Stimulation of gastric glucagon secretion by epinephrine administration in dogs

To determine the response of gastric A-cells to adrenergic substances, immunoreactive glucagon was determined simultaneously in the jugular vein and in the left gastroepiploic vein of totally depancreatized dogs. Under basal conditions a significant gradient of glucagon concentrations between the jugular and gastric veins was observed, whereas plasma insulin values were almost undetectable. Intravenous administration of epinephrine elicits a prompt and significant increase in glucagon concentrations in the gastric vein which persist during the time of hormone infusion. To ensure adequate adrenergic blockade, blockers were infused before epinephrine administration. Accordingly, after phentolamine, the infusion of epinephrine failed to increase gastric glucagon concentrations, while after propranolol, epinephrine induced a significant release of gastric glucagon. These results indicate that epinephrine stimulates gastric glucagon secretion and that this effect is mediated through alpha-adrenergic receptors.     

The effects of glucagon and epinephrine on two preparations of cardiac mitochondria

The effects of $\text{in}$$\text{vivo}$ administration in epinephrine on calcium uptake were measured in two preparations of heart mitochondria, intermyofibrillar (IMF) and subsarcolemmal (SSL) using either ⁴⁵Ca²⁺ or murexide to follow calcium movement. The administration of either hormones resulted in an increased calcium uptake in both preparation of mitochondria subsequently isolated. This increase might be the consequence of the increased State 3 respiration, also evoked by hormones. The possibility is raised that the inotropic actions of glucagon and epinephrine might be partially mediated by mitochondria.     

Effects of epinephrine, glucagon and insulin on glucose metabolism of planaria

Epinephrine and insulin increased glucose uptake in Planaria, but epinephrine did so to a much grater extent. Glucagon proved to be without effect. The experiments support earlier results according to which in unicellular and invertebrate organisms membrane patterns can be found, which are similar to those of higher organisms and behave like receptors.     

Insulin and glucagon immunoreactivity during high-intensity exercise under opiate blockade

Eight fit men [maximum oxygen consumption (O_2max) 64.6 (1.9) ml · kg⁻¹ · min⁻¹, aged 28.3 (1.7) years (SE in parentheses) were studied during two treadmill exercise trials to determine the effect of endogenous opioids on insulin and glucagon immunoreactivity during intense exercise (80% O_2max). A double-blind experimental design was used with subjects undertaking the two exercise trials in counterbalanced order. Exercise trials were 20 min in duration and were conducted 7 days apart. One exercise trial was undertaken following administration of naloxone (N; 1.2 mg; 3 ml) and the other after receiving a placebo (P; 0.9% NaCl saline; 3 ml). Prior to each experimental trial a flexible catheter was placed into an antecubital vein and baseline blood samples were collected. Immediately after, each subject received either a N or P bolus injection. Blood samples were also collected after 20 min of continuous exercise (running). Glucagon was higher (P < 0.05), while insulin was lower (P < 0.05), during exercise compared with pre-exercise values in both trials. However, glucagon was higher (P < 0.05) in the P than in the N exercise trial [141.4 (8.3) ng · l⁻¹ vs 127.2 (7.6) ng · l⁻¹]. There were no differences in insulin during exercise between the P and N trials [50.2 (4.3) pmol · l⁻¹ vs 43.8 (5) pmol · l⁻¹]. These data suggest that endogenous opioids may augment the glucagon response during intense exercise. Accepted: 15 June 1996     

Solubilization of glucagon and epinephrine sensitive adenylate cyclase from rat liver plasma membranes

Hormonally sensitive adenylate cyclase has been solubilized from rat liver plasma membranes using Triton X-305 in Tris buffers containing mercaptoethanol and MgCl₂. The solubilized enzyme was stimulated 5 fold by NaF, 7 fold by glucagon and 20 fold by epinephrine. Criteria for solubilization included lack of sedimentation at 100,000 × g for one hour, the absence of particulate material in the 100,000 × g supernatant when examined by electron microscopy, and inclusion of hormonally sensitive adenylate cyclase activity in Sephadex G 200 gels. The molecular weight of the solubilized, hormonally sensitive enzyme was approximately 200,000 in the presence of Triton X-305.     

