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Glucagon Kinetics in Fasting: Physiological Elevations in Serum 3,5,3'-Triiodothyronine Increase the Metabolic Clearance Rate of Glucagon^*

Kyle Metabolic Unit, Clinical Investigation Service, Walter Reed Army Medical Center, Washington, D.C. 20012; Endocrine Service, the National Naval Medical Center, and the Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20014; Nichols Institute for Endocrinology, San Pedro, California 90731

Address requests for reprints to: Kenneth D. Barman, M. D., Kyle Metabolic Unit, Endocrine-Metabolism Service, Walter Reed Army Medical Center, Washington, D. C. 20012.

We have attempted to determine if the elevated plasma glucagon concentration and delayed MCR of glucagon (MCRg) observed during caloric restriction are related to the decreased serum T₃ that also occurs during fasting. Twelve obese subjects received a 3-h iv glucagon infusion during a 4-day fed period (1000 kCal/day) and again on approximately the third fasting day. Five patients fasted without receiving exogenous T₃ (control group), whereas seven subjects fasted but also received 5 fig T₃ orally every 4 h (T₃ group) to maintain approximately the same serum T₃ levels in the fed and fasting periods. Glucagon production rates (GPR) were derived by multiplying the MCRg by the respective basal plasma glucagon concentrations.

In the control group, the MCRg was 442 ± 55 ml/m² ·min in the postabsorptive state and decreased to 312 ± 49 ml/m² ·min (P < 0.025) during fasting, whereas in the T₃-treated group, the postabsorptive MCRg was 304 ± 22 ml/m²·min and increased during fasting to 417 ± 47 ml/m²·min (P < 0.025). The GPRs in the control group were statistically unaltered between the fed (27.7 ± 3.0 ng/m²·min) and fasted (22.9 ± 1.8 ng/m²·min) intervals, but GPR increased from 37.9 ±6.1 ng/m² ·min during fasting to 49.2 ±9.1 ng/m²·min when T₃ was administered (5 jug every 4 h). The net plasma glucose increment in response to glucagon decreased from 18 mg/dl (fed) to 5 mg/dl (fast) in the control patients and from 10 mg/dl (fed) to 7 mg/dl (fast) in the T₃-treated subjects. In the T₃-treated patients, serum T₃ averaged 124 ng/dl during both feeding and fasting, and rT₃ was 55 ± 6 ng/dl during feeding and 49 ± 5 ng/dl during fasting.

In summary, the results from this study indicate that during fasting 1) slight physiological alterations in serum T₃ influence the MCRg, and 2) T₃ increases the GPR and blocks the customary fasting-induced rise in rT₃. Conceivably, decreased T₃ is an arly event in the fasting state which serves to decrease the MCRg, a process which subsequently regulates glucose homeostasis.

^* The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or reflecting the views of the Department of the Army or the Department of Defense.

Received March 10, 1980.