MAINTENANCE OF EUGLYCEMIA IS IMPAIRED IN GLUCONEOGENESIS-INHIBITED IRON-DEFICIENT RATS AT REST AND DURING EXERCISE

To evaluate the hypothesis that mild iron deficiency increases depende nce upon gluconeogenesis, control and mildly iron-deficient (Hb = 80 /- 2 g/L) rats were injected with mercaptopicolinic acid (MPA), a know n inhibitor of gluconeogenesis, or with injection vehicle (sham) and s tudied at rest or after 30 min of treadmill running (13.4 m/min, 0% gr ade). Liver glycogen concentration was lower in resting iron-deficient rats than in resting control rats, but iron deficiency did not influe nce arterial substrates or hormones in sham treated rats. Glucose and insulin concentrations were less in resting control and iron-deficient MPA-treated rats than in sham-treated animals. However, arterial lact ate was greater in resting iron-deficient MPA-treated rats than contro l MPA-treated animals, and glucagon and epinephrine were greater in re sting iron-deficient MPA-treated rats than in iron-deficient sham-trea ted animals, indicating that gluconeogenesis is more important to main tenance of euglycemia in resting iron-deficient animals than in contro ls. Moderate exercise stimulated glucose metabolism in iron-deficient rats, as evidenced by the lower arterial glucose and higher arterial l actate when compared with resting iron-deficient rats. However, MPA tr eatment did not clearly establish differences between iron-deficient a nd control rats after exercise. Therefore, changes in substrate and ho rmone concentrations in resting iron-deficient MPA-treated rats indica te that dependence on gluconeogenesis for maintenance of euglycemia is greater at rest with dietary iron deficiency. Furthermore, consistent with previously published results for severely iron-deficient rats, r esults from the present investigation indicate that dependence on gluc ose metabolism is greater during moderate exercise in mildly iron-defi cient rats.