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

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.

Metabolism ◽  
1982 ◽  
Vol 31 (9) ◽  
pp. 884-895 ◽  
Author(s):  
Oluf Pedersen ◽  
Elisabeth Hjøllund ◽  
Niels Schwartz Sørensen

PLoS ONE ◽  
2014 ◽  
Vol 9 (2) ◽  
pp. e88684 ◽  
Author(s):  
John A. Corbin ◽  
Vinay Bhaskar ◽  
Ira D. Goldfine ◽  
Daniel H. Bedinger ◽  
Angela Lau ◽  
...  

Diabetologia ◽  
1985 ◽  
Vol 28 (5) ◽  
pp. 286-290 ◽  
Author(s):  
T. Suzuki ◽  
H. Makino ◽  
A. Kanatsuka ◽  
S. Kuribayashi ◽  
N. Hashimoto ◽  
...  

1980 ◽  
Vol 238 (3) ◽  
pp. E267-E275
Author(s):  
J. N. Livingston ◽  
B. J. Purvis

The plant lectin (wheat germ agglutinin, WGA) produces several alterations in the ability of fat cells to bind and respond to insulin. Although WGA markedly stimulated glucose oxidation, it caused only a modest stimulation of glucose transport. WGA (0.25-20 micrograms/ml) increased the binding of insulin by adipocytes, apparently by increasing the binding affinity of the insulin receptor. With low WGA concentrations (0.25-2.5 micrograms/ml), the elevation in binding was accompanied by an increase in the sensitivity of the adipocytes to insulin stimulation of glucose transport. However, the sensitivity of these cells to vitamin K5 and H2O2 was not altered. With higher WGA concentrations (5-20 micrograms/ml), stimulation of the glucose transport system by insulin, vitamin K5, or H2O2 was markedly inhibited, an effect that is reversed by the addition of ovomucoid. These findings suggest that low WGA concentrations increase the affinity of the insulin receptor and the insulin sensitivity of the cells. At higher concentrations, the lectin appears to act at another site(s) to inhibit the activation of the transport system by insulin or other agents.


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