The Prevalence of Metabolic Syndrome according to the Degree of Glucose Metabolism Impairment

당 대사 장애 정도에 따른 대사증후군 이환 정도

Kong, Mi-Hee;Choi, Hyun-Kook;Jung, An-Jin;Ahn, Byeong-Hun;Kim, Bom-Taeck;Kim, Kwang-Min
공미희;최현국;정안진;안병훈;김범택;김광민

  • Published : 20060300

Abstract

Background: The metabolic syndrome is a cluster of related cardiovascular risk factors and it is the cause of morbidity and mortality in cardiovascular diseases. Recently, new diagnostic criteria of glucose metabolism impairment has been recommended. The purpose of this study was to estimate the difference of cardiovascular risk by investigating the prevalence of metabolic syndrome according to the degree of glucose metabolism impairment. Methods: A population of 757 subjects was selected from a database of individuals who visited a health promotion center. We classified these subjects into 5 groups [Normal, Isolated impaired glucose tolerance (I-IGT), Isolated impaired fasting glucose (I-IFG), combined IGT with IFG (IGT/IFG) and Diabetes]. We compared the general characteristics, Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) and the prevalence of metabolic syndrome in these groups. Results: HOMA-IR and the prevalence of metabolic syndrome in the IGT/IFG and the Diabetes group were significantly greater than the Normal group. HOMA-IR and the prevalence of metabolic syndrome of the I-IGT and the I-IFG group were not significantly different with the Normal group. Conclusion: The insulin resistance and the prevalence of metabolic syndrome in the IGT/IFG group was significantly greater than the Normal group, and its presence may increase the risk of cardiovascular diseases. Therefore, it is important to control other combined metabolic disorders to prevent cardiovascular events after effective selection for IGT/ IFG.

연구배경: 대사증후군은 심혈관 질환의 위험요인들을 포괄하는 군집개념이며, 심혈관 질환의 이환 및 사망의 원인이다. 최근 심혈관 위험요인 중 하나인 당 대사 장애의 분류가 새로이 제시되었다. 본 연구에서는 새로이 제시된 분류를 기준으로 하여 당 대사 장애 정도에 따른 대사증후군의 이환 정도를 살펴봄으로써 심혈관 질환의 위험정도의 차이가 있는지를 알아보고자 하였다. 방법: 경기도 소재 대학병원에 건강검진을 위해 방문한 사람을 대상으로 최종 757명을 선발하여 이들의 당 대사 장애 정도에 따라 정상군, 순수내당능장애군, 순수공복혈당장애군, 혼합혈당장애군, 당뇨군으로 총 다섯 그룹으로 나누었다. 이 다섯 그룹에 대한 일반적 특징 및 공복인슐린과 Homeostasis Model Assessment of Insulin Resistance (HOMA- IR) 그리고 대사증후군 항목의 이환 정도를 비교하였다. 결과: 혼합혈당장애군(HOMA-IR: 2.3${\pm}$1.5, 대사증후군 이환 항목수: 1.91${\pm}$1.13)과 당뇨군(HOMA-IR: 2.7${\pm}$2.0, 대사증후군 이환 항목수: 2.11${\pm}$1.07)이 정상군(HOMA-IR: 1.6${\pm}$0.7, 대사증후군 이환 항목수: 1.35${\pm}$1.08)보다 HOMA- IR과 대사증후군 이환 항목수가 유의하게 증가하였다(P<0.05). 순수내당능장애군(HOMA-IR: 1.7${\pm}$0.8, 대사증후군 이환 항목수: 1.43${\pm}$1.06)과 순수공복혈당장애군(HOMA-IR: 1.9${\pm}$1.0, 대사증후군 이환 항목수: 1.51${\pm}$1.11)은 정상군과 비교하여 HOMA-IR과 대사증후군 이환 항목수의 차이가 없었다. 정상군과 비교하여 공복혈당장애군이 대사증후군에 이환될 교차곱비(Odds ratio)는 4.45 (95% CI: 2.41${\sim}$8.21), 혼합혈당장애군은 7.44 (95% CI: 4.00${\sim}$13.83), 당뇨군은 9.69 (95% CI: 5.47${\sim}$17.16)로 유의한 증가를 보였다. 결론: 공복혈당장애군과 혼합혈당장애군 그리고 당뇨군의 경우 유의하게 대사증후군에 이환될 교차곱비가 증가되어 있었다. 특히 혼합혈당장애군과 당뇨군의 경우는 유의한 인슐린 저항성증가와 높은 대사증후군 이환 정도를 보여 다른 군에 비해 심혈관 위험이 높은 군으로 보인다.

