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Insulin sensitivity and insulin secretion at birth in intrauterine growth retarded infants
Sajita Setia1, M G Sridhar, Vishnu Bhat
1Department of Biochemistry, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry, India. saj_setiya@yahoo.co.in
Insights
Intrauterine growth retarded (IUGR) infants at birth are hypoglycemic, hypoinsulinemic, and show increased insulin sensitivity with decreased pancreatic beta-cell function. Insulin levels correlate more strongly with ponderal index than birth weight in these infants.
Area of Science:
- Neonatal Metabolism
- Endocrinology
- Perinatal Medicine
Background:
- Intrauterine growth restriction (IUGR) affects fetal development, potentially impacting neonatal metabolic status.
- Understanding the endocrine profile of IUGR infants at birth is crucial for early intervention and long-term health outcomes.
Purpose of the Study:
- To investigate insulin sensitivity, insulin secretion, and the relationship between insulin levels, birth weight, and ponderal index in newborns with IUGR at birth.
Main Methods:
- A comparative study involving 30 IUGR and 30 healthy term newborns delivered vaginally.
- Cord blood samples were collected at delivery to measure plasma glucose and insulin levels.
Main Results:
- IUGR newborns exhibited lower plasma glucose and insulin levels compared to healthy controls.
- Insulin sensitivity was significantly higher in IUGR infants, indicated by G/I ratio, HOMA IS, and QUICKI.
- Pancreatic beta-cell function, assessed by I/G ratio, was decreased in IUGR infants. Insulin levels showed a stronger correlation with ponderal index than birth weight in both groups.
Conclusions:
- At birth, IUGR infants present with hypoglycemia, hypoinsulinemia, enhanced insulin sensitivity, and reduced pancreatic beta-cell function.
- Insulin levels demonstrate a more robust correlation with ponderal index than with birth weight in IUGR neonates.
Aim:
To study insulin sensitivity, secretion and relation of insulin levels with birth weight and ponderal index in intrauterine growth retarded (IUGR) infants at birth.
Methods:
We studied 30 IUGR and 30 healthy newborns born at term by vaginal delivery in Jipmer, Pondicherry, India. Cord blood was collected at the time of delivery for measurement of plasma glucose and insulin.
Results:
When compared with healthy newborns, IUGR newborns had lower plasma glucose levels (mean 2.3+/-0.98 versus 4.1+/-0.51 mmol/L, p<0.001); lower plasma insulin levels (mean 4.5+/-2.64 versus 11.03+/-1.68 microU/L, p<0.001); higher insulin sensitivity calculated using G/I ratio (mean 11.6+/-5.1 versus 6.7+/-0.31, p<0.001), HOMA IS (mean 5.5+/-6.0 versus 0.53+/-0.15, p<0.001), and QUICKI (mean 0.47+/-0.12 versus 0.34+/-0.02, p<0.001); and decreased pancreatic beta-cell function test measured as I/G (mean 0.10+/-0.037 versus 0.15+/-0.006, p<0.001). A positive correlation was identified between insulin levels and birth weight in both the healthy control group (r2 = 0.17, p = 0.024) and IUGR group (r2 = 0.13, p = 0.048). However correlation of insulin levels with ponderal index was much more confident in both healthy control (r2 = 0.90, p<0.001) and IUGR groups (r2 = 0.28, p = 0.003). Insulin status correlated both with birth weight and ponderal index more confidently in control group than in IUGR group.
Conclusion:
At birth, IUGR infants are hypoglycaemic, hypoinsulinaemic and display increased insulin sensitivity and decreased pancreatic beta-cell function. Insulin levels correlate with ponderal index much more confidently than with birth weight.
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