Growth hormone and insulin-like growth factors I and II produce distinct alterations in glucose metabolism in 3T3-F442A adipocytes.
Open Access
- 1 December 1985
- journal article
- research article
- Published by Proceedings of the National Academy of Sciences in Proceedings of the National Academy of Sciences
- Vol. 82 (24) , 8724-8728
- https://doi.org/10.1073/pnas.82.24.8724
Abstract
In 3T3-F442A adipocytes, human growth hormone (hGH) stimulates glucose oxidation in 4 hr. A maximal increase is evident at hGH concentrations of 50-100 ng/ml and rarely exceeds 50% above control. The stimulation is transient; after 48 hr of incubation with GH, glucose oxidation is significantly suppressed to 35% below control values. In view of the concept that insulin-like growth factors (IGF) may mediate the effects of GH, we compared the effects of hGH (500 ng/ml) and several preparations of IGF on glucose metabolism in 3T3 adipocytes. After 4 hr of incubation, IGF-I from human plasma stimulated glucose oxidation in a dose-related manner, producing a 10-fold increase at 50 ng/ml. Methionyl-IGF-I produced by recombinant DNA techniques was 85-88% as effective as IGF-I. IGF-II stimulated glucose oxidation 3-fold at 50 ng/ml after 4 hr of incubation. In contrast to the suppression observed with hGH after 48 hr, all three of the IGF preparations stimulated glucose oxidation after 48 hr of incubation and were as effective as they were after 4 hr. When each of the IGF preparations was tested (at 5 ng/ml) in combination with hGH, both the stimulatory and suppressive effects of GH were superimposed on the stimulation by the IGFs. Thus, the stimulatory properties of IGF differed from those of GH in that the maximum extent to which IGF increased glucose oxidation, compared with hGH, was as much as 20-fold greater. Furthermore, all of the IGF preparations stimulated glucose oxidation after 48 hr under conditions in which hGH suppressed glucose metabolism. Thus, it is unlikely that extracellular IGFs mediate the effects of hGH on glucose metabolism in 3T3-F442A adipocytes.Keywords
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