SummaryThe age-related changes in fasting arterial levels of energy substrates and insulin were studied at birth and/or 6 wk in eleven baboon infants. In addition, the renal contribution to glucose release in the primate infant was estimated. Arterial blood glucose levels were similar in six fasted newborns and in nine fasted 6-wkold infants. Arterial blood lactate, alanine, pyruvate, glutamate, and glutamine levels were significantly higher ( P < 0.01) in the new born animals, and /3-hydroxybutyrate was significantly higher in the older animals ( P < 0.001). Arterial plasma insulin levels were low in both groups. Levels of blood glucose in the inferior vena cava below the renal vein were significantly lower than levels in the aorta ( P < 0.01). In contrast, levels of blood glucose in the inferior vena cava above the renal vein were significantly higher than in the aorta ( P < 0.05). Computed renal vein glucose levels were higher than those in the aorta ( P < 0.01). In the newborn infants, there was significant renal uptake of lactate, pyruvate, glycerol, and glutamine ( P < 0.01), and release of /I-hydroxybutyrate ( P < 0.05). In the older animals, there was renal uptake of alanine, lactate, pyruvate, and glycerol ( P 0.01). Mean cardiac output per kg body weight did not differ significantly in the newborn and Cwk-old infants.Lactate uptake was potentially responsible for 59% of mean renal glucose output in the newborn and 76% of mean renal glucose output in the older infant. Net renal glucose release in eight Cwkold infants was estimated to be 3.5 + 1.1 pM/min*kg (95% confidence limits, 0.7 < 3.5 < 6.2). Net renal glucose release in three newborn infants was 4.7, 5.4, and 19.8 pM/min*kg. There was a significant linear relationship between arterial lactate levels and renal glucose production in the older infants ( P < 0.05).Extremely low arterial pH was associated with increased renal glucose release in the newborn, and high arterial pH with decreased or absent glucose release in the Cwk-old animals.
SpeculationThe primate infant kidney has a capacity for gluconeogenesis which is apparently enhanced by acidosis and lactate availability. In the stressed human neonate, it is possible that renal gluconeogenesis could be a significant and uncontrolled source of new glucose, leading to hyperglycemia.The renal contribution to gluconeogenesis is significant in fasting man and in lower mammalian species (14, 23). However, the role of renal glucose production in energy metabolism in the young animal has not been well studied. Most information concerning gluconeogenesis in infancy has been derived from studies in the rat. Gluconeogenesis in developing rat kidney cortex may be identified in late fetal life (30). In contrast, the ability to a d a~t to fasting by increased hepatic glu~oneo~enesis is acqiired poinatally in this species (10). The relative contribution of the kidneys to glucose production in the young of higher mammalian species and the primate neonate and infant, in particular, is unknown.To investigate the r...