Keywords

References

  1. 통계청. 2000년 사망원인통계연보;2001
  2. Pi-Sunyer Fx. Medical hazards of obesity. Ann Intern Med 1993;119:655-60 https://doi.org/10.7326/0003-4819-119-7_Part_2-199310011-00006
  3. Manson JE, Stampfer MJ, Hennekens CH, Willett WC. Body weight and longevity. JAMA 1987;257:353-8 https://doi.org/10.1001/jama.257.3.353
  4. 장명래, 이운창, 신홍석, 조주연, 안재억, 김주자. 비만도와 비만의 유형에 따른 혈압, 혈당, 그리고 혈중 지질 및 지단 백과의 관계. 가정의학회지 1994;15:1076-87
  5. DeFronzo RA, Ferrannini E. Insulin resistance: a multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease. Diabetes Care 1991;14:173-94 https://doi.org/10.2337/diacare.14.3.173
  6. Haffner SM. The insulin resistance syndrome revisited. Diabetes Care 1996;19:275-7 https://doi.org/10.2337/diacare.19.3.275
  7. Meigs JB, D'Agostino RB Sr, Wilson PW, Cupples LA, Nathan DM, Singer DE. Risk variable clustering in the insulin resistance syndrome. The framingham offspring study. Diabetes 1997;46:1594-600 https://doi.org/10.2337/diabetes.46.10.1594
  8. Reaven GM. Banting lecture 1988: role of insulin resistance in human disease. Diabetes 1988;37:1595-607 https://doi.org/10.2337/diabetes.37.12.1595
  9. Ferrannini E, Haffner SM, Mitchell BD, Stern MP. Hyperinsulinemia: the key feature of a cardiovascular and metabolic syndrome. Diabetologia 1991;3:416-22
  10. Bonadonna RC, Groop L, Kraemer N, Ferrannini E, Del Prato S, DeFronzo RA. Obesity and insulin resistance in humans: a dose response study. Metabolism 1990;39:452-9 https://doi.org/10.1016/0026-0495(90)90002-T
  11. National Cholesterol Education Program. Executive Summary of the Third Report of National Cholesterol Education Program (NCEP) Expert Panel on Detection. Evaluation and treatment of high blood cholesterol in adults. JAMA 2001; 285:2486-97 https://doi.org/10.1001/jama.285.19.2486
  12. World Health Organization. Diabetes mellitus: report of a WHO Study Group. Geneva: World Health Org.;1985 (Tech. Rep. Ser., no. 727)
  13. Report of the Expert Committee on the diagnosis and classification of diabetes mellitus. Diabetes Care 1997;20:1183-97 https://doi.org/10.2337/diacare.20.7.1183
  14. Shaw JE, Zimmet PZ, de Courten M, Dowse GK, Chitson P, Gareeboo H, et al. Impaired fasting glucose or impaired glucose tolerance. What best predicts future diabetes in Mauritius? Diabetes Care 1999;22:399-402 https://doi.org/10.2337/diacare.22.3.399
  15. Gabir MM, Hanson RL, Dabelea D, Imperatore G, Roumain J, Bennett PH, et al. Plasma glucose and prediction of microvascular disease and mortality: evaluation of 1997 American Diabetes Association and 1999 World Health Organization criteria for diagnosis of diabetes. Diabetes Care 2000;23:1113-8 https://doi.org/10.2337/diacare.23.8.1113
  16. Larsson H, Berglund G, Lindgarde F, Ahren B. Comparison of ADA and WHO criteria for diagnosis of diabetes and glucose intolerance. Diabetologia 1998;41:1124-5 https://doi.org/10.1007/s001250051040
  17. World Health Organization: Definition, Diagnosis and Classification of Diabetes Mellitus and its Complication: report of a WHO consultation. Part 1: diagnosis and classification of diabetes mellitus. Geneva:World Health Org.;1999
  18. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985;28:412-9 https://doi.org/10.1007/BF00280883
  19. WHO West Pacific Region. The Asia-Pacific perspective; reading obesity and its treatment. IOTF;2000
