Glucagon in doses of 0.25 or 1.0 mg. was injected rapidly, intravenously, into healthy normal subjects. There was a striking rise in arterial immunoreactive insulin levels within one minute of the start ot the injection before any change in arterial glucose concentration occurred Plasma insulin levels reached their peak within ten minutes and began to fall thereafter. In contrast, blood glucose levels were highest twenty to thirty minutes after the injection. A second glucagon injection during the hyperglycemic phase produced a larger rise in plasma insulin than the first. During constant infusions of smaller amounts of glucagon, the insulinogenic effect of glucagon was usually only apparent if blood glucose levels were raised. The effect of consecutive forty-minute intravenous infusions of glucagon (10μg./min.), glucose (0.5 gm./min.) and a glucagon-glucose (5μg. and 250 mg./min., respectively) on plasma insulin and arterio-venous blood glucose differences in six healthy normal subjects was studied. Plasma insulin levels were two to five times higher during glucose infusions alone, despite similar peak arterial blood glucose levels during the infusions. Similar results were obtained in other subjects during separate infusions of glucose and glucagon. Total body glucose clearance, judged by the rate of fall in arterial blood glucose levels, was faster after glucagon- than after glucose-induced hyperglycemia. Forearm A-V blood glucose differences were not obviously greater during glucagon, in spite of the higher plasma insulin levels, than during glucose infusions. Possible reasons for the failure of forearm A-V blood glucose differences to reflect accurately total peripheral glucose assimilation under these experimental conditions are discussed, and it is suggested that the co-existence of hyperglucagonemia and hyperinsulinemia may tend to favor incorporation of glucose into adipose tissue rather than muscle. Plasma glucagon levels were measured by immunoassay and the half-life was about ten minutes. The results provide evidence of a direct effect of glucagon upon insulin secretion. The suggestion is made that the insulinogenic effect of glucagon is physiological importance and is due to accelerated intra-β-cell glycogenolysis.

Interrelationship of Glucagon, Insulin and Glucose: The Insulinogenic Effect of Glucagon

The sections in this article are:


1
Embryonic and Postembryonic Histogenesis of Adipose Tissue
1.1
Occurrence and Appearance of the Primitive Organs of the White Adipose Tissue

1.2
Storage of Fat in the Primitive Organs

1.3
Histogenesis of the Primitive Organs and Their Reticuloendothelial Nature

1.4
Blood Cell Formation in Primitive Organs

1.5
Persistence of the Fat Organ After Loss of the Fat

1.6
Development of the Brown Adipose Tissue




2
Growth and Spreading of Adipose Tissue

The development of adipose tissue

http://www.jbc.org/content/235/9/2600.full.pdf

Effect of insulin on the metabolism of adipose tissue from hyperthyroid rats.

The sections in this article are:


1
I. Introduction

2
II. Physiological role of Brown Adipose Tissue as a Quantitatively Important site of Heat Production
2.1
A. Heat Production by Brown Adipose Tissue During Arousal From Hibernation

2.2
B. Changes in Brown Adipose Tissue of Nonhibernating Species During Exposure to Cold Environment




3
III. Other Possible Functions of Brown Adipose Tissue

4
IV. Suitability of Brown Adipose Tissue for the Study of Metabolic Mechanisms in Adipose Tissue

5
V. Summary

The physiological role of brown adipose tissue1

The sections in this article are:


1
Preparation of Fat Cells

2
Morphology of Fat Cell and Stromal-Vascular Fractions

3
Metabolism of Glucose and Response to Insulin

4
Effects of Other Hormones on Glucose Metabolism

5
Potassium Requirement for Insulin Response by Fat Cells

6
Effects of Lipolytic Hormones on Fatty Acid and Glycerol Release

The metabolism of isolated fat cells

The permeability of tissues toward glucose was explored in rats under various hormonal and environmental influences. The velocity constant K expressing the rate of disappearance of glucose from blood after rapid intravenous injection of a small load of glucose was critically analyzed as an index of glucose utilization. Acute treatments with large doses of glucagon and hydrocortisone led only to negligible effects on K. One hour after epinephrine injection, the persisting hyperglycemia appeared to be due more to increased liver glycogenolysis than to inhibition of glucose utilization. A marked enhancement of K developed 2 hours after a moderate dose. As expected, severe insulin hypoglycemia was accompanied by a sharp increase in K; this was followed by a drasticdecrease during the restoration to normal of the blood glucose level. A single injection of thyroxin led to a rapid increase in K and to a small degree of hyperglycemia. After pretreatment of the animals with thyroxine, the moderate hyperglycemia pe...

Effects of hormones on glucose utilization in fasted rats.

The acute administration of carbutamide was found to have a hypoglycemic effect in fasted normal mice, while it had no definite effect on the already low blood sugar levels of fasted obese hyperglycemic mice. Chronic oral treatment with carbutamide did not modify the food intake and weight increases of either type of mice during the seven weeks treatment. In obese-hyperglycemic mice no improvement of the “diabetes” was observed, both in fed and fasted states. Lean littermates, whether fasted or fed, showed a reversal of the direction of effect of a single dose. These animals were, rather paradoxically, rendered paradiabetic after four weeks of treatment, and responded to glucagon and growth hormone with a reaction similar to that seen in untreated obesehyperglycemic mice.

Aelita Jurjevics

Papers

Effects of hormones on glucose utilization in fasted rats.

Effects of acute and chronic treatments with carbutamide (BZ-55) on obese-hyperglycemic mice and their lean littermates.