TY - JOUR
T1 - Glucagon kinetics in fasting
T2 - Physiological elevations in serum 3,5,3'-triiodothyronine increase the metabolic clearance rate of glucagon
AU - Burman, Kenneth D.
AU - Smallridge, Robert C.
AU - Jones, Linda
AU - Ramos, Elizabeth A.
AU - O'brian, John T.
AU - Wright, Frances D.
AU - Wartofsky, Leonard
PY - 1980/11
Y1 - 1980/11
N2 - 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 μg 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 μg 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 early event in the fasting state which serves to decrease the MCRg, a process which subsequently regulates glucose homeostasis.
AB - 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 μg 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 μg 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 early event in the fasting state which serves to decrease the MCRg, a process which subsequently regulates glucose homeostasis.
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U2 - 10.1210/jcem-51-5-1158
DO - 10.1210/jcem-51-5-1158
M3 - Article
C2 - 7419689
AN - SCOPUS:0019182312
SN - 0021-972X
VL - 51
SP - 1158
EP - 1165
JO - Journal of Clinical Endocrinology and Metabolism
JF - Journal of Clinical Endocrinology and Metabolism
IS - 5
ER -