THE EFFECT OF FOOD INTAKE ON INSULIN RECEPTOR IN MAN

1979 ◽  
Vol 90 (3) ◽  
pp. 473-480 ◽  
Author(s):  
R. De Pirro ◽  
A. Bertoli ◽  
A. V. Greco ◽  
A. S. Gelli ◽  
R. Lauro
Keyword(s):  
Food Intake ◽  
Insulin Receptor ◽  
Normal Subjects ◽  
Insulin Binding ◽  
Specific Cell ◽  
Cell Binding ◽  
Metabolic Pattern ◽  
Receptor Affinity ◽  
Rapid Changes ◽  
Effect Of Food

ABSTRACT Insulin binding to circulating monocytes was studied in 22 normal volunteers before and 1, 3 and 5 h after a 1400 Kcal meal. Results indicate that 3 h after food intake there is an increase in the specific cell binding fraction (P < 0.001) with a change in receptor affinity. Data emerging from the present study demonstrate that there are rapid changes in insulin receptor properties during the day. These changes probably play a role in the regulation of the hormonal and metabolic pattern in normal subjects.

scholarly journals The effect of malnutrition on insulin binding to rat erythrocytes

1992 ◽  
Vol 67 (2) ◽  
pp. 279-286 ◽  
Author(s):  
Hazel M. Payne-Robinson ◽  
Richard Brown
Keyword(s):  
Insulin Receptor ◽  
Insulin Binding ◽  
Rat Erythrocytes ◽  
Receptor Affinity ◽  
And Control ◽  
Specific Insulin

Insulin binding to erythrocyte receptors was compared in malnourished and control rats. Percentage specific insulin binding to malnourished rat erythrocytes was significantly lower than to control erythrocytes (P < 0.001). The low insulin binding in the malnourished rat erythrocytes was accompanied by low insulin receptor affinity (P = 0.035).

Effect of L-Dopa Administration on Insulin Binding: Possible Role of Growth Hormone in Regulation of Insulin Receptor Affinity

1982 ◽  
Vol 14 (07) ◽  
pp. 342-345
Author(s):  
M. Iwasaki ◽  
M. Kobayashi ◽  
S. Ohgaku ◽  
H. Maegawa ◽  
Y. Shigeta
Keyword(s):  
Growth Hormone ◽  
Insulin Receptor ◽  
Insulin Binding ◽  
Receptor Affinity

A STUDY OF INSULIN RECEPTORS IN HUMAN MONONUCLEAR LEUCOCYTES

1976 ◽  
Vol 83 (3) ◽  
pp. 556-564 ◽  
Author(s):  
Oluf Pedersen ◽  
Henning Beck-Nielsen
Keyword(s):  
Silicone Oil ◽  
Insulin Receptors ◽  
Insulin Binding ◽  
Cell Number ◽  
Receptor Interaction ◽  
Specific Cell ◽  
Cell Binding ◽  
Temperature Dependent ◽  
Normal Body Weight ◽  
Mononuclear Leucocytes

ABSTRACT Insulin binding sites were demonstrated in human mononuclear leucocytes by use of a technique which includes isolation of mononuclear leucocytes from defibrinated blood and separation of cell bound and free [125I] insulin with silicone oil. The binding was time and temperature dependent. At 15°C equilibrium was reached after 90 min and a plateau maintained for at least 50 min. Incubations were carried out at 4°C, 15°C and 37°C. Maximal binding was obtained at 15°C. The optimum pH for insulin receptor interaction occurred at about 8. [125I] insulin binding to mononuclear leucocytes was demonstrated to be a linear function of cell number concentration over a range of 17–70× 106×ml−1. The binding was a displaceable function of native insulin concentration. In a group of 21 young healthy persons with normal body weight we found a mean specific cell binding fraction of 1.92 ± 0.58 (s) × 10−2. Analysis of the equilibrium between insulin and its receptor revealed an apparent heterogeneity of insulin receptors.

Bidirectional alteration of insulin receptor affinity by different forms of physical exercise

1984 ◽  
Vol 246 (2) ◽  
pp. E153-E159 ◽  
Author(s):  
G. Michel ◽  
T. Vocke ◽  
W. Fiehn ◽  
H. Weicker ◽  
W. Schwarz ◽  
...  
Keyword(s):  
Physical Exercise ◽  
Insulin Receptor ◽  
Serum Insulin ◽  
Insulin Binding ◽  
Bicycle Exercise ◽  
Post Exercise ◽  
Receptor Affinity ◽  
Receptor Number ◽  
Serum Components

