Birth-weight, insulin levels, and HOMA-IR in new-borns at term

E. Narayanan, S. Selvakumar, A. T. Arasar Seeralar


Background: Abnormal birth weight babies are prone to develop adverse metabolic and cardiovascular outcomes later in life. There is dearth of knowledge regarding correlation of birth-weight with hyperinsulinemia and insulin resistance in term newborns.

Methods: Prospective cohort study was done in Institute of Obstetrics and Gynecology, Egmore, Madras Medical College from time period of May 2016 to November 2016. Inclusion criteria were newborns with gestational age between 38 to 41 weeks of normal pregnancies of healthy mothers aged 18 to 39 years. Incomplete/unclear data about mother’s health status, diabetes, history of gestational diabetes, hypertension, pre-eclampsia, eclampsia and conditions influencing glucose metabolism were exclusion criteria. In the first phase, cutoff point of HOMA-IR (homeostatic model assessment of insulin resistance) was established in 33 AGA neonates with birth-weight >2500 g and <4000 g. In the second phase, 34 term neonates were enrolled to determine whether LGA/SGA is related with hyperinsulinemia and elevated HOMA-IR. Serum insulin and serum glucose was obtained from cord blood. Hyperinsulinemia was defined by serum insulin levels ≥12.60 μU/mL and HOMA-IR ≥2.34. Multiple logistic regression analysis and Mann Whitney test was used to find association between birth-weight with hyperinsulinemia and HOMA-IR index.

Results: A total of 67 newborns were enrolled; 24, 10, and 33 with SGA, LGA and AGA respectively. Hyperinsulinemia was more prevalent in 16 newborns particularly in SGA (p=0.01), whereas HOMA-IR was noted in 13 neonates (p=0.06). Multiple logistic regression analysis revealed LGA had a strong association with hyperinsulinemia (p=0.02) and HOMA-IR (p=0.02).

Conclusions: Study revealed term LGA is associated with hyperinsulinemia and elevated HOMA-IR at birth.


Birth weight, Hyperinsulinemia, HOMA-IR, Insulin, Insulin resistance

Full Text:



Helmrich SP, Ragland DR, Leung RW, Paffenbarger Jr RS. Physical activity and reduced occurrence of non-insulin-dependent diabetes mellitus. N Engl J Med. 1991;325:147-52.

Jovanovic L. Type 2 diabetes trends in offspring of type 2 diabetic mothers. Diabetes Care. 2000;23:1219-20.

Petitt DJ, Aleck KA, Baird HR, Carraher MJ, Bennett PH, Knowler WC. Congenital susceptibility to NIDDM: Role or intrauterine environment. Diabetes. 1988;37:622-8.

Jaquet D, Trégouët DA, Godefroy T, Nicaud V, Chevenne D, Tiret L, et al. Combined effects of genetic and environmental factors on insulin resistance associated with reduced fetal growth. Diabetes. 2002;51:3473-8.

Phillips DI, McLeish R, Osmond C, Hales CN. Fetal growth and insulin resistance in adult life; role of plasma triglyceride and non-esterified fatty acids. Diabet Med. 1995;12:796-801.

Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985;28:412-9.

Vohr BR, Lipsitt LP, Oh W. Somatic growth of children of diabetic mothers with reference to birth sizes. J Pediatr. 1980;97:196-9.

Sahasrabuddhe A, Pitale S, Raje D, Sagdeo MM. Cord blood levels of insulin and glucose in full term pregnancies. J Assoc Physicians India. 2013;61(6):378-82.

Simental-Mendía LE, Castañeda-Chacón A, Rodríguez-Morán M, Guerrero-Romero F. Birth-weight, insulin levels, and HOMA-IR in newborns at term Simental-Mendía et al. BMC Pediatr. 2012;12:94.

Catalano PM, Presley L, Minium J, Hauguel-de Mouzon S. Fetuses of obese mothers develop insulin resistance in utero. Diabetes Care. 2009;32:1076-80.

Hofman PL, Regan F, Jackson WE, Jefferies C, Knight DB, Robinson EM, et al. Premature birth and later insulin resistance. N Engl J Med. 2004;351:2179-86.