Glucagon kinetics in fasting: Physiological elevations in serum 3,5,3'-triiodothyronine increase the metabolic clearance rate of glucagon

K. D. Burman, Robert Christian Smallridge, L. Jones, E. A. Ramos, J. T. O'Brien, F. D. Wright, L. Wartofsky

Research output: Contribution to journalArticle

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Abstract

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 T 3 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 T 3 (control group), whereas seven subjects fasted but also received 5 μg T 3 orally every 4 h (T 3 group) to maintain approximately the same serum T 3 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/m 2.min in the postabsorptive state and decreased to 312 ± 49 ml/m 2.min (P < 0.025) during fasting, whereas in the T 3-treated group, the postabsorptive MCRg was 304 ± 22 ml/m 2.min and increased during fasting to 417 ± 47 ml/m 2.min (P < 0.025). The GPRs in the control group were statistically unaltered between the fed (27.7 ± 3.0 ng/m 2.min and fasted (22.9 ± 1.8 ng/m 2.min) intervals, but GPR increased from 37.9 ± 6.1 ng/m 2.min during fasting to 49.2 ± 9.1 ng/m 2.min when T 3 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 T 3-treated subjects. In the T 3-treated patients, serum T 3 averaged 124 ng/dl during both feeding and fasting, and rT 3 was 55 ± 6 ng/dl durig 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 T 3 influence the MCRg, and 2) T 3 increases the GPR and blocks the customary fasting-induced rise in rT 3. Conceivably, decreased T 3 is an early event in the fasting state which serves to decrease the MCRg, a process which subsequently regulates glucose homeostasis.

Original languageEnglish (US)
Pages (from-to)1158-1165
Number of pages8
JournalJournal of Clinical Endocrinology and Metabolism
Volume51
Issue number4
StatePublished - 1980
Externally publishedYes

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Metabolic Clearance Rate
Triiodothyronine
Glucagon
Fasting
Kinetics
Serum
Plasmas
Control Groups
Ground penetrating radar systems
Glucose
Caloric Restriction

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

Glucagon kinetics in fasting : Physiological elevations in serum 3,5,3'-triiodothyronine increase the metabolic clearance rate of glucagon. / Burman, K. D.; Smallridge, Robert Christian; Jones, L.; Ramos, E. A.; O'Brien, J. T.; Wright, F. D.; Wartofsky, L.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 51, No. 4, 1980, p. 1158-1165.

Research output: Contribution to journalArticle

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abstract = "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 T 3 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 T 3 (control group), whereas seven subjects fasted but also received 5 μg T 3 orally every 4 h (T 3 group) to maintain approximately the same serum T 3 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/m 2.min in the postabsorptive state and decreased to 312 ± 49 ml/m 2.min (P < 0.025) during fasting, whereas in the T 3-treated group, the postabsorptive MCRg was 304 ± 22 ml/m 2.min and increased during fasting to 417 ± 47 ml/m 2.min (P < 0.025). The GPRs in the control group were statistically unaltered between the fed (27.7 ± 3.0 ng/m 2.min and fasted (22.9 ± 1.8 ng/m 2.min) intervals, but GPR increased from 37.9 ± 6.1 ng/m 2.min during fasting to 49.2 ± 9.1 ng/m 2.min when T 3 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 T 3-treated subjects. In the T 3-treated patients, serum T 3 averaged 124 ng/dl during both feeding and fasting, and rT 3 was 55 ± 6 ng/dl durig 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 T 3 influence the MCRg, and 2) T 3 increases the GPR and blocks the customary fasting-induced rise in rT 3. Conceivably, decreased T 3 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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AU - Wartofsky, L.

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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 T 3 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 T 3 (control group), whereas seven subjects fasted but also received 5 μg T 3 orally every 4 h (T 3 group) to maintain approximately the same serum T 3 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/m 2.min in the postabsorptive state and decreased to 312 ± 49 ml/m 2.min (P < 0.025) during fasting, whereas in the T 3-treated group, the postabsorptive MCRg was 304 ± 22 ml/m 2.min and increased during fasting to 417 ± 47 ml/m 2.min (P < 0.025). The GPRs in the control group were statistically unaltered between the fed (27.7 ± 3.0 ng/m 2.min and fasted (22.9 ± 1.8 ng/m 2.min) intervals, but GPR increased from 37.9 ± 6.1 ng/m 2.min during fasting to 49.2 ± 9.1 ng/m 2.min when T 3 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 T 3-treated subjects. In the T 3-treated patients, serum T 3 averaged 124 ng/dl during both feeding and fasting, and rT 3 was 55 ± 6 ng/dl durig 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 T 3 influence the MCRg, and 2) T 3 increases the GPR and blocks the customary fasting-induced rise in rT 3. Conceivably, decreased T 3 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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