These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Insulin-like growth factor I stimulates active Na(+)-K+ transport in rat soleus muscle.
    Author: Dørup I, Clausen T.
    Journal: Am J Physiol; 1995 May; 268(5 Pt 1):E849-57. PubMed ID: 7762637.
    Abstract:
    The functional homology between insulin and insulin-like growth factor I (IGF-I) comprises effects on growth and glucose metabolism. Because insulin stimulates the Na(+)-K+ pump, IGF-I might exert a similar effect. We show here that IGF-I increases 42K and 86Rb uptake and the efflux of 22Na in isolated rat soleus muscle. This leads to a significant decrease (21-55%, P < 0.001) in intracellular Na+ and a small increase in intracellular K+. In extensor digitorum longus (EDL) muscle, similar effects were observed. The stimulation of K+ uptake and the reduction in intracellular Na+ in the soleus were blocked by ouabain, indicating that they reflect an acute stimulation of active Na(+)-K+ transport. This conclusion was further supported by the observation that the [3H]ouabain binding rate was significantly increased by IGF-I. IGF-I increased ouabain-suppressible 42K or 86Rb uptake by 56 and 54%, respectively. The effects of IGF-I and epinephrine on ouabain-suppressible 86Rb influx in rat soleus were additive, whereas the effects of insulin and IGF-I were similar and nonadditive. The effects of IGF-I were seen down to a concentration of 10(-8) M, which is unlikely to stimulate the insulin receptor, and it is therefore plausible that IGF-I exerts its effect on Na(+)-K+ transport through its own receptor. IGF-I may play a role in the maintenance of muscle Na+ and K+ contents also in vivo, especially in patients treated with IGF-I.
    [Abstract] [Full Text] [Related] [New Search]