Effects of glucagon and epinephrine on the rat liver: oxidative phosphorylation and ultrastructure

Twenty minutes after i.v. injection of 1.5 micrograms/100 g epinephrine, the phosphorylation rates of rat liver mitochondria were increased by 30-40%. Treatment with cycloheximide or actinomycin D 20 min before epinephrine or glucagon (10 micrograms/100 g, i.v.) injection blocked much of the respiratory activation by these hormones. The treatment with glucagon or epinephrine (20 min) provoked an important development of rough endoplasmic reticulum of which cisternae were closely associated with the mitochondria, and an appearance of abundant ribosomes. We observed close structural contact between mitochondria, and also between smooth endoplasmic reticulum membranes and mitochondria. Thus, glucagon and epinephrine provoked an early stimulation of mRNA and protein synthesis which could be involved in the activation of mitochondrial energy metabolism.     

Different effects of glucagon and epinephrine on the kinetic properties of liver glycogen synthase

Kinetic constants of glycogen synthase (M0.5 for glucose-6-P and S0.5 for UDP-glucose) were determined after hepatocytes isolated from starved rats were incubated with either glucagon or epinephrine. Incubation with these hormones resulted in an increase in both S0.5 and M0.5. However, the action of glucagon resulted in great modifications on S0.5 whereas epinephrine affected mainly M0.5. Therefore, glucagon and epinephrine alter the kinetic properties of glycogen synthase provoke the phosphorylation of glycogen synthase at different site(s) acting through different mechanisms.     

Differential effects of insulin, epinephrine, and glucagon on rat hepatocyte mitochondrial activity

Oxidation of [2,3-14C]succinate carbons in the mitochondrial Krebs cycle was used as a probe to investigate the effects of insulin, epinephrine, glucagon, and 2,4-dinitrophenol (2,4-DNP) on isolated rat hepatocytes. Epinephrine, glucagon, and 2,4-DNP had a far greater stimulatory effect on 14CO2 formation from [2,3-14C]succinate than insulin. Unlike insulin, epinephrine and glucagon had no significant effect on the anabolic utilization of succinate carbons for protein synthesis. Our results suggest that although epinephrine, glucagon, and 2,4-DNP enhance the movement of tracer carbons through the Krebs cycle, only insulin is capable of enhancing amphibolite utilization for protein synthesis.     

Role of GTP in epinephrine and glucagon activation of adenyl cyclase of liver plasma membrane

Purified liver plasma membranes isolated from adrenalectomized rats are characterized by a high sensitivity to glucagon and fluoride and an unusual sensitivity to epinephrine, thus allowing a comparative study of the two hormonal responses. GTP appears to be an essential factor for the effects of both hormones, since it enhances the responses to glucagon as well as epinephrine. GTP has no effect upon the fluoride activation, yet it increases the basal cyclase activity. Therefore GTP requirement seems to be a general feature of the liver adenyl cyclase system.     

Kaluresis independent K-homeostasis: glucagon and B receptor blockade in pancreatectomized dogs

Seventy minutes post pancreatectomy, in dogs that are K loaded - made abruptly hyperkalemic and "life threatened" - by infusion with 2 mEgKC1/kg-/hr until prelethal ECG changes of hyperkalemic cardiotoxicity appear, a kaluresis independent K homeostatic mechanism transfers about 2/3 of administered K to intracellular fluid. Treatment of K loaded pancreatectomized dogs with glucagon or a B receptor blockading dosage of propranolol does not alter the proportion transferred, but treatment with glucagon and propranolol reduces it. It appears that in pancx dogs there is a reciprocal relation between insulin and B receptor mediated K transfer and that glucagon is involved in activity of the kaluresis independent K homeostatic mechanism.