OJIM  Vol.4 No.4 , December 2014
Association between Homa Index and Vascular Endothelial Dysfunction in Type 2 Diabetic Patients
Abstract: Introduction: In recent years, flow mediated dilatation (FMD) has become a popular technique in cardiovascular medicine. HOMA-IR was accepted to determine the insulin sensitivity as a valuable standard. In this study, we evaluated the association between HOMA-IR (homeostasis model assessment of insulin resistance) and vascular endothelial dysfunction, as assessed by endothelium- dependent flow-mediated dilatation (FMD) and nitroglycerin-mediated dilatation (NMD), in type 2 Diabetic (DM) patients. Material and Methods: Eighty four (84) consecutive out-patients were enrolled. HOMA-IR was calculated as fasting insulin (μU/ml) multiplied by fasting plasma glucose (FPG) (mg/dl) and divided by 405. The ultrasound method for measuring FMD and NMD has been used. Out of 84 patients, 42 patients were in control group and 42 patients were in diabetic group, which were further subdivided into two groups based on HOMA-IR > 3.0 and above was considered as Group I and HOMA IR < 3.0 and below was considered as Group II. Fasting Plasma Glucose (mmol/dl) (7.74 ± 2.56, 6.81 ± 1.9, p < 0.001) and Fasting Insulin (μU/dl) (13.26 ± 8.09, 6.65 ± 2.36, p < 0.001) were statistically significant in Group I. The baseline mean FMD in controls and cases (Group I and Group II) was 15.36 ± 9.56, 4.15 ± 2.29, 12.21 ± 6.24 (p < 0.001) respectively. By logistic regression analysis the factors which were effective on FMD percentage change (<5.5%) in Group I were BMI (p < 0.02), plasma Insulin (p < 0.04) and triglycerides (p < 0.02). There was a negative co-relation for FMD, NMD and HOMA-IR. Discussion: We conclude that increased HOMA-IR in hyperglycaemic patients is associated with severe endothelial dysfunction which is the marker of the atherosclerosis. Thus the measurement of endothelial vasomotor function which is a comprehensive analysis of atherosclerotic burden may provide a better predictive value of future cardiovascular events than the analysis of each of the traditional risk factors alone.
Cite this paper: Kumari, N. , Raju, I. , Devi, M. and Praveen, M. (2014) Association between Homa Index and Vascular Endothelial Dysfunction in Type 2 Diabetic Patients. Open Journal of Internal Medicine, 4, 123-129. doi: 10.4236/ojim.2014.44019.

[1]   Gokce, N., Keaney Jr., J.F., Hunter, L.M., Watkins, M.T., Nedeljkovic, Z.S., Menzoian, J.O. and Vita, J.A. (2003) Predictive Value of Noninvasively Determined Endothelial Dysfunction for Long-Term Cardiovascular Events in Patients with Peripheral Vascular Disease. Journal of the American College of Cardiology, 41, 1769-1775.

[2]   Karatzis, E.N., Ikonomidis, I., Vamvakou, G.D., Papaioannou, T.G., Protogerou, A.D., Andreadou, I., Voidonikola, P.T., Karatzi, K.N., Papamichael, C.M. and Lekakis, J.P. (2006) Long-Term Prognostic Role of Flow-Mediated Dilatation of the Brachial Artery after Acute Coronary Syndromes without ST Elevation. American Journal of Cardiology, 98, 1424-1428.

[3]   Rossi, R., Nuzzo, A., Origliani, G. and Modena, M.G. (2008) Prognostic Role of Flow-Mediated Dilation and Cardiac Risk Factors in Post-Menopausal Women. Journal of the American College of Cardiology, 51, 997-1002.

[4]   Shechter, M., Issachar, A., Marai, I., Koren-Morag, N., Freinark, D., Shahar, Y., Shechter, A. and Feinberg, M.S. (2009) Long-Term Association of Brachial Artery Flow-Mediated Vasodilation and Cardiovascular Events in Middle-Aged Subjects with No Apparent Heart Disease. International Journal of Cardiology, 134, 52-58.

[5]   Yeboah, J., Folsom, A.R., Burke, G.L., Johnson, C., Polak, J.F., Post, W., Lima, J.A., Crouse, J.R. and Herrington, D.M. (2009) Predictive Value of Brachial Flow-Mediated Dilation for Incident Cardiovascular Events in a Population-Based Study: The Multi-Ethnic Study of Atherosclerosis. Circulation, 120, 502-509.

