BIOLOGICAL TRANSPORT 



The action by insulin on two entirely distinct transport proc- 

 esses (for sugars and for amino acids) deserves close attention. We 

 should not infer, however, that a decompartmentalization has oc- 

 curred, i.e., that barriers to diffusion have been removed, since 

 these solutes do not move simply by diffusion. Instead the trans- 

 ports in question are mediated; the uptake of amino acids appears 

 in most cases to be concentrative. For a-aminoisobutyric acid, 

 Akedo and Christensen (1962b) have shown that the diffusion con- 

 stant is not modified by insulin, but that insulin influences instead 

 a mediated process in such a way that the apparent K m is strongly 

 decreased. 



The finding by Barrnett and Ball (1960) that the frequency of 

 invagination and pinocytosis of the cells of the epididymal fat pad, 

 as estimated by electron microscopy (Figure 31), is increased by 

 insulin, may be taken as another indication that the cell membrane 

 has been affected in a general way, and not simply with reference 

 to the mediation of sugar transport. We have already seen the diffi- 

 culties in supposing that the extra sugar enters by the increased 

 pinocytosis per se. More likely, the increased frequency of invagina- 

 tion reflects a modification of the membrane associated with an 

 increased responsiveness to entering solutes. The transport of sodium 

 and potassium ions is also known to be influenced by insulin (Man- 

 ery et al., 1956; Smillie and Aianery, 1960; Kernan, 1961). Note 

 that steroids also modify a variety of apparently unrelated trans- 

 ports in other cells and tissues. It is striking how frequently hor- 

 mones seem to act on a generalized transport property of the 

 plasma membrane rather than on a single specific transport. 



Randle (1956) has shown that glucose entry into muscle is also 

 accelerated by the absence of oxygen or by the presence of 2,4- 

 dinitrophenol, salicylate, or other agents (Randle and Smith, 1958). 

 A common effect that can be attributed to these agencies is a de- 

 creased availability of high-energy phosphate. Hence Randle has 

 suggested that insulin may act by diverting high-energy phosphate 

 away from a presumed repressive effect on sugar transport. In ap- 

 parent contrast, the action of dinitrophenol on a-aminoisobutyric 

 acid transport is inhibitory rather than insulin-like (Akedo and 

 Christensen, 1962b). Such transport of a-aminoisobutyric acid into 

 the isolated diaphragm becomes uphill when insulin is added; being 

 an uphill transport it presumably requires ATP and, as would be 

 expected, is antagonized by 2,4-dinitrophenol. Under these condi- 

 tions, the conclusion that insulin modifies transport by diverting 



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