ENDOCRINOLOGY OF TRANSPORT 



Cyclic AMP was shown to stimulate water migration and sodium 

 transport when it was applied at 1- to 10-m/l/ levels to the serosal 

 surface of the toad bladder. Theophylline at a 40-m/W level also 

 produced this action. The effects of a submaximal dose each of 

 vasopressin and theophylline were additive. Each agent was ineffec- 

 tive when applied to the mucosal surface. The action of all three 

 was blocked by 1-mM N-ethylmaleimide and by p-chloromercuri- 

 benzoate. An actual increase in the level of the cyclic anhydride in 

 toad bladder under the action of vasopressin has not yet been shown. 

 This proposal has special interest in that it supplies possible transport- 

 modifving actions for several more hormones. 



Insulin 



Apparently as "a voice in the wilderness" urging attention to 

 the importance of transport and its control, Rudolph Hober sug- 

 gested in 1914, before insulin was known, that diabetes might well 

 be a disease of sugar transport by the cell membrane (Levine, 1961). 

 Lundsgaard showed in 1939 that insulin accelerated sugar uptake 

 by perfused striated muscle. Levine and his associates showed, be- 

 ginning in 1949 (see also Levine, 1961), that insulin accelerates the 

 entry of sugars into the cellular compartment as estimated for the 

 whole organism. This action has since been confirmed specifically 

 for a number of isolated tissues, including particularly the heart, the 

 diaphragm, and the epididymal fat pad. These tissues are believed 

 not to concentrate sugars and may appear not to admit them to 

 all the cellular space; nevertheless, the entry at least into muscle is 

 mediated in the absence as well as in the presence of insulin. The 

 diaphragm of the insulin-treated rat in situ appears to take up D-xy- 

 lose to a level twice as high as the plasma level (Eichhorn and 

 Hechter, 1961). The possibility that the outward transport can be 

 uphill has received insufficient attention. 



The isolated diaphragm takes up a number of amino acids 

 faster when insulin is added. These amino acids include a-amino- 

 isobutyric acid (Kipnis and Noall, 1958), glycine (Manchester and 

 Young, 1960; cf. Manchester, 1961), also L-methionine and L-proline, 

 and a number of model amino acids (Akedo and Christensen, 

 1962b). A tentative impression that this action occurs only for 

 abnormal amino acids is not correct. More probably the hormone 

 acts on only one of two mediating systems (the so-called "A" media- 

 tor) for neutral amino acids discussed in Chapter 4. 



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