[6]   Widlansky, M.E., Gokce, N., Keaney Jr., J.F. and Vita, J.A. (2003) The Clinical Implications of Endothelial Dysfunction. Journal of the American College of Cardiology, 42, 1149-1160.

[7]   Halcox, J.P., Donald, A.E., Ellins, E., Witte, D.R., Shipley, M.J., Brunner, E.J., Marmot, M.G. and Deanfield, J.E. (2009) Endothelial Function Predicts Progression of Carotid Intima-Media Thickness. Circulation, 119, 1005-1012.

[8]   Kelm, M. (2002) Flow-Mediated Dilatation in Human Circulation: Diagnostic and Therapeutic Aspects. American Journal of Physiology—Heart and Circulatory Physiology, 282, H1-H5.

[9]   Defronzo, R.A., Tobin, J.D. and Andres, R. (1979) Glucose Clamp Technique: A Method for Quantifying Insulin Secretion and Resistance. American Journal of Physiology, 237, 214-223.

[10]   Pacini, G. and Bergman, R.N. (1986) MINMOD: A Computer Program to Calculate Insulin Sensitivity and Pancreatic Responsivity from the Frequently Sampled Intravenous Glucose Tolerance Test. Computer Methods and Programs in Biomedicine, 23, 113-122.

[11]   Shen, S.W., Reaven, G.M. and Farquhar, J.W. (1970) Comparison of Impedance to Insulin Mediated Glucose Uptake in Normal Subjects and in Subjects with Latent Diabetes. Journal of Clinical Investigation, 49, 2151-2160.

[12]   Korytkowski, M.T., Berga, S.L. and Horwitz, M.J. (1995) Comparison of the Minimal Model and the Hyperglycaemic Clamp for Measuring Insulin Sensitivity and Acute Insulin Response to Glucose. Metabolism, 44, 1121-1125.

[13]   Matthews, D.R., Hosker, J.P., Rudenski, A.S., et al. (1985) Homeostasis Model Assessment: Insulin Resistance and Beta-Cell Function from Fasting Plasma Glucose and Insulin Concentrations in Man. Diabetologia, 28, 412-419.

[14]   Zeng, G., Nystrom, F.H., Ravichandran, L.V., et al. (2000) Roles for Insulin Receptor, P13 Kinase, and Akt in Insulin-Signalling Pathways Related to Production of Nitric Oxide in Human Vascular Endothelial Cells. Circulation, 101, 1539-1545.

[15]   Kuboki, K., Jiang, Z.Y., Takahara, N., et al. (2000) Regulation of Endothelial Constitutive Nitric Oxide Synthase Gene Expression in Endothelial Cells and in Vivo: A Specific Vascular Action of Insulin. Circulation, 101, 676-681.

[16]   Cardillo, C., Kilcoyne, C.M., Nambi, S.S., et al. (1998) Vasodilator Response to Systemic but Not to Local Hyperinsulinemia in the Human Forearm. Hypertension, 32, 740-745.

[17]   Ross, R. (1999) Atherosclerosis—An Inflammatory Disease. American Heart Journal, 138, 419-420.

[18]   Steinberg, H.O., Chaker, H., Leaming, R., et al. (1996) Obesity/Insulin Resistance Is Associated with Endothelial Dysfunction. Implications for the Syndrome of Insulin Resistance. The American Society for Clinical Investigation, 97, 2601-2610.

[19]   Tooke, J.E. (1995) Micro Vascular Function in Human Diabetes: A Physiologic Perspective. Diabetes, 44, 721-726.

[20]   King, G.L. and Wakasaki, H. (1992) Theoretical Mechanisms by Which Hyperglycaemia and Insulin Resistance Could Cause Cardiovascular Diseases in Diabetes. Diabetes Care, 22, 31-37.

[21]   Kitta, Y., Obata, J., Nakamura, T., et al. (2009) Persistent Impairment of Endothelial Vasomotor Function Has a Negative Impact on Outcome in Patients with Coronary Artery Disease. Journal of the American College of Cardiology, 53, 323-330.

[22]   Yoda, K., Inaba, M., Hamamata, K., Yoda, M., et al. (2014) Association between Glycemic Control and Morning Blood Pressure Surge with Vascular Endothelial Dysfunction in Type 2 Diabetic Patients. Diabetes Care, 37, 644-650.

[23]   Karabag, T., Kaya, A., Yavuz, S., et al. (2007) The Relation of HOMA Index with Endothelial Functions Determined by Flow Mediated Dilatation Method among Hyperglcemic Patients. Indian Heart Journal, 59, 463-467.