STUDIES ON THE PATHOGENESIS OF DIABETES IN ACROMEGALY

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.

1967 ◽  
Vol 55 (2) ◽  
pp. 305-329 ◽  
Author(s):  
Erol Cerasi ◽  
Rolf Luft

ABSTRACT In a previous paper it was shown that 15 out of 85 healthy subjects with a normal intravenous glucose tolerance demonstrated a low plasma insulin response to glucose infusion which was similar to that obtained in diabetic subjects. In the present paper it has been shown that the type of insulin response to glucose infusion was the same when the test was repeated. Low insulin responders to glucose infusion, as a group, also showed low insulin response to intravenous tolbutamide and oral glucose. This indicates that the type of insulin response is characteristic for a given subject irrespective of the stimulation used. There seemed to be no difference in the occurrence of diabetes in the family history of the groups of low and high insulin responders.


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.


Diabetes ◽  
1968 ◽  
Vol 17 (1) ◽  
pp. 17-26 ◽  
Author(s):  
J. S. Soeldner ◽  
R. E. Gleason ◽  
R. F. Williams ◽  
M. J. Garcia ◽  
D. M. Beardwood ◽  
...  

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.


1983 ◽  
Vol 55 (2) ◽  
pp. 512-517 ◽  
Author(s):  
G. W. Heath ◽  
J. R. Gavin ◽  
J. M. Hinderliter ◽  
J. M. Hagberg ◽  
S. A. Bloomfield ◽  
...  

Physically trained individuals have a markedly blunted insulin response to a glucose load and yet have normal glucose tolerance. This phenomenon has generally been ascribed to long-term adaptations to training which correlate with maximal oxygen uptake (VO2max) and reduced adiposity. Our study was undertaken to test the hypothesis that residual effects of the last bouts of exercise play an important role in this phenomenon. Eight well-trained subjects stopped training for 10 days. There were no significant changes in VO2max (58.6 +/- 2.2 vs. 57.6 +/- 2.1 ml/kg), estimated percent body fat (12.5 +/- 0.7 vs. 12.5 +/- 0.8%), or body weight. The maximum rise in plasma insulin concentration in response to a 100-g oral glucose load was 100% higher after 10 days without exercise than when the subjects were exercising regularly. Despite the increased insulin levels, blood glucose concentrations were higher after 10 days without exercise. Insulin binding to monocytes also decreased with physical inactivity. One bout of exercise after 11 days without exercise returned insulin binding and the insulin and glucose responses to an oral 100-g glucose load almost to the initial “trained” value. These results support our hypothesis.


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