Effect of Cortisone on Carbohydrate Metabolism Measured by the "Glucose Assimilation Coefficient"

Diabetes ◽  
1954 ◽  
Vol 3 (3) ◽  
pp. 205-209 ◽  
Author(s):  
P. A. Bastenie ◽  
V. Conard ◽  
J. R. M. Franckson
1990 ◽  
Vol 45 (1-2) ◽  
pp. 125-128
Author(s):  
M. Ataur Rahman ◽  
Hasna Begum ◽  
Abdus Samad ◽  
S. Shahjehan

Abstract Hyperglycemia is an important independent risk factor in the development of coronary artery disease. Sixty one patients suffering from chronic and acute myocardial infarction out of which 12 patients were diabetic and 10 normal control subjects were investigated. The patients without diabetes and control subjects were subjected to oral and intravenous glucose tolerance tests. It was observed that the post load glucose level of most of the patients and fasting insulin level of patients without diabetes were higher as compared with control subjects. From the intravenous glucose tolerance test, half life of glucose and glucose assimilation coefficient were determined. Half life of glucose was increased significantly and glucose assimilation coefficient was decreased in the patients with myocardial infarction as compared with those of control subjects. The observations confirm that carbohydrate intolerance in myocardial infarction is not due to suppression of insulin secretion but due to peripheral utilization.


1960 ◽  
Vol XXXV (IV) ◽  
pp. 551-559 ◽  
Author(s):  
P. R. Bouman ◽  
W. Dermer

ABSTRACT Hemidiaphragms of adrenalectomized rats which had been nembutalized prior to decapitation, were incubated under aerobic conditions and the glucose uptake and glycogen deposition were measured. Addition of adrenaline in vitro induced marked glycogen degradation and a relative small decrease in glucose uptake. Pretreatment with adrenaline in vivo, however, appeared to increase glycogen deposition in vitro while glucose uptake increased to an equivalent extent. This effect was attributed to the low initial glycogen content induced by this treatment. Double exposure to adrenaline by administering this substance both in vivo and in vitro, neither affected glucose uptake nor glycogen deposition as compared with untreated control diaphragms. However, there was a significant difference in the glycogen level at which both groups metabolized, this level being extremely low in diaphragms doubly exposed to adrenaline. It was concluded that the action of adrenaline on muscular carbohydrate metabolism consists basically of three different stages: 1. A temporary initial stage during which glucose assimilation is inhibited secondarily to glycogen degradation. 2. A second stage, in which the occurrence of inhibition of glucose assimilation is determined by the fact whether in the corresponding control tissue the glucose uptake is raised in favour of glycogen deposition. 3. A stage of recovery induced by discontinuing the exposure to adrenaline. This stage is characterized by glycogen deposition and an equivalent rise in glucose assimilation.


1967 ◽  
Vol 28 (5) ◽  
pp. 914-919 ◽  
Author(s):  
Frank W. Cervenko ◽  
Nicholas M. Greene

1981 ◽  
Vol 98 (4) ◽  
pp. 603-608 ◽  
Author(s):  
J. E. Eigenmann ◽  
R. Y Eigenmann

Abstract. The combined effects of oestradiol and medroxyprogesterone acetate on growth hormone (GH) levels and carbohydrate metabolism were studied in 6 ovariohysterectomized dogs, which previously had shown moderate increments in GH after medroxyprogesterone acetate (MPA) administration. Oestradiol (Oe2) implants were administered 5 months after the last MPA injection, when MPA and GH levels tended to decrease. Following Oe2 administration GH levels rose significantly. Single MPA injections (100 mg) given 20 days after Oe2-priming were followed by still further increased GH levels. These GH levels were several-fold higher than GH levels achieved by previous MPA administration alone. GH levels decreased in 3 dogs after 35 days and remained elevated in the other 3 dogs as long as 70 days after MPA administration with Oe2 priming. Glucose assimilation became impaired and insulin response to a glucose load increased in relation to elevated GH levels. Oe2-primed control dogs, which received no MPA, failed to develop elevated GH levels. These findings indicate (1) that Oe2 and MPA induce overproduction in ovariohysterectomized dogs synergistically (2) that GH levels of the magnitude evoked are associated with glucose intolerance and insulin resistance.


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