INSULIN RESPONSE TO GLUCOSE INFUSION DURING PREGNANCY. A PROSPECTIVE STUDY OF HIGH AND LOW INSULIN RESPONDERS WITH NORMAL CARBOHYDRATE TOLERANCE

1974 ◽  
Vol 75 (1) ◽  
pp. 87-104 ◽  
Author(s):  
Karin Edström ◽  
Erol Cerasi ◽  
Rolf Luft
Keyword(s):  
Fasting Blood Glucose ◽  
Insulin Response ◽  
Glucose Infusion ◽  
Intravenous Glucose ◽  
K Value ◽  
Endogenous Insulin ◽  
High Insulin ◽  
Insulin Response To Glucose ◽  
A Prospective Study ◽  
Low Insulin Response

ABSTRACT A decreased insulin response to glucose administration has been suggested to be a prerequisite for the development of diabetes mellitus. Factors that increase the demand for insulin in the organism may precipitate diabetes in subjects with a low insulin response to a glucose infusion test (GIT). Since it is well-known that pregnancy is a diabetogenic factor, its effect on the carbohydrate metabolism of subjects with a low insulin response was studied. During pregnancy, the insulin response of the low responders was enhanced as in the controls, but at all stages the insulin response was significantly less than in the controls. None of the subjects developed glucose intolerance during pregnancy. The fasting blood glucose and plasma insulin levels and the k-value in intravenous glucose tolerance tests (IVGTT) were modified according to similar patterns in both groups. The sensitivity to endogenous insulin was significantly greater in the low insulin responders but was reduced to a greater extent than in the controls towards the end of pregnancy. In four of the 11 low insulin responders the initial insulin response to glucose in the last trimester was lower than in mid-pregnancy. This occurred only in one out of 14 high insulin responders. It is suggested that gestational diabetes occurs in those low insulin responders who demonstrate either a dramatic decrease in insulin sensitivity, or limitations in the enhancement of insulin release, or, more likely both conditions.

FURTHER STUDIES ON HEALTHY SUBJECTS WITH LOW AND HIGH INSULIN RESPONSE TO GLUCOSE INFUSION

1967 ◽  
Vol 55 (2) ◽  
pp. 305-329 ◽  
Author(s):  
Erol Cerasi ◽  
Rolf Luft
Keyword(s):  
Healthy Subjects ◽  
Insulin Response ◽  
Glucose Infusion ◽  
Oral Glucose ◽  
Intravenous Glucose ◽  
The Family ◽  
High Insulin ◽  
History Of ◽  
Insulin Response To Glucose ◽  
Plasma Insulin Response

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.

GLUCOSE TOLERANCE IN NEWBORN INFANTS OF HEALTHY MOTHERS: ITS RELATIONSHIP TO THE MOTHERS' INSULIN RESPONSE TO GLUCOSE INFUSION

1975 ◽  
Vol 78 (1) ◽  
pp. 44-53 ◽  
Author(s):  
Karin Edström ◽  
Erol Cerasi ◽  
Rolf Luft ◽  
Bengt Persson ◽  
Berlil Thalme
Keyword(s):  
Glucose Tolerance ◽  
Newborn Infants ◽  
Insulin Response ◽  
Late Pregnancy ◽  
Mean Difference ◽  
Glucose Infusion ◽  
K Value ◽  
High Insulin ◽  
The Mean ◽  
Low Insulin Response

ABSTRACT It has earlier been postulated that a low insulin response to a glucose infusion is characteristic for the prediabetic individual (Cerasi & Luft 1967c). There is also evidence that some infants of individuals with low insulin response might have a carbohydrate metabolism that is in some respects similar to that of newborn infants to diabetic mothers (Edström et al. 1974). In the present study 15 infants to low insulin responders (ILR) and 22 infants to high insulin responders (IHR) were subjected to an intravenous glucose load (IVGTT) at 2–24 h age. A significant difference in glucose tolerance was found between the groups, the mean k-value for the ILR being 1.39 ± 0.41 and that for the IHR 1.05 ± 0.09 (P < 0.05). No mothers were found to have a gestational diabetes (with the possible exception of one low insulin responders) but during late pregnancy the mean k-value at IVGTT in the low responders decreased from nonpregnant values (the mean difference being 0.41 ± 0.20, P < 0.025) while the high responders did not show a corresponding decrease (mean difference 0.12 ± 0.25, P > 0.05). No other differences between the groups of infants that could influence the k-value could be found apart from the mothers being low or high insulin responders. Our findings show that a low insulin response in the mothers might affect the glucose tolerance of the foetus even in the absence of continuous maternal hyperglycaemia in late pregnancy.

INSULIN RESPONSE TO GLUCOSE INFUSION IN DIABETIC AND NON-DIABETIC MONOZYGOTIC TWIN PAIRS. GENETIC CONTROL OF INSULIN RESPONSE?

1967 ◽  
Vol 55 (2) ◽  
pp. 330-345 ◽  
Author(s):  
Erol Cerasi ◽  
Rolf Luft
Keyword(s):  
Diabetes Mellitus ◽  
Chronic Pancreatitis ◽  
Healthy Subjects ◽  
Insulin Response ◽  
Monozygotic Twin ◽  
Glucose Infusion ◽  
Striking Similarity ◽  
Insulin Response To Glucose ◽  
Genetically Determined ◽  
Low Insulin Response

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.

