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. 2016 Sep 1;8(3):270-5.
doi: 10.4274/jcrpe.2819. Epub 2016 Apr 18.

Indices of Glucose Homeostasis in Cord Blood in Term and Preterm Newborns

Afzal Ahmad, M S Rukmini  1 , Charu Yadav, Ashish Agarwal, Poornima A Manjrekar, Anupama Hegde
Affiliations

Indices of Glucose Homeostasis in Cord Blood in Term and Preterm Newborns

Afzal Ahmad et al. J Clin Res Pediatr Endocrinol. .

Abstract

Objective: According to the thrifty phenotype hypothesis, intrauterine malnutrition has a role in the etiology of type 2 diabetes. This study was planned to determine the early alterations in indices of glucose homeostasis (glucose, insulin, and cortisol) in term and preterm newborns and the correlations of glucose, insulin, and cortisol levels with insulin resistance indices.

Methods: A descriptive study comprising 35 term and 35 preterm newborns was carried out from December 2013 to June 2015. Venous cord blood was collected and plasma glucose was analyzed by the glucose oxidase-peroxidase method in an auto analyzer. Serum insulin and cortisol levels were assessed by the enzyme-linked immunosorbent assay. Homeostasis model assessment of insulin resistance (HOMA-IR), quantitative insulin sensitivity check index and glucose insulin ratio were calculated to assess insulin resistance. The data on physical and metabolic parameters were analyzed using standard tests for statistical significance.

Results: In term newborns, mean glucose and cortisol levels (83.6±17.4 mg/dL and 11.88±5.78 µg/dL, respectively) were significantly higher than those in preterm infants (70.4±15.8 mg/dL and 8.9±4.6 µg/dL, respectively). Insulin and HOMA-IR levels were found higher in preterm newborns (10.8±4.8 µIU/mL and 1.52±0.66, respectively) than in term newborns (7.9±2.7 µIU/mL and 1.19±0.29, respectively). Insulin was found to positively correlate with HOMA-IR, whereas cortisol was negatively correlated with HOMA-IR in both term and preterm newborns.

Conclusion: Higher insulin levels and HOMA-IR values in the cord blood of preterm newborns support the theory of intrauterine origin of metabolic diseases.

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