AJP - Regulatory, Integrative and Comparative Physiology, Vol 244, Issue 5 667-R675, Copyright © 1983 by American Physiological Society
Ketone-glucose interaction in fed, fasted, and fasted-infected sheep
A. G. Radcliffe, R. R. Wolfe, M. F. Colpoys, F. Muhlbacher and D. W. Wilmore
Ketosis following starvation was suppressed by hindlimb infection in seven
fasted sheep. Glucose production determined following the primed constant
infusion of [6-3H(N)]glucose was elevated in the fasted-infected animals
(9.50 +/- 1.11 mmol X kg-1 X min-1 (mean +/- SE) versus fasted controls
(5.56 +/- 2.2). To determine if the ketonemia following sepsis contributed
to the increased glucogenesis associated with catabolic disorder, glucose
production and arterial substrates were measured before and after infusion
of sodium-DL-beta-hydroxybutyrate (beta-OHB, 20 mumol X kg-1 X min-1) in
fed, fasted, and fasted-infected animals. Following 3 h of beta-OHB
infusion in the awake conditioned animals, beta-OHB and acetoacetate blood
concentrations more than doubled. With infusion, blood glucose and alanine
concentrations decreased in the fed and fasted sheep but not in the
fasted-infected group. Glucose production fell significantly from 10.11 +/-
1.33 to 8.44 +/- 1.05 in the fed animals and from 5.05 +/- 0.28 to 4.11 +/-
0.33 in the fasted group. Glucose production was unaffected by beta-OHB
infusion in the fasted-infected animals (9.50 +/- 1.83 vs. 9.11 +/- 1.44).
The accelerated rate of glucose production in sheep following infection is
not a consequence of the hypoketonemic state associated with sepsis.
