AN ANALOGUE COMPUTER MODEL FOR THE INSULIN RESPONSE TO GLUCOSE INFUSION

1967 ◽  
Vol 55 (1) ◽  
pp. 163-183 ◽  
Author(s):  
Erol Cerasi ◽  
Bertil Andersson
Keyword(s):  
Blood Glucose ◽  
Glucose Uptake ◽  
Computer Model ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Quantitative Information ◽  
Glucose Infusion ◽  
Analogue Computer ◽  
Dynamic Factors ◽  
Insulin Response To Glucose

ABSTRACT 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.

An analogue computer model for the insulin response to glucose infusion

SIMULATION ◽  
1971 ◽  
Vol 16 (6) ◽  
pp. 243-255 ◽  
Author(s):  
Erol Cerasi ◽  
Bertil Andersson
Keyword(s):  
Blood Glucose ◽  
Glucose Uptake ◽  
Computer Model ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Quantitative Information ◽  
Glucose Infusion ◽  
Analogue Computer ◽  
Dynamic Factors ◽  
Insulin Response To Glucose

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.

DIMINISHED SENSITIVITY OF THE INSULIN RESPONSE TO GLUCOSE FOLLOWING GROWTH HORMONE INFUSION IN MAN

1976 ◽  
Vol 81 (4) ◽  
pp. 735-742 ◽  
Author(s):  
Ulf Adamson ◽  
Erol Cerasi
Keyword(s):  
Growth Hormone ◽  
Blood Glucose ◽  
Insulin Release ◽  
Dose Response ◽  
Plasma Insulin ◽  
Insulin Dose ◽  
Insulin Response ◽  
Insulinogenic Index ◽  
K Value ◽  
Insulin Response To Glucose

ABSTRACT The acute effect of growth hormone (GH) administration on the dose-kinetics of glucose-stimulated insulin release was investigated in eight healthy, non-obese male subjects. The glucose-insulin dose-response relationship in these subjects was established by performing glucose infusions at three different dose levels. In a second series of experiments, the glucose infusions were preceded by a 30 min infusion of GH (40 μg/kg body weight), terminated 60 min before administration of glucose. GH induced small but significant reductions in the basal levels of blood glucose and plasma insulin. The glucose tolerance (k-value) was diminished after GH at all glucose doses. Both the initial late phases of insulin response to glucose were impaired following GH treatment. This effect was most pronounced when the intermediary glucose dose (eliciting a blood glucose level around 300 mg/100 ml) was used. Thus, the insulinogenic index (whole period of stimulation) was reduced by GH to 88.9 ± 7.6, 60.4 ± 7.1 and 74.3 ± 11.0% of the respective controls when the smallest, the intermediate, and the largest glucose loads, respectively, were given. The blood glucose-plasma insulin dose-response curves were shifted to the right of the control ones when glucose infusion was preceded by GH. These findings suggest that GH diminishes the sensitivity of the islet for the insulin releasing action of glucose. Some possible mechanisms by which GH may modify insulin release are discussed.

Appetite regulation by carbohydrate: role of blood glucose and gastrointestinal hormones

1996 ◽  
Vol 271 (2) ◽  
pp. E209-E214 ◽  
Author(s):  
J. H. Lavin ◽  
G. Wittert ◽  
W. M. Sun ◽  
M. Horowitz ◽  
J. E. Morley ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Eating Behavior ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Gastrointestinal Hormones ◽  
Glucose Infusion ◽  
Gastrointestinal Hormone ◽  
Intravenous Glucose ◽  
Intraduodenal Infusion ◽  
Glucose Levels

To investigate the mechanisms by which intestinal carbohydrate affects eating behavior, seven fasted, healthy male volunteers received intraduodenal infusions of glucose or saline over a 90-min period while blood glucose levels were matched by use of intravenous glucose and saline infusions. A second study examined the effect of intraduodenal glucose on eating behavior when the gastrointestinal hormone response was inhibited by intravenous octreotide. Intravenous glucose infusion did not affect hunger or satiety. In contrast, intraduodenal infusion of glucose suppressed hunger, increased fullness and satiety ratings, reduced energy intake, and resulted in higher plasma insulin responses compared with the intravenous glucose infusion. Octreotide abolished the plasma insulin response to intraduodenal glucose and reversed the changes in ratings and eating behavior. This study has shown that the effects of intestinal glucose on appetite are not mediated via an increase in blood glucose but are likely to reflect small intestinal stimulation of release of either insulin or intestinal incretins.

