Increased glucose dependence in resting, iron-deficient rats.

Abstract

Rates of blood glucose and lactate turnover were assessed in resting iron-deficient and iron-sufficient (control) rats to test the hypothesis that dependence on glucose metabolism is increased in iron deficiency. Male Sprague-Dawley rats, 21 days old, were fed a diet containing either 6 mg iron/kg feed (iron-deficient group) or 50 mg iron/kg feed (iron-sufficient group) for 3-4 wk. The iron-deficient group became anemic, with hemoglobin levels of 6.4 +/- 0.2 compared with 13.8 +/- 0.3 g/dl for controls. Rats received a 90-min primed continuous infusion of D-[6-3H]glucose and sodium L-[U-14C]lactate via a jugular catheter. Serial samples were taken from a carotid catheter for concentration and specific activity determinations. Iron-deficient rats had significantly (P less than 0.05) higher blood glucose (7.1 +/- 0.3 vs. 6.1 +/- 0.2 mM) and lactate concentrations than controls (1.0 +/- 0.1 vs. 0.8 +/- 0.1 mM). The iron-deficient group had a significantly higher glucose turnover rate (67 +/- 2 vs. 58 +/- 4 mumol . kg-1 . min-1) than the control group. Significantly more metabolite recycling in iron-deficient rats was indicated by greater incorporation of 14C (from infused [14C]-lactate) into blood glucose. Assuming a carbon crossover correction factor of 2, half of blood glucose arose from lactate in deficient animals. By comparison, only 25% of glucose arose from lactate in controls. Lack of a difference in lactate turnover (irreversible disposal) rates between deficient rats and controls (191 +/- 26 vs. 163 +/- 15 mumol . kg-1 . min-1) was attributed to 14C recycling.(ABSTRACT TRUNCATED AT 250 WORDS)