J Korean Diabetes Assoc.
2000 Oct;24(5):541-551.
Limitation of Validity of Homeostasis Model Assessment as a Index of Insulin Resistance
- Affiliations
-
- 1Department of Internal Medicine, Yonsei University College of Medicine.
- 2Department of Food and Nutrition, Yonsei University College of Ecology.
- 3Department of Internal Medicine, Pouchon Cha University College of medicine.
Abstract
-
BACKGROUND: Homeostasis model assessment of insulin resistance (HOMAIR) 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 HOMA cell function (Homeostasis model assessment of cell
function) were calculated with formula described by Matthews [HOMAIR: fasting
insulin ( U/mL) X fasting glucose (mmol/L) / 22.5, HOMA cell function: 20 X fasting insulin
( U/mL) / (fasting glucose (mmol/L) - 3.5)]. 2-hour euglycemic (5 mmol/L) hyper
insulinemic (717 pmol/L) clamp test were carried out.
RESULTS
The strong inverse correlation (r=-0.658, <0.001) was shown between log
transformed HOMAIR and total glucose disposal rates. The agreement of two
methodes in the categorization according to insulin resistance was moderate
(weighed kappa=0.45). The magnitude of correlation coefficients were smaller in
subjects with lower BMI (BMI < 23.7 kg/m2, r = -0.441 vs BMI > or = 23.7 kg/m2, r = -0.693,
p = 0.0183), lower HOMA cell function (HOMA cell function < 57.2, r = -0.514 vs HOMA
cell function > or = 57.2, r = -0.773, p = 0.0091) and higher fasting glucose levels (fasting
glucose < 102 mg/dL, r = -0.697 vs fasting glucose > or = 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.