Development and Application of a Radioimmunoassay for Plasma Glucagon

1974 ◽  
Vol 20 (5) ◽  
pp. 566-570 ◽  
Author(s):  
Mark A Sperling ◽  
Paul V DeLamater ◽  
Mirtha Kazenelson ◽  
Robert H Fiser ◽  
Delbert A Fisher
Keyword(s):  
Children And Adolescents ◽  
Coefficient Of Variation ◽  
Oral Feeding ◽  
Oral Glucose ◽  
Plasma Glucagon ◽  
Human Infants ◽  
Glucose Loading ◽  
Pancreatic Glucagon ◽  
Assay Conditions ◽  
Glucagon Concentration

Abstract We report sensitive radioimmunoassay procedures for glucagon-like immunoreactivity and for pancreatic glucagon, with use of antisera generated in rabbits by the injection of glucagon covalently coupled to thyroglobulin. Optimum assay conditions were determined. These assays have absolute limits of sensitivity of 10 to 20 pg, an intra-assay coefficient of variation of 8%, and an inter-assay coefficient of variation of up to 22%. In human infants 30 minutes after birth, glucagon concentration was 227 ± 27 pg/ml (SEM), and glucagon-like immunoreactivity increased sharply with oral feeding. In children and adolescents, plasma glucagon concentrations during fasting, the increase in response to arginine stimulation, and the suppression after oral glucose loading were similar to values previously reported in adults. Problems inherent in the methodology for measuring plasma glucagon are discussed.

The influence of oral glucose loading on the insulin response to i.v. glucagon in children and adolescents

Metabolism ◽  
1976 ◽  
Vol 25 (3) ◽  
pp. 277-280 ◽  
Author(s):  
Z. Josefsberg ◽  
E. Flatau ◽  
M. Doron ◽  
Z. Laron
Keyword(s):  
Children And Adolescents ◽  
Insulin Response ◽  
Oral Glucose ◽  
Glucose Loading

Contribution of hepatic glycogenolysis to glucose production in humans in response to a physiological increase in plasma glucagon concentration

Diabetes ◽  
1995 ◽  
Vol 44 (2) ◽  
pp. 185-189 ◽  
Author(s):  
I. Magnusson ◽  
D. L. Rothman ◽  
D. P. Gerard ◽  
L. D. Katz ◽  
G. I. Shulman
Keyword(s):  
Glucose Production ◽  
Plasma Glucagon ◽  
Glucagon Concentration

Induction of renal phosphoenolpyruvate carboxykinase mRNA: suppressive effect of glucose

1989 ◽  
Vol 257 (1) ◽  
pp. F145-F151
Author(s):  
A. S. Pollock
Keyword(s):  
Metabolic Acidosis ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Suppressive Effect ◽  
Oral Glucose ◽  
Prolonged Fasting ◽  
Glucose Loading ◽  
Glucose Administration ◽  
Liver And Kidney ◽  
Gluconeogenic Enzyme ◽  
Effect Of Glucose

The mRNA for the important gluconeogenic enzyme phosphoenolpyruvate carboxykinase (GTP) (PEPCK; EC 4.1.1.32) is expressed in liver and kidney. In the kidney, acidosis is a unique and potent stimulus, whereas insulin, the major counterregulatory hormone of gluconeogenesis, has no effect. In this study, we find that oral glucose administration to rats rapidly decreases the abundance of renal PEPCK mRNA by 50–72%. This reduction takes place in normal euglycemic, in insulin-induced hypoglycemic, and in streptozotocin-induced hyperglycemic diabetic animals. The effect of glucose is not seen in the presence of metabolic acidosis, whether induced by NH4Cl or by prolonged fasting. Therefore, it appears that oral glucose loading is a physiological suppressor of renal PEPCK message abundance, although not in acidosis.

Hepatic glycogen in humans. I. Direct formation after oral and intravenous glucose or after a 24-h fast

1989 ◽  
Vol 257 (2) ◽  
pp. E145-E157 ◽  
Author(s):  
J. Radziuk
Keyword(s):  
Glucose Infusion ◽  
Hepatic Glycogen ◽  
Oral Glucose ◽  
Metabolic Clearance ◽  
Glucose Load ◽  
Fasting Period ◽  
Intravenous Glucose ◽  
Glucose Loading ◽  
Constant Rate ◽  
Direct Formation

The formation of hepatic glycogen by the direct pathway is assessed in humans 1) after a 12-h fast and oral loading (100 g) or 2) intravenous infusion (90 g) and 3) after a 24-h fast and the same oral glucose load. The methodology used is based on the double tracer method. [3–3H]glucose is infused at a constant rate for the determination of the metabolic clearance of glucose. [1–14C]glucose is administered with the glucose load. One hour after absorption or the intravenous glucose infusion is terminated, a glucagon infusion is initiated to mobilize the glycogen labeled with [1-14C]glucose and formed during the absorptive period. At this time a third tracer, [6-3H]glucose, is administered to measure glucose clearance. It was found that after the 12-h fast and oral glucose loading 7.2 +/- 1.1 g of hepatic glycogen appears to be formed directly from glucose compared with 8.4 +/- 1.0 g after the same load and a 24-h fast and 8.5 +/- 0.4 g after a 12-h fast and an equivalent intravenous glucose infusion. When the amount of label ([14C]glucose) mobilized that was not corrected for metabolic recycling was calculated, the data suggested that the amount of glycogen formed by gluconeogenic pathways was probably at least equal to that formed by direct uptake. It was also approximately 60% greater after a 24-h fast. It can be concluded that the amount of hepatic glycogen formed directly from glucose during glucose loading is not significantly altered by the route of entry or the extension of the fasting period to 24 h. The data suggest, however, that gluconeogenetic formation of glycogen increases with fasting.

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