Cord blood levels of insulin, cortisol and HOMA2-IR in very preterm, late preterm and term newborns

Afzal Ahmad, Rukmini Mysore Srikantiah, Charu Yadav, Ashish Agarwal, Poornima Ajay Manjrekar, Anupama Hegde

Research output: Contribution to journalArticle

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Abstract

Introduction: Alteration in the glucose homeostasis is still the major cause of morbidity and mortality in the newborns. Intrauterine undernutrition plays an important role in causing adult insulin resistance and diabetes but the exact cause is still unknown. Aim: To estimate the plasma glucose, serum insulin and cortisol levels at birth in newborns at different gestational age.Materials and Methods: The present cross-sectional study conducted from December 2014 to June 2015 included 58 newborns enrolled as per the inclusion criteria and further categorized into Group I (very preterm; n=19; gestational age < 32 weeks), Group II (late preterm; n=20; gestational age between 32-37 weeks) and Group III (full term; n=19; gestational age >37 weeks) newborns. Venous Cord Blood (VCB) was collected and plasma glucose was analysed by GOD-POD (Glucose Oxidase-Peroxidase) method in auto analyser whereas serum insulin and cortisol were analysed by ELISA (Enzyme Linked Immunosorbent Assay). HOMA2-IR (Homeostatic Model Assessment) calculator was used to assess insulin resistance. All parametric data was expressed as mean±SD and analysed using ANOVA with Tukey’s as the Post-Hoc test. Correlation analysis was done using Pearson’s correlation co-efficient with scatter plot as the graphical representation. Results: Significantly increased insulin and HOMA2-IR levels were found in group I (13.7±4.7μIU/mL and 1.6±0.58 respectively) when compared to group II (8.3±2.9μIU/mL and 0.93±0.2 respectively) and group III (8.3±2.1μIU/mL and 1.03±0.26 respectively). A positive correlation between cortisol levels and gestational age (r = 0.6, n = 58, p < 0.001) and a negative correlation between insulin and gestational age (r = -0.654, n = 58, p < 0.001) was observed in the study population. Conclusion: Increased levels of insulin and HOMA2-IR as seen in the very preterm newborns signify the predisposition of these newborns to development of diabetes in later stages of life. The inverse association of cortisol and insulin with gestational age suggests that cortisol could also be responsible for impaired β cell function and insulin sensitivity.

Original languageEnglish
Pages (from-to)BC05-BC08
JournalJournal of Clinical and Diagnostic Research
Volume10
Issue number5
DOIs
Publication statusPublished - 01-05-2016

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Fetal Blood
Hydrocortisone
Blood
Gestational Age
Insulin
Insulin Resistance
Glucose
Medical problems
Glucose Oxidase
Serum
Malnutrition
Plasmas
Immunosorbents
Analysis of Variance
Homeostasis
Cross-Sectional Studies
Enzyme-Linked Immunosorbent Assay
Parturition
Analysis of variance (ANOVA)
Morbidity

All Science Journal Classification (ASJC) codes

  • Clinical Biochemistry

Cite this

@article{baab0dcc9d144d00bba5471598691220,
title = "Cord blood levels of insulin, cortisol and HOMA2-IR in very preterm, late preterm and term newborns",
abstract = "Introduction: Alteration in the glucose homeostasis is still the major cause of morbidity and mortality in the newborns. Intrauterine undernutrition plays an important role in causing adult insulin resistance and diabetes but the exact cause is still unknown. Aim: To estimate the plasma glucose, serum insulin and cortisol levels at birth in newborns at different gestational age.Materials and Methods: The present cross-sectional study conducted from December 2014 to June 2015 included 58 newborns enrolled as per the inclusion criteria and further categorized into Group I (very preterm; n=19; gestational age < 32 weeks), Group II (late preterm; n=20; gestational age between 32-37 weeks) and Group III (full term; n=19; gestational age >37 weeks) newborns. Venous Cord Blood (VCB) was collected and plasma glucose was analysed by GOD-POD (Glucose Oxidase-Peroxidase) method in auto analyser whereas serum insulin and cortisol were analysed by ELISA (Enzyme Linked Immunosorbent Assay). HOMA2-IR (Homeostatic Model Assessment) calculator was used to assess insulin resistance. All parametric data was expressed as mean±SD and analysed using ANOVA with Tukey’s as the Post-Hoc test. Correlation analysis was done using Pearson’s correlation co-efficient with scatter plot as the graphical representation. Results: Significantly increased insulin and HOMA2-IR levels were found in group I (13.7±4.7μIU/mL and 1.6±0.58 respectively) when compared to group II (8.3±2.9μIU/mL and 0.93±0.2 respectively) and group III (8.3±2.1μIU/mL and 1.03±0.26 respectively). A positive correlation between cortisol levels and gestational age (r = 0.6, n = 58, p < 0.001) and a negative correlation between insulin and gestational age (r = -0.654, n = 58, p < 0.001) was observed in the study population. Conclusion: Increased levels of insulin and HOMA2-IR as seen in the very preterm newborns signify the predisposition of these newborns to development of diabetes in later stages of life. The inverse association of cortisol and insulin with gestational age suggests that cortisol could also be responsible for impaired β cell function and insulin sensitivity.",
author = "Afzal Ahmad and Srikantiah, {Rukmini Mysore} and Charu Yadav and Ashish Agarwal and Manjrekar, {Poornima Ajay} and Anupama Hegde",
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Cord blood levels of insulin, cortisol and HOMA2-IR in very preterm, late preterm and term newborns. / Ahmad, Afzal; Srikantiah, Rukmini Mysore; Yadav, Charu; Agarwal, Ashish; Manjrekar, Poornima Ajay; Hegde, Anupama.

