Functional Enteroinsular Axis in Full-Term Newborn Infants

Abstract

ABSTRACT. The term "enteroinsular axis" refers to the AGA, appropriate for gestational age enhancement of insulin release by hormones secreted from SGA, small for gestational age the gut. Gastric inhibitory polypeptide (GIP) is one of theLGA, large for gestational age major hormones that mediates this function. The purpose IDM, infant of diabetic mother of the present study was to examine whether the enteroin-IRI, immunoreactive insulin sular axis is functional in newborn infants born at term gestation. Between d 2 and d 4 of life, glucose was infused for 2 h intravenously or orogastrically to 44 fullterm newborn infants, of whom 18 were appropriate for gestational age, nine large for gestational age, eight small for gestational age; nine infants were born to diabetic mothers. Glucose was infused at either 8 mg/kg/min intravenously or 16 mg/kg/min orogastrically to achieve similar plasma glucose concentrations. Plasma insulin and GIP concentrations were compared. Plasma GIP concentration increased significantly with enteral glucose administration in all infants but remained unchanged with parenteral glucose infusion. The responses of plasma insulin and the insulin/ glucose ratio were significantly greater in infants receiving enterally than parenterally infused glucose. However, when glucose was infused orogastrically at a lower rate (8 mg/ kg/min), plasma GIP concentrations rose, but no enhancement of insulin response was detected, suggesting the importance of the role of circulating glucose in the "enteroinsular axis". The infants of diabetic mothers and the large-for-gestational-age infants had more rapid insulin response to orogastrically administered glucose, but their GIP responses were similar to that of normal infants. These findings suggest that, at term gestation, the newborn infants have a "functional" enteroinsular axis in response to glucose, i.e. the rising plasma GIP contributed in part to the enhanced insulin response to enterally infused glucose. However, the more rapid insulin response to enteral glucose in the infant of diabetic mothers probably results from the effect of intrauterine hyperglycemia. Our data could not separate the role of GIP in insulin response to enteral glucose in the infants of diabetic mothers. (Pediatr Res 25:490-495, 1989)

Relationships Between Early Nutrition and Blood Glucose Concentrations in Very Preterm Infants

“…There are a number of possible mechanisms for this. Enteral feeding stimulates the enteroinsular axis and, in the term infant, may be necessary for the production of glucose‐dependent insulinotropic peptide (35), an incretin which acts to depolarize the beta‐cell membrane and stimulate insulin secretion (36), potentially improving an infant's responsiveness to increasing BGCs. Small, early enteral feed volumes may also have a maturational effect on hepatic glut‐2 receptors via the direct portal venous delivery of carbohydrate to the liver (37,38), and thus allowing for more accurate hepatic sensing of BGCs, and potentially dampening inappropriate hepatic gluconeogenesis (39).…”