GLUCOSE TOLERANCE AND INSULIN RESPONSE DURING DAILY CONTINUOUS LOW-DOSE ORAL CONTRACEPTIVE TREATMENT

1969 ◽  
Vol 62 (2) ◽  
pp. 242-250 ◽  
Author(s):  
U. Larsson-Cohn ◽  
B. Tengström ◽  
L. Wide
Keyword(s):  
Glucose Tolerance ◽  
Blood Glucose Concentration ◽  
Fasting Blood Glucose ◽  
Insulin Response ◽  
Continuous Treatment ◽  
Intravenous Glucose ◽  
Dose Oral ◽  
Glucose Tolerance Tests ◽  
Insulin Response To Glucose ◽  
Intravenous Glucose Tolerance Tests

ABSTRACT Intravenous glucose tolerance tests and insulin determinations were performed on 37 women at different stages of the menstrual cycle and after one, three and twelve months of daily continuous treatment with 0.5 mg of norethindrone or 0.5 mg of chlormadinone acetate. The fasting blood glucose concentration, the k-values (percentage disappearance rate of glucose per minute) and the insulin response to glucose administration were compared. No statistically significant differences were found between the values obtained on two occasions before treatment, and during treatment.

STUDIES ON THE PATHOGENESIS OF DIABETES IN ACROMEGALY

1967 ◽  
Vol 56 (4) ◽  
pp. 593-607 ◽  
Author(s):  
Rolf Luft ◽  
Erol Cerasi ◽  
Carl Axel Hamberger
Keyword(s):  
Glucose Tolerance ◽  
Insulin Response ◽  
Normal Glucose Tolerance ◽  
Glucose Infusion ◽  
Intravenous Glucose ◽  
Highly Active ◽  
Normal Glucose ◽  
Insulin Response To Glucose ◽  
Active Acromegaly ◽  
Plasma Insulin Response

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.

OBESITY AS AN ADDITIONAL FACTOR IN THE PATHOGENESIS OF DIABETES

1968 ◽  
Vol 59 (2) ◽  
pp. 344-352 ◽  
Author(s):  
Rolf Luft ◽  
Erol Cerasi ◽  
Bo Andersson
Keyword(s):  
Glucose Tolerance ◽  
Plasma Insulin ◽  
Peripheral Resistance ◽  
Insulin Response ◽  
Intravenous Glucose ◽  
Endogenous Insulin ◽  
Intravenous Glucose Tolerance ◽  
Obese Subjects ◽  
Insulin Response To Glucose ◽  
Plasma Insulin Response

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.

Physical Fitness and Insulin Sensitivity in Human Subjects with a Low Insulin Response to Glucose

1994 ◽  
Vol 87 (2) ◽  
pp. 187-192 ◽  
Author(s):  
Jan Pigon ◽  
Jan Karlsson ◽  
Claes-Göran Östenson
Keyword(s):  
Body Weight ◽  
Insulin Sensitivity ◽  
Exercise Capacity ◽  
Insulin Response ◽  
Trained Subjects ◽  
C Peptide ◽  
Healthy Men ◽  
High Insulin ◽  
Insulin Response To Glucose ◽  
Low Insulin Response

1. We have assessed insulin secretion, insulin sensitivity, exercise capacity and muscle fibre composition in healthy men with a low insulin response to glucose (low insulin responders and endurance-trained subjects) and in healthy men with a normally high insulin response. Low insulin responders have been considered as prediabetic subjects. 2. During glucose infusion, low insulin responders and endurance-trained subjects had acute-phase (0-10 min) insulin responses that were 26% (P < 0.001) and 31% (P < 0.001), and C-peptide responses that were 35% (P < 0.001) and 42% (P < 0.01), respectively of the responses in high insulin responders. Also, the late-phase (10-60 min) insulin and C-peptide responses were lower in low insulin responders and endurance-trained subjects. Endurance-trained subjects, compared with high and low insulin responders, had higher insulin sensitivity (blood glucose concentration during a somatostatin-insulin-glucose infusion test 3.6 ± 0.4 versus 6.3 ± 0.6 mmol/l in high insulin responders, P < 0.01, and 5.5 ± 0.4 mmol/l in low insulin responders, P < 0.01), exercise capacity (4.2 ± 0.2 versus 3.0 ± 0.2 W/kg body weight, P < 0.001, and 2.8 ± 0.1 W/kg body weight, P < 0.001) and a higher percentage of slow-twitch fibres (58.2 ± 5.2 versus 38.5 ± 3.5%, P < 0.01 and 40.9 ± 3.0%, P < 0.001). 3. In conclusion, we demonstrate that low insulin responders exhibited decreased insulin and C-peptide responses to glucose, despite normal insulin sensitivity and exercise capacity. Thus, the low insulin response in low insulin responders reflects a true impairment of insulin release and not a compensatory decrease due to increased insulin sensitivity. The insulin response to glucose in endurance-trained subjects was also decreased, probably due to increased insulin sensitivity.

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