Data obtained over the last two years pertinent to the thiol redox model for the modulation of hexose transport activity by insulin is summarized. The model proposes that activation of hexose transport in fat cells involves sulfhydryl oxidation to the disulfide form in a key protein component of the
Common pathway for the induction of hexose transport by insulin and stress
โ Scribed by A. P. Warren; C. A. Pasternak
- Publisher
- John Wiley and Sons
- Year
- 1989
- Tongue
- English
- Weight
- 646 KB
- Volume
- 138
- Category
- Article
- ISSN
- 0021-9541
No coin nor oath required. For personal study only.
โฆ Synopsis
The effect of stress (heat shock, arsenite, or Semliki Forest virus lSFV1 infection) on the induction of increased hexose transport has been compared with that of insulin. All four treatments increase the V, , , , , for transport by BHK cells three-to five-fold, with little effect (< 40% decrease) on K , .
Hydrogen peroxide and phenylarsine oxide (PAC)) prevent the increase in hexose transport induced by stress treatments as effectively as they do that induced by insulin. Pinocytosis is not affected by any of the four treatments. On the other hand, the induction by insulin is sensitive to amiloride, whereas that by arsenite is not. Rat embryo fibroblasts, which respond poorly to insulin, respond well to arsenite, heat shock, or SFV infection. It is concluded that the stress response is mediated by certain compounds that may be comnion to those required for the action of insulin, but that those compounds act at a stage subsequent to the function of the insulin receptor.
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