In: Journal of Clinical and Diagnostic Research, Vol. 10, No. 5, 01.05.2016, p. BC05-BC08.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Cord blood levels of insulin, cortisol and HOMA2-IR in very preterm, late preterm and term newborns

AU - Ahmad, Afzal

AU - Srikantiah, Rukmini Mysore

AU - Yadav, Charu

AU - Agarwal, Ashish

AU - Manjrekar, Poornima Ajay

AU - Hegde, Anupama

PY - 2016/5/1

Y1 - 2016/5/1

N2 - Introduction: Alteration in the glucose homeostasis is still the major cause of morbidity and mortality in the newborns. Intrauterine undernutrition plays an important role in causing adult insulin resistance and diabetes but the exact cause is still unknown. Aim: To estimate the plasma glucose, serum insulin and cortisol levels at birth in newborns at different gestational age.Materials and Methods: The present cross-sectional study conducted from December 2014 to June 2015 included 58 newborns enrolled as per the inclusion criteria and further categorized into Group I (very preterm; n=19; gestational age < 32 weeks), Group II (late preterm; n=20; gestational age between 32-37 weeks) and Group III (full term; n=19; gestational age >37 weeks) newborns. Venous Cord Blood (VCB) was collected and plasma glucose was analysed by GOD-POD (Glucose Oxidase-Peroxidase) method in auto analyser whereas serum insulin and cortisol were analysed by ELISA (Enzyme Linked Immunosorbent Assay). HOMA2-IR (Homeostatic Model Assessment) calculator was used to assess insulin resistance. All parametric data was expressed as mean±SD and analysed using ANOVA with Tukey’s as the Post-Hoc test. Correlation analysis was done using Pearson’s correlation co-efficient with scatter plot as the graphical representation. Results: Significantly increased insulin and HOMA2-IR levels were found in group I (13.7±4.7μIU/mL and 1.6±0.58 respectively) when compared to group II (8.3±2.9μIU/mL and 0.93±0.2 respectively) and group III (8.3±2.1μIU/mL and 1.03±0.26 respectively). A positive correlation between cortisol levels and gestational age (r = 0.6, n = 58, p < 0.001) and a negative correlation between insulin and gestational age (r = -0.654, n = 58, p < 0.001) was observed in the study population. Conclusion: Increased levels of insulin and HOMA2-IR as seen in the very preterm newborns signify the predisposition of these newborns to development of diabetes in later stages of life. The inverse association of cortisol and insulin with gestational age suggests that cortisol could also be responsible for impaired β cell function and insulin sensitivity.

AB - Introduction: Alteration in the glucose homeostasis is still the major cause of morbidity and mortality in the newborns. Intrauterine undernutrition plays an important role in causing adult insulin resistance and diabetes but the exact cause is still unknown. Aim: To estimate the plasma glucose, serum insulin and cortisol levels at birth in newborns at different gestational age.Materials and Methods: The present cross-sectional study conducted from December 2014 to June 2015 included 58 newborns enrolled as per the inclusion criteria and further categorized into Group I (very preterm; n=19; gestational age < 32 weeks), Group II (late preterm; n=20; gestational age between 32-37 weeks) and Group III (full term; n=19; gestational age >37 weeks) newborns. Venous Cord Blood (VCB) was collected and plasma glucose was analysed by GOD-POD (Glucose Oxidase-Peroxidase) method in auto analyser whereas serum insulin and cortisol were analysed by ELISA (Enzyme Linked Immunosorbent Assay). HOMA2-IR (Homeostatic Model Assessment) calculator was used to assess insulin resistance. All parametric data was expressed as mean±SD and analysed using ANOVA with Tukey’s as the Post-Hoc test. Correlation analysis was done using Pearson’s correlation co-efficient with scatter plot as the graphical representation. Results: Significantly increased insulin and HOMA2-IR levels were found in group I (13.7±4.7μIU/mL and 1.6±0.58 respectively) when compared to group II (8.3±2.9μIU/mL and 0.93±0.2 respectively) and group III (8.3±2.1μIU/mL and 1.03±0.26 respectively). A positive correlation between cortisol levels and gestational age (r = 0.6, n = 58, p < 0.001) and a negative correlation between insulin and gestational age (r = -0.654, n = 58, p < 0.001) was observed in the study population. Conclusion: Increased levels of insulin and HOMA2-IR as seen in the very preterm newborns signify the predisposition of these newborns to development of diabetes in later stages of life. The inverse association of cortisol and insulin with gestational age suggests that cortisol could also be responsible for impaired β cell function and insulin sensitivity.

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