scholarly journals Glucose tolerance and plasma insulin response to intravenous glucose infusion and test meal in rats with microencapsulated islet allografts

Diabetologia ◽  
1991 ◽  
Vol 34 (8) ◽  
pp. 542-547 ◽  
Author(s):  
W. M. Fritschy ◽  
J. H. Strubbe ◽  
G. H. J. Wolters ◽  
R. van Schilfgaarde
1967 ◽  
Vol 56 (4) ◽  
pp. 593-607 ◽  
Author(s):  
Rolf Luft ◽  
Erol Cerasi ◽  
Carl Axel Hamberger

ABSTRACT Plasma insulin response to glucose infusion was found to be markedly increased in 20 patients with active acromegaly and with normal intravenous glucose tolerance. The insulin response was more pronounced in patients with highly active acromegaly than in those showing moderately active disease. In five patients with active acromegaly and with decreased glucose tolerance the insulin response was delayed and smaller than normal, i. e. similar to that seen in diabetic subjects without acromegaly. After successful treatment of the acromegaly insulin response to glucose infusion was normalized in the patients with normal glucose tolerance. In those with decreased glucose tolerance the diabetic type of insulin response remained unchanged even when the glucose tolerance was normalized. It is suggested that diabetes in connection with acromegaly develops only in prediabetic individuals, i.e. subjects with decreased insulin response to hyperglycaemia, who are unable to overcome the diabetogenic effect of growth hormone by compensatory hyperinsulinism.


1968 ◽  
Vol 59 (2) ◽  
pp. 344-352 ◽  
Author(s):  
Rolf Luft ◽  
Erol Cerasi ◽  
Bo Andersson

ABSTRACT Plasma insulin response to glucose infusion was measured in obese subjects with normal and decreased intravenous glucose tolerance. In obese non-diabetic subjects there was insulin hyperresponsiveness to glucose accompanied by peripheral resistance to endogenous insulin. In the obese diabetic subjects insulin response was of the type seen in non-obese diabetics; in no such instance could insulin hyperresponsiveness to glucose be obtained. It is suggested that obesity precipitates diabetes only in subjects with preexisting impairment of insulin response, i. e. in prediabetics. Subjects with unimpaired insulin secreting capacity would overcome the diabetogenic effect of obesity by compensatory hyperinsulinism.


1967 ◽  
Vol 55 (2) ◽  
pp. 278-304 ◽  
Author(s):  
Erol Cerasi ◽  
Rolf Luft

ABSTRACT Plasma insulin concentration was measured during a standardized glucose infusion test (GIT) in 85 healthy subjects with a normal glucose tolerance and in 28 patients with manifest diabetes mellitus or decreased glucose tolerance. Each test was evaluated with the aid of an analogue computer model, and parameters characterizing different parts of the insulin curve during GIT were obtained. Large variations existed in all parameter values both in the normal and diabetic groups, and the overlapping between the two groups was considerable. In 15 out of 85 healthy subjects the plasma insulin response during GIT was of the diabetic type as judged from the frequency distribution of the computer parameters (low values). The similarity was still more striking when the characteristics of the insulin curves in these 15 subjects were compared with those in patients with mild diabetes or with a decreased glucose tolerance only. It is postulated that this type of low insulin response reflects a derangement of the release of insulin into the circulation, and that it marks an alteration which probably is a prerequisite for the development of diabetes mellitus. In this sense, these subjects may be considered to be potential diabetics.


Diabetologia ◽  
1974 ◽  
Vol 10 (S1) ◽  
pp. 667-670 ◽  
Author(s):  
A. Gutzeit ◽  
A. Rabinovitch ◽  
P. P. Studer ◽  
P. A. Trueheart ◽  
E. Cerasi ◽  
...  

Diabetes ◽  
1987 ◽  
Vol 36 (2) ◽  
pp. 179-186 ◽  
Author(s):  
R. A. Sicree ◽  
P. Z. Zimmet ◽  
H. O. King ◽  
J. S. Coventry

1983 ◽  
Vol 245 (6) ◽  
pp. E575-E581 ◽  
Author(s):  
A. L. Vallerand ◽  
J. Lupien ◽  
L. J. Bukowiecki

The metabolic interactions of cold exposure, cold acclimation, and starvation on glucose tolerance and plasma insulin levels were studied in precannulated, unrestrained, and unanesthetized rats. Cold exposure (48 h at 5 degrees C) significantly reduced the insulin response to intravenous glucose injection (P less than 0.01) while improving glucose tolerance (P less than 0.01). Starvation (48 h at 25 degrees C) also reduced the insulin response (P less than 0.01) but did not significantly alter glucose tolerance. “Accelerated starvation” induced by starving rats for 48 h at 5 degrees C dramatically reduced both basal and glucose-stimulated insulin levels while even improving glucose tolerance, resulting in a 15-fold reduction in the insulinogenic index. Cold acclimation (3 wk at 5 degrees C) induced essentially the same alterations as cold exposure. Approximately reversed changes were observed when cold-acclimated rats were returned to a warm environment for 15–18 h. Results from these studies indicate that 1) cold exposure and starvation, but not cold acclimation, act synergistically in decreasing the sensitivity and/or the capacity of pancreatic islets for secreting insulin in response to glucose stimulation; 2) glucose tolerance and possibly insulin sensitivity of peripheral tissues are enhanced by cold exposure and starvation, although glucose tolerance is improved by cold exposure only, not by starvation; 3) an improved glucose tolerance with barely detectable plasma insulin levels was obtained in cold-starved rats under normal physiological conditions.


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