Jk. Linderman et al., LACTATE IS ESSENTIAL FOR MAINTENANCE OF EUGLYCEMIA IN IRON-DEFICIENT RATS AT REST AND DURING EXERCISE, The American journal of physiology, 264(4), 1993, pp. 662-667
To evaluate the hypothesis that lactate supply is essential to maintai
n euglycemia during iron deficiency, female Sprague-Dawley rats were a
ssigned to iron-sufficient (50 mg Fe2+/kg diet, +Fe) or iron-deficient
(15 mg Fe2+/kg diet, -Fe) dietary groups and were injected with a spe
cific beta2-adrenergic inhibitor, ICI 118,551 (1.0 mg/kg body wt). Rat
s were studied at rest or after 30 min of running at 13.4 m/min 0% gra
de. Dietary iron deficiency decreased hemoglobin concentration 38%, bu
t resting arterial concentrations of glucose ([Glc]), lactate ([La]),
or alanine ([Ala]) were unaffected. Administration of ICI 118,551 (bet
a2-blockade) decreased [La] and [Glc] 52 and 32% in resting -Fe rats,
respectively. beta2-Blockade attenuated the exercise-induced rise in [
La] and decreased [Glc] 31% in exercising -Fe rats. [Ala] were unaffec
ted by iron deficiency or exercise but decreased 24 and 18% because Of
beta2-blockade in resting and exercising +Fe rats. Iron deficiency de
pleted resting liver glycogen concentration 45%, with no additional ef
fect of exercise or beta2-blockade. beta-Blockade decreased arterial i
nsulin and increased arterial glucagon concentrations in resting -Fe a
nd +Fe rats. During exercise glucagon concentration increased signific
antly more in -Fe than +Fe rats. Decreased arterial [La] with a corres
ponding decrease in arterial [Glc] in response to beta2-blockade suppo
rt the contention that lactate supply is critical to maintenance of eu
glycemia in -Fe rats at rest and during exercise.