Insulin binding of monocytes and erythrocytes was studied in untrained male volunteers after 15 min of exhaustive bicycle exercise (EE) and several days later after moderate exercise (ME) for 90 min. Insulin receptor affinity decreased after EE in monocytes (26.4% decrease; P less than 0.01) and in erythrocytes (10.4%; P less than 0.05) with no change in receptor number. After ME, however, binding to monocytes was enhanced by 15.2% (P less than 0.05) due to increased receptor affinity. The number of circulating monocytes was markedly increased after both forms of exercise, averaging 105% after EE and 57% after ME. The bidirectional effect on monocyte insulin binding could be reproduced in vitro by incubation of preexercise cells with post-exercise serum: 12.4% (P less than 0.05) decrease with EE serum and 6.1% (P less than 0.05) increase with ME serum. The effect was prevented by overnight dialysis. These results suggest that physical exercise not only entails adjustment of serum insulin but also of cellular hormone sensitivity, presumably through the mediation of low-molecular-weight serum components.

scholarly journals Reversible reduction of insulin receptor affinity by ATP depletion in rat adipocytes

1983 ◽  
Vol 214 (1) ◽  
pp. 203-207 ◽  
Author(s):  
H J Steinfelder ◽  
H G Joost
Keyword(s):  
Insulin Receptor ◽  
Plasma Membranes ◽  
Insulin Receptors ◽  
Insulin Binding ◽  
Dissociation Rate ◽  
Atp Depletion ◽  
Metabolic Inhibitor ◽  
Receptor Affinity ◽  
Rat Fat Cells ◽  
Reversible Reduction

The effects of the metabolic inhibitor NaN3 on insulin receptors in isolated rat fat-cells were investigated. The agent reduced insulin binding in parallel to a decrease of the ATP content of cells. Both effects were observed in the same concentration range of NaN3, and were fully reversible. According to the binding curves the affinity rather than the number of receptors was reduced. Kinetic experiments revealed an increased dissociation rate of the insulin-receptor complex. The effects outlasted cell disruption, since the receptor affinity was still lowered in plasma membranes obtained from NaN3-treated cells. Thus an inhibition of insulin internalization could not account for the observed effects. It is suggested that the observed ATP-dependence of insulin receptor affinity reflects a reversible structural alteration of the receptor, or of some closely related membrane protein.

BESTIMMUNG DER INSULINAKTIVITÄT IM MENSCHLICHEM SERUM NACH GLUKOSEBELASTUNG ALS PRÜFUNG DER FUNKTIONSFÄHIGKEIT DES PANKREAS

1963 ◽  
Vol 42 (3) ◽  
pp. 437-452 ◽  
Author(s):  
H. Daweke
Keyword(s):  
Blood Sugar ◽  
Pancreatic Insufficiency ◽  
Normal Subjects ◽  
Insulin Binding ◽  
Epididymal Adipose Tissue ◽  
Moderate Increase ◽  
Glucose Loading ◽  
Before And After ◽  
Oral Hypoglycaemic Drugs ◽  
Severity Of The Disease

Using the method of glucose-1-14C oxydation to 14CO2 on the rat epididymal adipose tissue, the insulin-like activities (ILA) in the serum have been compared before and after oral loading with glucose in normal subjects, in maturity-onset diabetics and in insulin-requiring diabetics. In maturity-onset diabetics mean fasting values were found to be 30% below normal while in insulin-requiring diabetics they were 85% above normal. In normal subjects there was observed, 30 minutes after glucose loading, a moderate increase in blood sugar together with an increase of ILA of 222% above the starting value; in maturity-onset diabetics the increase in ILA was only 106% while the blood sugar was markedly increased. After glucose loading in maturity-onset diabetics, the total amount of insulin detected during the period of the experiment was, on the average, only 45% of that found in normal subjects. In insulin requiring diabetics there was no increase but, on the contrary, a steady decrease of the ILA values, while the blood sugar excessively increased. In general ILA values were higher than those in maturity-onset diabetics. No difference in response was found between maturity-onset diabetics treated with diet alone and those treated with diet and oral hypoglycaemic drugs. In contrast to the absolute ILA values, the index of insulin reserve, is of value in assessing the functional capacity of the pancreas. This index decreases progressively with the severity of the disease and reaches a maximum of 54% of the normal in maturity-onset diabetics, which can satisfactorily be explained by pancreas insufficiency. Only in some cases of insulin-requiring diabetics was an insulin reserve still detectable. The biological inactivity of the insulin circulating in the blood can be deduced from the increased ILA-values, as compared with those found in maturity-onset diabetics. Obviously some of this insulin can be released by the addition of glucose. It is likely that, in addition to pancreatic insufficiency, insulin-binding or insulin-inactivating antibodies play a part in the pathogenesis of insulin-requiring diabetes.

scholarly journals Characterization of a membrane regulator of insulin receptor affinity.

1983 ◽  
Vol 258 (11) ◽  
pp. 6875-6881 ◽  
Author(s):  
J T Harmon ◽  
J A Hedo ◽  
C R Kahn
Keyword(s):  
Insulin Receptor ◽  
Receptor Affinity
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