scholarly journals Correlation between insulin receptor binding in isolated fat cells and insulin sensitivity in obese human subjects.

1976 ◽  
Vol 58 (6) ◽  
pp. 1435-1441 ◽  
Author(s):  
L C Harrison ◽  
F I Martin ◽  
R A Melick
Keyword(s):  
Insulin Sensitivity ◽  
Insulin Receptor ◽  
Receptor Binding ◽  
Human Subjects ◽  
Fat Cells ◽  
Isolated Fat Cells ◽  
Insulin Receptor Binding ◽  
Obese Human

Insulin receptor binding and insulin action in human fat cells: Effects of obesity and fasting

Metabolism ◽  
1982 ◽  
Vol 31 (9) ◽  
pp. 884-895 ◽  
Author(s):  
Oluf Pedersen ◽  
Elisabeth Hjøllund ◽  
Niels Schwartz Sørensen
Keyword(s):  
Insulin Receptor ◽  
Receptor Binding ◽  
Insulin Action ◽  
Fat Cells ◽  
Insulin Receptor Binding

scholarly journals Insulin-sensitive phosphodiesterase and insulin receptor binding in fat cells from spontaneously obese rats

Diabetologia ◽  
1985 ◽  
Vol 28 (5) ◽  
pp. 286-290 ◽  
Author(s):  
T. Suzuki ◽  
H. Makino ◽  
A. Kanatsuka ◽  
S. Kuribayashi ◽  
N. Hashimoto ◽  
...  
Keyword(s):  
Insulin Receptor ◽  
Receptor Binding ◽  
Fat Cells ◽  
Insulin Receptor Binding ◽  
Obese Rats

Insulin binding and action on fat cells from young healthy females and males

1982 ◽  
Vol 243 (2) ◽  
pp. E158-E167 ◽  
Author(s):  
O. Pedersen ◽  
E. Hjollund ◽  
H. O. Lindskov
Keyword(s):  
Glucose Metabolism ◽  
Cell Surface ◽  
Insulin Receptor ◽  
Glucose Transport ◽  
Receptor Binding ◽  
Glucose Utilization ◽  
Insulin Binding ◽  
Fat Cells ◽  
Insulin Receptor Binding ◽  
Rate Limiting

Insulin binding and action were studied in fat cells from the gluteal region of young healthy subjects. Fat cells from females were larger than those of males, had higher insulin receptor binding and higher rates of noninsulin-stimulated and maximally insulin-stimulated rates of methylglucose transport and glucose metabolism when these data were expressed per cell number. However, when insulin binding and insulin effects were expressed per cell surface, which may be physiologically more relevant, no sex differences were found in insulin binding and glucose transport, whereas noninsulin-stimulated and maximally insulin-stimulated glucose metabolism was still significantly increased in female fat cells. The latter indicates postreceptor differences in glucose metabolism between females and males. The insulin concentrations causing half-maximal responses (a measure of the sensitivity to insulin) of glucose transport, glucose metabolism and lipolysis were similar in fat cells from the two sexes, which is consistent with the comparable values of insulin receptor binding when adjusted to cell surface. Studies of rate-determining steps for the glucose utilization of human fat cells showed that glucose transport was not the rate-limiting step at physiological glucose concentrations. Moreover, at physiological glucose levels, glucose metabolism exhibited a decreased maximal insulin responsiveness and an increased insulin sensitivity when compared with glucose metabolism at low glucose concentrations at which glucose transport is rate limiting for the fat cell glucose utilization.

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