Mr. Myers et Kc. Klasing, Low glucokinase activity and high rates of gluconeogenesis contribute to hyperglycemia in barn owls (Tyto alba) after a glucose challenge, J NUTR, 129(10), 1999, pp. 1896-1904
Barn owls (Tyto alba) and leghorn chickens were fed a low protein high gluc
ose (33.44% protein, 23.67% glucose) or a high protein low glucose (55.35%
protein, 1.5% glucose) diet. After an intravenous glucose infusion, the pea
k in plasma glucose was not affected by diet in either species and was 22.6
and 39.4 mmol/L in chickens and barn owls, respectively. Glucose levels re
turned to normal within 30 min in chickens, but remained elevated for 3.5 h
in barn owls. An oral glucose challenge also resulted in greater and longe
r hyperglycemia in barn owls than in chickens. The activities of hepatic gl
ucokinase, malic enzyme and phosphoenolpyruvate carboxykinase of barn owls
were 16, 35, and 333% of the levels in chickens. Malic enzyme (P = 0.024) w
as less affected by dietary glucose level in barn owls than in chickens. Cu
ltured hepatocytes from chickens produced 43% more glucose from lactate tha
n hepatocytes from barn owls and, conversely, barn owl hepatocytes produced
87% more glucose from threonine than chickens (P = 0.001). Gluconeogenesis
from lactate was greatly suppressed by high media glucose in chicken hepat
ocytes but not in those of barn owls (P = 0.0001 for species by glucose lev
el interaction). When threonine was the substrate, gluconeogenesis was supp
ressed by increased glucose in both species but to a greater relative exten
t in chickens (P = 0.007 for species by glucose level interaction). Owls we
re glucose intolerant at least in part because of low hepatic glucokinase a
ctivity and an inadequate suppression of gluconeogenesis in the presence of
exogenous glucose, apparently because they evolved with large excesses of
amino acids and limited glucose in their normal diet.