THE PLASMA INSULIN RESPONSE TO GLUCOSE INFUSION IN HEALTHY SUBJECTS AND IN DIABETES MELLITUS

1967 ◽  
Vol 55 (2) ◽  
pp. 278-304 ◽  
Author(s):  
Erol Cerasi ◽  
Rolf Luft
Keyword(s):  
Diabetes Mellitus ◽  
Glucose Tolerance ◽  
Healthy Subjects ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Normal Glucose Tolerance ◽  
Glucose Infusion ◽  
Analogue Computer ◽  
Plasma Insulin Concentration ◽  
Plasma Insulin Response

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.

scholarly journals The B2 Receptor of Bradykinin Is Not Essential for the Post-Exercise Increase in Glucose Uptake by Insulin-Stimulated Mouse Skeletal Muscle

2011 ◽  
pp. 511-519 ◽  
Author(s):  
G. G. SCHWEITZER ◽  
C. M. CASTORENA ◽  
T. HAMADA ◽  
K. FUNAI ◽  
E. B. ARIAS ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Glucose ◽  
Glucose Uptake ◽  
Insulin Action ◽  
Plasma Insulin ◽  
Treadmill Exercise ◽  
Post Exercise ◽  
Skeletal Muscle Glucose Uptake ◽  
Glucose Plasma ◽  
Exercise Induced

Bradykinin can enhance skeletal muscle glucose uptake (GU), and exercise increases both bradykinin production and muscle insulin sensitivity, but bradykinin’s relationship with post-exercise insulin action is uncertain. Our primary aim was to determine if the B2 receptor of bradykinin (B2R) is essential for the post-exercise increase in GU by insulin-stimulated mouse soleus muscles. Wildtype (WT) and B2R knockout (B2RKO) mice were sedentary or performed 60 minutes of treadmill exercise. Isolated soleus muscles were incubated with [3H]-2-deoxyglucose ±insulin (60 or 100 μU/ml). GU tended to be greater for WT vs. B2RKO soleus with 60 μU/ml insulin (P=0.166) and was significantly greater for muscles with 100 μU/ml insulin (P<0.05). Both genotypes had significant exercise-induced reductions (P<0.05) in glycemia and insulinemia, and the decrements for glucose (~14 %) and insulin (~55 %) were similar between genotypes. GU tended to be greater for exercised vs. sedentary soleus with 60 μU/ml insulin (P=0.063) and was significantly greater for muscles with 100 μU/ml insulin (P<0.05). There were no significant interactions between genotype and exercise for blood glucose, plasma insulin or GU. These results indicate that the B2R is not essential for the exercise-induced decrements in blood glucose or plasma insulin or for the post-exercise increase in GU by insulin-stimulated mouse soleus muscle.

POTENTIATION OF INSULIN RELEASE BY GLUCOSE IN MAN

1975 ◽  
Vol 79 (3) ◽  
pp. 511-534 ◽  
Author(s):  
Erol Cerasi
Keyword(s):  
Blood Glucose ◽  
Insulin Release ◽  
Dose Response ◽  
Pancreatic Beta Cell ◽  
Insulin Response ◽  
Initial Response ◽  
Normal Glucose Tolerance ◽  
Glucose Infusion ◽  
Clear Cut ◽  
The Right

ABSTRACT Glucose-induced potentiation of glucose-induced insulin release was quantitatively evaluated in 14 non-obese subjects with normal glucose tolerance but decreased insulin response, and in six non-obese patients with mild, adult-onset diabetes, by measuring the insulin responses to two consecutive glucose infusion tests, administered with 40 or 70 min interval. Enhancement of the second insulin response occurred in both groups. In low insulin responders, the dose-response relationship between blood glucose and plasma insulin was flatter and shifted to the right when compared to the control. Pretreatment with glucose increased strikingly the slope of this relationship, the responses now being within the normal range. The enhancement induced by glucose seems to be of multiplicative type. In mildly diabetic subjects, insulin response to glucose infusion was low and sluggish, only a minor initial response being observed. Pretreatment with glucose modified the profile of the insulin response, a clear-cut initial response of greater magnitude being obtained at least in some of the patients. The sensitivity of the islet to the potentiating action of glucose was higher in low insulin responders than in controls, the minimal glucose concentration needed to induce potentiation of the forthcoming response being much lower. The dose-response curve for the relationship between the blood glucose level of the preinfusion period and the percentual enhancement of the insulin response obtained at the second stimulation was, in low insulin responders, higher than and shifted to the left of the curve of the control subjects. In the group of diabetics, sensitivity for potentiation by glucose seemed not different from the controls. These studies indicate that the ability of glucose to initiate insulin release and its ability to generate time-bound potentiation in the islet correspond to two distinct functions. In the early stages of the diabetic syndrome, only the recognition of glucose as the initiator of an insulinogenic signal is impaired. The pancreatic beta-cell in these subjects seems to recognize normally glucose as the promotor of the potentiation.

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