Abstract
Summary: The effects of cortisol injection (0.2 mg/g body wt) at birth and of triglyceride feeding (20 mg/g body wt) 13 hr after birth have been studied in 16-hr-old fasted newborn rats. Cortisol produced a 10% decrease in body weight and in protein concentrations of carcass, hindlimb muscle, and liver. Furthermore, cortisol induced a 60% fall in carcass lipid levels. Cortisol caused a 2-fold increase in fasting blood glucose level. This effect resulted from a stimulation of gluconeogenesis (as shown by the 2− to 3-fold rise in the rate of conversion of labeled lactate or alanine to glucose). Several factors influenced this response: 1) increase in circulating gluconeogenic substrates (lactate, pyruvate, alanine,' proline, and glutamine), 2) increase in plasma glucagon, 3) a small rise in plasma free fatty acids (FFA) arising from the catabolism of endogenous lipids, thereby providing additional energy for the hepatic conversion of gluconeogenic substrates to glucose. A concurrent decrease in glucose utilization was unlikely since: 1) the rate of glucose disappearance after an ip glucose load was similar in fasted and cortisol-treated newborns, and 2) the rise in plasma insulin occurring after cortisol injection would ordinarily tend to increase glucose utilization.
Triglyceride feeding was associated with a 2-fold rise in fasting blood glucose. This effect was secondary to a stimulation of gluconeogenesis by provision of free FFA, as demonstrated by the 2.5-fold increase hi the conversion in vivo of labeled lactate and alanine into glucose.
In newborn rats injected with cortisol, the levels of both plasma FFA and blood ketone bodies remained far below those in suckling newborns of the same age. The combination of cortisol injection at birth with triglyceride feeding 13 hr after birth caused a 3-fold increase in blood glucose levels in the 16-hr-old newborn rats. The stimulating effects of cortisol on gluconeogenesis were potentiated by triglyceride feeding, as shown by the 3− to 4-fold increase in the rate of lactate or alanine conversion to glucose. However, cortisol markedly decreased the ketosis induced by triglyceride feeding and increased plasma triglycerides.
Speculation: Corticosteroids have been used in the treatment of symptomatic hypoglycemia in newborn infants. In fasted newborn rats, cortisol partially prevents hypoglycemia, but at the cost of increased protein catabolism. Moreover, cortisol has an antiketogenic effect, thus decreasing the availability of ketones as alternate fuel for brain metabolism and as precursor for brain lipid synthesis. If such data can be extrapolated to the human newborn, the prolonged use of corticosteroids in the treatment of neonatal hypoglycemia seems less physiologic than adequate parenteral energy substrate provision in the form of intralipid and gluconeogenic precursors (lactate, ammo acids, and glycerol).
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Ferre, P., Pegorier, JP., Assan, R. et al. Influence of Exogenous Cortisol and Triglyceride Feeding on Glucose Homeostasis in the Fasted Newborn Rat. Pediatr Res 12, 751–756 (1978). https://doi.org/10.1203/00006450-197807000-00002
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DOI: https://doi.org/10.1203/00006450-197807000-00002