  20. Davies MJ, Raymond NT, Day JL, Hales CN, Burden AC. Impaired glucose tolerance and fasting hyperglycaemia have different characteristics. Diabet Med 2000;17:433-40 https://doi.org/10.1046/j.1464-5491.2000.00246.x
  21. Snehalatha C, Ramachandran A, Sivasankari S, Satyavani K, Vijay V. Insulin secretion and action show differences in impaired fasting glucose and impaired glucose tolerance in Asian Indians. Diabetes Metab Res Rev 2003;19:329-32 https://doi.org/10.1002/dmrr.388
  22. Conget I, Fernandez Real JM, Costa A, Casamitjana R, Ricart W. Insulin secretion and insulin sensitivity in relation to glucose tolerance in a group of subjects at a high risk for type 2 diabetes mellitus. Med Clin 2001;116:491-2 https://doi.org/10.1016/S0025-7753(01)71882-9
  23. Guerrero-Romero F, Rodriguez-Moran M. Impaired glucose tolerance is a more advanced stage of alteration in the glucose metabolism than impaired fasting glucose. J Diabetes Complications 2001;15:34-7 https://doi.org/10.1016/S1056-8727(00)00131-8
  24. Fuller JH, Shipley MJ, Rose G, Jarrett RJ, Keen H. Coronary heart disease risk and impaired glucose tolerance: the Whitehall Study. Lancet 1980;1:1373-6
  25. Decode Study Group. Glucose tolerance and cardiovascular mortality: comparison of fasting and 2-hour diagnostic criteria. Arch Intern Med 2001;161:397-405 https://doi.org/10.1001/archinte.161.3.397
  26. Burchfiel CM, Hamman RF, Marshall JA, Baxter J, Kahn LB, Amirani JJ. Cardiovascular risk factors and impaired glucose tolerance: the San Luis Valley Diabetes Study. Am J Epidemiol 1990;131:57-70 https://doi.org/10.1093/oxfordjournals.aje.a115485
  27. Hanefield M, Temelkova-Kurktschiev T. The postprandial state and the risk of atherosclerosis. Diabet Med 1997;14:S6-11 https://doi.org/10.1002/(SICI)1096-9136(199708)14:3+3.3.CO;2-8
  28. Will new diagnostic criteria for diabetes mellitus change phenotype of patients with diabetes? Reanalysis of European epidemiological data. DECODE Study Group on behalf of the European Diabetes Epidemiology Study Group. BMJ 1998; 317:371-5 https://doi.org/10.1136/bmj.317.7155.371
  29. Weyer C, Bogardus C, Pratley RE. Metabolic characteristics of individuals with impaired fasting glucose and/or impaired glucose tolerance. Diabetes 1999;48:2197-203 https://doi.org/10.2337/diabetes.48.11.2197
  30. Hanefeld M, Temelkova-Kurktschiev T, Schaper F, Henkel E, Siegert G, Koehler C. Impaired fasting glucose is not a risk factor for atherosclerosis. Diabet Med 1999;16:212-8 https://doi.org/10.1046/j.1464-5491.1999.00072.x
  31. Rathmann W, Giani G, Mielck A. Cardiovascular risk factors in newly diagnosed abnormal glucose tolerance: comparison of 1997 ADA and 1985 WHO criteria. Diabetologia 1999;42: 1268-9 https://doi.org/10.1007/s001250051305
  32. de Vegt F, Dekker JM, Stehouwer CD, Nijpels G, Bouter LM, Heine RJ. The 1997 American Diabetes Association criteria versus the 1985 World Health Organization criteria for the diagnosis of abnormal glucose tolerance: poor agreement in the Hoorn Study. Diabetes Care 1998;21:1686-90 https://doi.org/10.2337/diacare.21.10.1686
  33. Vaccaro O, Ruffa G, Imperatore G, Iovino V, Rivellese AA, Riccardi G. Risk of diabetes in the new diagnostic category of impaired fasting glucose: a prospective analysis. Diabetes Care 1999;22:1490-3 https://doi.org/10.2337/diacare.22.9.1490
  34. Knowler WC, Barrett-Connor E, Fowler SE, Hamman RF, Lachin JM, Walker EA, et al. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 2002;346:393-403 https://doi.org/10.1056/NEJMoa012512