Effect of glucagon on serum insulin, plasma glucose and free fatty acids in man

Crockford, P. M.; Porte, Daniel; Wood, Francis C.; Williams, Robert H.

doi:10.1016/0026-0495(66)90032-1

Cited by 106 publications

(37 citation statements)

References 20 publications

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“…Glucagon, per se, is a potent stimulus to insulin secretion as is the hyperglycemia produced [8,12,191. The slope and magnitude of the insulin and blood sugar response obtained in the adult dog resemble the data reported by CROCKFORD et al [8] obtained in human adults during a 3-h glucagon infusion. In the puppy, glucagon infusion with the attendant hyperglycemia elicited a minimal rise in insulin levels.…”

Section: Discussionmentioning

confidence: 99%

Glucose Production and Utilization in the Newborn Puppy

1970

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A steady-state radioglucose dilution technique was used to determine new glucose production in six newborn (1-4 days) and two adult dogs in the postabsorptive state, and during a 90-min glucagon infusion.Basal new glucose production rates were 2.0 and 2.2 mg/kg body weight per minute in the adults. In contrast, basal rates in the newborn were 2-4 times (4.1-7.9 mg/kg/min) the values for the adults.During glucagon-induced hyperglycemia in the adult, glucose production increased to 2.5 times the basal level, while plasma glucose concentration rose to a peak at 30 min. The newborn dog responded with only a 40% increment above basal production while glucose concentration rose continuously. The adult responded with a rise in plasma insulin level but no change was observed in the newborn. The fractional rate of glucose utilization during the glucagon-induced hyperglycemia was observed to decline in newborn dogs; no decline was observed in the adults. Glucose metabolism in the newborn differs from that in the adult dog as follows: I) basal glucose production and utilization per unit body weight are greater in the newborn; and 2) during glucagon-stimulated hyperglycemia the newborn adapts with less acceleration of both the production and the utilization of glucose. Speculation

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Section: Discussionmentioning

confidence: 99%

Glucose Production and Utilization in the Newborn Puppy

1970

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“…Maximum insulin congonemia, due to either endogenously released glucagon or exogecentration determined was 120 p.U/mi. At the highest dose of nous infusion, is associated with an immediate hyperglycemic glucagon utilized (1.0 mg/kg) this would cause a maximum eleresponse (9,29). Although the glycogenolytic and gluconeogenic vation of 0.2 p.U/ml in fetal plasma.…”

Section: Summary Speculationmentioning

confidence: 99%

Influence of Exogenous Glucagon on Fetal Glucose Metabolism and Ketone Production

et al. 1983

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(2, 28) have shown that certain adult glucagon secretogogues such as arginine or epinephrine could produce a significant fetal hyperglucagonemia. Recent work (13) suggests that elevation in fetal glucagon concentration may accompany prolonged maternal fasting.The physiologic function of fetal hyperglucagonemia is also open to question. A hyperglycemic response to pharmacologic injection has been suggested in in vivo preparations (6). In order to clarify the role of glucagon as a possible fetal metabolic regulatory hormone, we utilized the chronically catheterized fetal sheep as our model. Varying degrees of hyperglucagonemia were induced and alterations in fetal glucagon, insulin, glucose and ketone concentrations as well as umbilical glucose and ketone uptakes then noted. Summary SpeculationThe fetus in late gestation may respond to substrate deprivation by secretion of glucagon. If so, a modest but significant hyperglycemia would result, presumably the result of acute fetal glycogenolysis. The acute fetal metabolic adaptation to maternal starvation, however, if modified by glucagon, does not include utilization of ketones as alternate substrates.Acute glucagon injections were performed in chronically catheterized fetal lambs in late gestation to assess the fetal metabolic response to exogenous glucagon infusion. Glucagon dosages between 1 p,g/kg and 1 mg/kg induced significant fetal hyperglycemia by 15-30 min postinjection, with peak glucose values 130-180% of control. Increasing responsivity to the same dose/kg was noted to parallel increasing gestational age. In selected preparations in which umbilical venous catheters were implanted, glucagon injection caused an acute fall in the glucose/oxygen quotient and net umbilical glucose consumption. The fall in glucose consumption to 8% of control values occurred within 15 min of injection and suggests acute fetal glucose excretion, probably secondary to hepatic glycogenolysis. Glucagon injection in the neonatal lamb caused qualitatively similar increases in plasma glucose concentration but the quantitative responses were considerably greater. No change in fetal ,B-hydroxybutyrate (,B-ORD) concentration was noted after injection; nor did the fetal uptake or excretion of this ketone change. The neonatal ,B-ORD concentration was significantly different (P < 0.001) from fetal concentrations and did rise 14% above control after glucagon injection; thus, elevation of plasma glucagon in the fetus causes an acute hyperglycemia but, unlike the adult, does not induce a significant ketogenesis.Experimental design. Eleven pregnant ewes between 118-149 days of gestation were studied (Table 1). Term gestation in the sheep is 147 days. All but two had singleton fetuses. Intravenous sodium pentobarbital and spinal anesthesia were administered to each animal preoperatively. Polyvinyl catheters were then placed in a fetal pedal artery and vein as well as the maternal femoral artery for purposes of sampling and infusion. In five of the fetal lambs umbilical venous catheters were als...

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“…Naeh Glueagon erfolgt der Insulinanstieg deutlich frfiher als der Blutzuckergipfel, wie SAMozs et al [16] zum ersten Mal naehgewiesen haben. Naeh SAI,3IOLS et al und CROCKFOI~I) et al [2] stimuliert das Glueagon direkt die Insulinsekretion aus den beta-Zellen des Pankreas. Dies wurde yon V]~cc~IO et al [19] in vitro an isoliertem foetalem und in der Gewebekultur gehaltenem Pankreasgewebe best~Ltigt.…”

Section: Disl~ussion Und Schlu[3folgerungenunclassified

Immunologically measurable insulin (IMI) in normal, obese and obese, diabetic subjects after intravenous administration of glucose, tolbutamide and glucagon.

et al. 1967

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Immunologically measurable insulin (IMI) in normal, obese and obese, diabetic subjects after intravenous administration of glucose, tolbutamide and glucagon.Summary. Serum insulin levels (immunologically measurable insulin, IMI) in normal, obese and obese, diabetic subjects were determined following injection of glucose {0.33 g/kg), tolbutamide (1 g) and glucagon (1 rag). --In normal non-obese subjects an immediate (after one minute) increase of serum insulin levels was observed following the injection of glucose, tolbutamide or glucagon. 15 minutes after injection, the IMI-values were within the normal range. Obese subjects also react with an immediate increase of serum insulin levels following injection of glucose, tolbutamide or gtucagon; however, the IMIvalues were significantly higher than in normal subjects. Furthermore, in obese patients with slight diabetes, the IMI-levels after glucose or tolbutamide were definitely lower than those observed in normal non-obese subjects, although the levels following glucagon were of the same magnitude.-Apparently the increase of endogenous insulin in obese non-diabetic-patients after administration of glucose does not influence the glucose assimilation coefficient, K. I-Iyperinsulinism appears to be associated with obesity rather than with diabetes.

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Effect of glucagon on serum insulin, plasma glucose and free fatty acids in man

Cited by 106 publications

References 20 publications

Glucose Production and Utilization in the Newborn Puppy

Glucose Production and Utilization in the Newborn Puppy

Influence of Exogenous Glucagon on Fetal Glucose Metabolism and Ketone Production

Immunologically measurable insulin (IMI) in normal, obese and obese, diabetic subjects after intravenous administration of glucose, tolbutamide and glucagon.

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