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KCI 후보 SCIE SCOPUS
Homeostasis Model Assessment법을 이용한 인슐린저항성 평가의 한계
Limitation of Validity of Homeostasis Model Assessment as a Index of Insulin Resistance
차봉수(Bong Soo Cha),허갑범(Kap Bum Huh),윤용석(Yong Seok Yun),박석원(Seok Won Park),송영득(Young Duk Song),박효경(Hyo Kyung Park),김오연(Oh Yoen Kim),안철우(Chul Woo Ahn),남재현(Jae Hyun Nam),남수현(Su Hun Nam),이종호(Chong Ho Lee),임승길(Sung Gil Lim),김경래(Kyung Rae Kim),이현철(Hyun Chul Lee)
UCI I410-ECN-0102-2009-510-005459182
* 발행 기관의 요청으로 구매가 불가능한 자료입니다.

Background: Homeostasis model assessment of insulin resistance(HOMA) had been proposed as a simple and inexpensive alternative to other complex procedures measuring insulin resistance. We evaluated the validity of HOMAIR, comparing to total glucose disposal rate measured by euglycemic clamp test in 63 subjects with normal glucose tolerance, 21 with impaired glucose tolerance and 47 with type 2 DM. Methods: HOMAIR and HOMAβcell function (Homeostasis model assessment of βcell function) were calculated with formula described by Matthews (HOMAIR: fasting insulin (μU/mL) X fasting glucose (mmol/L) / 22.5, HOMAβcell function: 20 X fasting insulin (μU/mL)/(fasting glucose(mmol/L)- 3.5)). 2-hour euglycemic(5mmol/L) hyperinsulinemic (717pmol/L) clamp test were carried out. Results: The strong inverse correlation(r=-0.658, <0.001) was shown between log transformed HOMA and total glucose disposal rates. The agreement of two methodes in the categorization according to insulin resistance was moderate (weighed a =0.45). The magnitude of correlation coefficients were smaller in subjects with lower BMI (BMI < 23.7 kg/m2, r = -0441 vs BMI > 23.7 kg/m2, r = -0.693, p = 0.0183), lower HOMAβcell function (HOMAβcell function 57.2, r = -0.514 vs HOMAβcell function≥57.2, r = -0.773, p = 0.0091) and higher fasting glucose levels (fasting glucose < 102 mg/dL, r = -0.697 vs fasting glucose > 102 mg/dl, r = -0.59, p = 0.0735). The results of correlation analysis was not significant in diabetics with lower BMI. Conclusion: Limitation of validity of HOMAIR should be carefully considered in subjects with lower BMI and lower fasting insulin to glucose levels, such as lean type 2 diabetes with insulin secretory defects (J Kor Diabetes Asso 24:541 551, 2000).

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