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Laboratory for Human Performance Research and Department of Nutrition, The Pennsylvania State University, Noll Laboratory, University Park, PA 16802
Iron deficient (ID) and control (C) rats were studied to determine if severe iron deficiency alters insulinstimulated glucose disposal. Euglycemic hyperinsulinemic glucose clamps were conducted by infusing insulin (2 mu·kg-1·min-1, constant rate) for 120 min while maintaining euglycemia. In a 12-h fasted state, ID rats were hyperglycemic (109.4 ± 4.0 mg·dL-1 arterial plasma glucose, x ± SEM) when compared with C rats (86.9 ± 3.4 mg·dL-1) (P < 0.05). Even though insulin was infused identically on a per kilogram body weight basis for both groups, the resulting hyperinsulinemia was higher in ID rats (3.1 ± 0.27 ng·mL-1) compared with C rats (2.3 ± 0.4 ng·mL-1) at the end of the clamp. Glucose infusion rates required to maintain euglycemia were twofold higher in ID rats (27.0 ± 5.4 mg·kg-1·min-1) versus C rats (13.1 ± 3.3 mg·kg-1·min-1) (P < 0.05). Circulating lactic acid increased in both groups, and the concentrations in ID rats (3.2 ± 0.4 mmol·L-1) were significantly higher than those in C rats (1.8 ± 0.5 mmol·L-1) at the end of the clamp. When the efficiency of insulin to dispose glucose was evaluated by calculating the glucose disposal divided by the prevailing insulinemia, ID rats could dispose of almost twice the glucose per unit of insulin [9.0 ± 0.6 (mg·kg-1·min-1)/(ng·mL-1)] when compared with C rats [5.6 ± 0.9 (mg·kg-1·min-1)/(ng·mL-1)] (P < 0.05). The data indicate that insulin sensitivity is increased in ID rats and that ID rats cannot metabolize exogenous insulin as well as C rats.
KEY WORDS: insulin sensitivity iron deficiency
1 This study was supported in part by a Biomedical Research Support Grant to P. A. Farrell and by Public Health Service Grant No. DK39160 to J. Beard.
Manuscript received 1 December 1987. Revision accepted 27 April 1988.