Plasma Insulin Response to An Oral Glucose Load in Noncoronary Heart Disease

CHEST Journal ◽  
1971 ◽  
Vol 59 (2) ◽  
pp. 184-187
Author(s):  
Wilbert S. Aronow ◽  
John R. Kent
Diabetes ◽  
1975 ◽  
Vol 24 (12) ◽  
pp. 1066-1071 ◽  
Author(s):  
K. Yasuda ◽  
T. Sato ◽  
T. Furuyama ◽  
K. Yashinaga

Angiology ◽  
1998 ◽  
Vol 49 (9) ◽  
pp. 815-826 ◽  
Author(s):  
Shigeo Takata ◽  
Atsuhiro Shimakura ◽  
Satoru Sakagami ◽  
Yukio Nakamura ◽  
Hitoshi Ohkuwa ◽  
...  

Diabetes Care ◽  
2000 ◽  
Vol 23 (5) ◽  
pp. 710-712 ◽  
Author(s):  
Y. Tanaka ◽  
Y. Atsumi ◽  
K. Matsuoka ◽  
T. Onuma ◽  
R. Kawamori

1983 ◽  
Vol 104 (1) ◽  
pp. 85-90 ◽  
Author(s):  
X. Jeanrenaud ◽  
E. Maeder ◽  
E. Del Pozo ◽  
J. P. Felber

Abstract. The purpose of the present work was to study the effect of a methionine-enkephalin analogue (FK 33-824) on glucose tolerance in man. Groups of 5 to 8 normal subjects were given a 0.5 mg im injection of the drug or placebo just before a 100 g oral glucose load or a 0.5 g/kg iv glucose load. In the enkephalin analogue treated subjects, diminished insulin response to glucose was observed following the oral glucose load, with insulin values significantly lower than in the controls from time 10 to 90 min, but no corresponding change in the glucose curve. This effect was not observed when glucose was given iv in another group of 5 subjects in whom the significant blunting of the insulin response was accompanied by a significant decrease in glucose tolerance. These observations demonstrate that in man, enkephalin produces a decrease in insulin secretion in response to both oral and iv glucose loads. The absence of any marked impairment in glucose tolerance in the oral test in spite of the decreased insulin response suggests that enkephalin might have an additional effect in delaying glucose absorption.


1968 ◽  
Vol 58 (4) ◽  
pp. 643-654 ◽  
Author(s):  
Vivian Harding Asfeldt ◽  
Kai R. Jørgensen

ABSTRACT Transient, maximum stimulation with β1–24 corticotrophin has been carried out in nine normal fasting subjects, in two fasting diabetics without hypercorticism and in three fasting diabetics with hypercorticism. Fluorimetric determinations of corticosteroids and determinations of immunological detectable insulin in plasma and blood sugar were made during stimulation. No significant variation in the blood sugar or the plasma insulin during transient, maximum ACTH stimulation was found either in normal fasting subjects or in fasting diabetics with or without hypercorticism. Moreover, in two diabetics with hypercorticism the plasma insulin response was measured during an oral glucose tolerance test. After treatment for approximately seven months with glucocorticosteroids, a reduced glucose tolerance and an increased plasma insulin response were found in one of these two patients. Four and a half months after the termination of steroid treatment, normal glucose tolerance and normal insulin responses were observed. In one patient, after several years of hypercorticism, a reduced glucose tolerance and a markedly reduced plasma insulin response were found.


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