Background: Insulin resistance (IR) is a key factor in the etiology of type 2 diabetes mellitus, dyslipidemia, hypertension, vascular diseases and may have a role as well in stroke and coronary heart disease. Poor nutrition in fetal and early infant life and prematurity affects the development and activity of P cells of islets of Langerhans. Early changes in insulin and cortisol hormones levels affect glucose homeostasis and may later lead to IR and obesity. Aim of Study:The purpose of this study is to evaluate IR using homeostasis model assessment-insulin resistance (HO-MA-IR) and its relation to gestational age among full term (FT) and preterm infants (PT).Patients and Methods: Eighty newborn infants between 28 and 41 gestational weeks delivered by vaginal delivery (VD) or Caesarian Section (CS) were enrolled in this study. Three milliliters of umbilical venous blood were obtained immediately after birth to measure both insulin and cortisol levels by Enzyme-linked Immunosorbent Assay and glucose level, HOMA-IR and glucose insulin ratio (GIR) were calculated. Results:In this cross-sectional study, cord blood insulin and HOMA-IR levels were significantly higher in PT groups than FT groups with p-value <0.001. Other biochemical tests such as cord blood glucose, cortisol levels and GIR were higher in FT groups than PT groups with p-value: 0.01, <0.001 and <0.001 respectively. In the study population, An inverse relation was found between gestational age with insulin and HOMA-IR while a positive one was observed between gestational age with cortisol and glucose levels. Vaginal delivered FT and PT neonates had higher levels of cord blood cortisol than delivered by CS. Anthropometric measurements revealed highly statistically significant differences between FT and PT newborns with p-value <0.001. Conclusion:Increased levels of insulin and HOMA-IR in PT newborns signify its role as a risk factor for development of diabetes in these newborns later. Elevated level of cortisol in FT newborns more than PT reflects its role in fetal matu-
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