G, Alberiche M, Bonadonna RC, Saggiani F, Zenere M, Monauni T, Muggeo M. Homeostasis model assessment closely mirrors the glucose clamp technique In the assessment of insulin sensitivity. Diabetes Care. 2000. 23:57–63.
21. Anderson RL, Hamman RF, Savage PJ, Saad MF, Laws A, Kades WW, Sands RE, Cefalu W. Exploration of simple insulin sensitivity measures derived from frequently sampled intravenous glucose tolerance (FSIGT) tests: the Insulin Resistance Atherosclerosis Study. Am J Epidemiol. 1995. 142:724–732.
22. Emoto M, Nishizawa Y, Maekawa K, Hiura Y, Kanda H, Kawagishi T, Shoji T, Okuno Y, Morii H. Homeostasis model assessment as a clinical index of insulin resistance in type 2 diabetic patients treated with sulfonylureas. Diabetes Care. 1999. 22:818–822.
crossref
23. Wallace TM, Levy JC, Matthews DR. Use and abuse of HOMA modeling. Diabetes Care. 2004. 27:1487–1495.
crossref
TOOLS
Similar articles