Insulin resistance and beta cell dysfunction are core defects in type 2 diabetes (T2DM). Impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) are intermediate states in the transition in glucose tolerance from normal to T2DM, both of which are associated with increased conversion rate to T2DM. Understanding the metabolic abnormalities that lead to the development of IFG and IGT will help develop strategies to prevent the development of T2DM. in the present study, we have examined the metabolic abnormalities responsible for the development of IFG and IGT in Arab individuals. 43 subjects with NGT (n=17), isolated IFG (N=17) and isolated IGT (n=9) received 75-gram OGTT and plasma glucose, insulin and C-peptide concentrations were measured at baseline and every 15 minutes for 3 hours after the glucose drink. Insulin secretion was measured with the incremental area under the plasma insulin and C-peptide concentration curves and insulin sensitivity was measured with the Matsuda Index. Beta cell function was measured with the Disposition Index as the product of insulin secretion and insulin sensitivity indices. IGT subjects manifested severe insulin resistance compared to IFG and NGT subjects. The Matsuda Index was 3.7±0.4, 7.2±1.0 and 8.4±1.1, respectively (p<0.01 for IGT versus both IFG and NGT). Beta cell function measured with the Disposition Index from 0-180 minutes was markedly reduced in IGT subjects compared to IFG and NGT individuals, 6.5±1.2, 34.0±5.6 and 32.9±4.9, respectively, (p<0.05 for IGT versus IFG and NGT. However, insulin secretion during the first 30 minutes during the OGTT was reduced in both IFG and IGT compared to NGT, 68.1±8.1, 52.6±7.4, and 100.7±10.9, respectively, (p<0.01 for both IFG and IGT. Collectively, these results indicate that similar to other ethnic groups, distinct metabolic defect characterize IFG and IGT in Arabic individuals Acknowledgment: We would like to thank Sanaa Mansy and Evette Rofaeil for their excellent care of the study participants. Supported by Qatar Foundation grant NPRP 4-247-3-076 to MAG and MZ


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