Does Human Milk Insulin Help Program Infant Pancreatic Function? Variation in Neonatal Human Milk Insulin Is Associated with Later Measures of Infant Glycemic Control

Abstract

Abstract Objectives Whether variation in human milk (HM) insulin contributes to neonatal blood sugar regulation and pancreatic programming remains unknown. This pilot study investigates whether HM insulin concentrations correlate with infant pancreatic function in exclusively breastfed 5-month old infants. We hypothesize that neonatal exposure to elevated HM insulin will “under stimulate” the infant pancreas, resulting in an exaggerated glycemic response to oral glucose at 5 months. Methods Exclusively breastfed infants of normoglycemic mothers (NG; n = 5) and mothers with minor insulin resistance (IR; n = 5) were administered a 1.75 g/kg oral glucose challenge. Infant capillary glucose was assessed at Fasting (>2 hours), 30 minutes (T30) and 60 minute (T60) after glucose administration. Fasting HM insulin was measured at 2-weeks and 5-months. Repeated Measures ANOVA and linear regression analyses were utilized. Results Using repeated measures analysis, the IR group exhibited a more dramatic glycemic response to the glucose challenge (P = 0.031): exhibiting lower fasting glucose (P = 0.085; n = 10) and higher glucose excursion from fasting to T30 (P = 0.007) compared to the NG group. HM insulin did not differ between the NW and IR groups at 2-weeks or 5-months. However, higher HM insulin concentrations at 2-weeks did correlate with a more dramatic infant glycemic response to oral glucose at 5 months. Fasting HM insulin at 2 weeks was positively associated with infant glucose at T30 (P = 0.033) and with the increase in glucose from fasting to T30 (P = 0.081; n = 8). Furthermore, fasting HM insulin at 2-weeks was negatively associated with infant glucose at T60 (P = 0.031) and the change in glucose from T30-T60 (P = 0.032; n = 7). Conclusions These pilot results suggest that HM insulin may contribute to postnatal programming of infant pancreatic function such that chronic exposure to elevated HM insulin may result in a dampened pancreatic response to an oral glucose challenge. Confirmation in a larger sample size is necessary. Funding Sources NIH/NIDDK; The Gerber Foundation.