Long-term stability of low insulin responses to glucose in non-diabetic subjects

1992 ◽  
Vol 127 (1) ◽  
pp. 33-37 ◽  
Author(s):  
Michael Alvarsson ◽  
Valdemar E Grill ◽  
Alexandre Wajngot ◽  
Erol Cerasi ◽  
Suad Efendic

We investigated the stability of the insulin response to glucose in healthy subjects by making retrospective comparisons of insulin responses after two 60 min glucose infusion tests performed many years apart. The subjects (N =49) were divided into two lower and two higher quartiles as assessed by the incremental 0–10 min insulin area during the initial glucose infusion test. Ages were initially 32.3±2.8 years in lower quartiles and 26.6±1.1 in higher quartiles and body mass indexes 21.6±0.6 kg/m2 and 21.8±0.5, respectively. The interval between the first and second glucose infusion tests was 8.1±2.8 years for lower quartiles and 10.4±1.3 for higher quartiles. In lower quartiles, the 0–10 min insulin area at first testing was 157.1±15.9 mU/l × 10 min and at follow-up 202.2±26.6 (+ 29%, NS). In higher quartiles, the insulin area decreased from 654.8±70.6 mU/l × 10 min at first testing to 489.8±53.6 at follow-up (−25%, p<0.05). The 0–60 min glucose area did not change significantly between glucose infusion tests in lower quartiles (+ 5%), but did increase by 12% (p<0.005) in higher quartiles. Only one subject of the lowest quartile at first testing changed to higher quartiles at follow-up. Predictable "regression toward the mean" at follow-up was moderate, hence the individual insulin response to glucose was relatively stable with time. This finding is compatible with the hypothesis that genetic factors are of major importance for the insulin response to glucose.

1984 ◽  
Vol 64 (5) ◽  
pp. 300-301 ◽  
Author(s):  
Y. TERASHIMA ◽  
Y. ITOH ◽  
H. ITOH

Plasma glucose clearance rates were lower (P < 0.10) in wethers fed the high potassium (0.32% Mg-4.90% K) diet compared with those of the control (0.32% Mg-0.75% K). Insulin responses to glucose infusion and feeding tended to be reduced in wethers fed the high potassium diet as compared to the control. Key words: Sheep, high potassium diet, glucose utilization, insulin


1975 ◽  
Vol 79 (3) ◽  
pp. 502-510 ◽  
Author(s):  
Erol Cerasi

ABSTRACT If two consecutive glucose infusions are administered with 40 min of rest between, the insulin response to the second challenge is markedly potentiated. When the insulin response to the first glucose infusion was suppressed by 65 % with the aid of adrenaline, potentiation of the insulin response to the second infusion was not modified. This suggests that the generation of a state of enhancement in the islet does not necessitate that glucose exerts its insulin releasing action. It is postulated that islet glucose metabolism may be involved in producing the potentiation. Pretreatment of the subjects with a glucose infusion enhanced also the insulin responses to glucagon and to tolbutamide, given intravenously 50 min later. Thus, the potentiation generated by glucose is not restricted to the insulinogenic signal induced by glucose. The eventual role that the beta-cell adenylate cyclase may play in this respect is discussed.


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.


1967 ◽  
Vol 55 (2) ◽  
pp. 330-345 ◽  
Author(s):  
Erol Cerasi ◽  
Rolf Luft

ABSTRACT The insulin response during a standardized glucose infusion (GIT) was studied in a group of 13 monozygotic twin pairs previously registered as consisting of one diabetic/one non-diabetic member. At the time of the study three of the non-diabetic subjects had developed overt diabetes and three decreased glucose tolerance only. Of the non-diabetic members all but one (with diabetes due possibly to chronic pancreatitis in the sibling) showed an insulin response similar to that seen in diabetic subjects, and in healthy subjects previously assumed to be potential diabetics. The present study therefore supports our earlier suggestion that a low insulin response characterizes potential diabetes. There was a striking similarity between the insulin curves in the twin pairs, irrespective whether diabetes occurred in one, in both or in none of the members. It is suggested as a working hypothesis that the type of insulin response to glucose infusion is genetically determined, and that a low insulin response is a prerequisite for the development of diabetes mellitus.


1978 ◽  
Vol 89 (2) ◽  
pp. 329-338 ◽  
Author(s):  
B. Schulz ◽  
M. Ziegler ◽  
S. Witt ◽  
I. Rjasanowski ◽  
P. Heinke ◽  
...  

ABSTRACT The pancreatic glucagon (IRG) secretion pattern was studied during a 2 h glucose infusion test (12 mg/kg/min) in 21 controls as well as in 44 subjects showing different degrees of carbohydrate intolerance. The fasting IRG levels increased significantly from controls (98 ± 7.6 pg/ml) to chemical (144 ± 9 pg/ml) and mild maturity-onset-type diabetics (166 ± 12.2 pg/ml). During artificial hyperglycaemia the glucagon concentrations decreased slightly in all groups, but they remained at a higher level in early and overt diabetics1). The molar IRI-IRG ratios have been found to be diminished in patients displaying a disturbed carbohydrate tolerance. There was not any correlation between insulin and glucagon concentrations in the blood. The findings suggest that abnormalities of alpha cell function may be present in early and overt diabetes independent of beta cell responsiveness. The causal relationship of A and B cell function in glucose intolerant subjects has to be cleared in follow-up studies.


SIMULATION ◽  
1971 ◽  
Vol 16 (6) ◽  
pp. 243-255 ◽  
Author(s):  
Erol Cerasi ◽  
Bertil Andersson

An analogue computer model has been constructed for the analysis of the interrelationship between blood glucose and plasma insulin concentrations during glucose infusion. The model presented gives quantitative information on the effect of plasma insulin on glucose uptake, the total amount of glucose taken up by the tissues at a given time, the effect of blood glucose on the release of stored and newly formed insulin, and the rapidity by which plasma insulin is increased in response to hyperglycaemia. Such an analogue computer model might be a useful tool in the investigation of the various dynamic factors involved in the glucose- insulin interrelationship.


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.


Diabetologia ◽  
1980 ◽  
Vol 19 (1) ◽  
pp. 15-20 ◽  
Author(s):  
P. M. Fisher ◽  
H. W. Sutherland ◽  
P. D. Bewsher

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