The metabolic response of the canine neonate to twenty-four hours of fasting

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The metabolic effects of 24 hours of neonatal fasting in unanesthetized dogs were compared to fasting for three hours during the first day of life. Blood glucose, lactate, and ketones were unaltered while FFA (0.94 ± 0.07 v 0.70 ± 0.04 mmol/L, P < .001), glycerol (0.21 ± 0.01 v 0.12 ± 0.01 mmol/L, P < .01), and triglycerides (0.41 ± 0.03 v 0.23 ± 0.03 mmol/L, P < .01) were lower at 24 hours. Glucose production and lactate and alanine turnover were unaffected while palmitate turnover declined (8.8 ± 0.7 v 5.1 ± 0.5 μmol/kg/min, P < .01). Oxygen consumption decreased (6.9 ± 0.4 v 6.0 ± 0.3 mL/kg/min, P < .02) while RQ increased (0.79 ± 0.02 v 0.86 ± 0.03, P < 0.05) at 24 hours. Hepatic glycogen content declined (575 ± 37 to 266 ± 32 μmol/g, P < .001) and could account for a GP of 12 μmol/kg/min between 3 and 24 hours of age. Both gluconeogenesis from lactate and alanine increased, together accounting for 7% and 21% of glucose production at 3 and 24 hours. The increment in gluconeogenesis may be facilitated by augmented hepatic cytosolic phosphoenolpyruvate carboxykinase at 24 hours (1.8 ± 0.2 v 14.1 ± 0.8 nmol/min mg protein, P < .01). Despite the decline in VO 2, hepatic ATP and energy charge were unaltered by 24 hours of fasting. These data suggest that FFA availability diminishes during a prolonged neonatal canine fast resulting in lower VO 2. Furthermore, as FFA availability declines, glucose utilization becomes the predominant precursor for energy production. As hepatic glycogen becomes depleted, gluconeogenesis must now constitute a greater proportion of systemic glucose production. Nevertheless, VO 2 is not maintained. The paradoxical stability of hepatic ATP with lower VO 2 suggests that hepatic ATP utilization may have also declined.