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P. 246 et seq. [8J H. L. , Ed. by P. D. Boyer, H. Lardy, and K. Myrback, Vol. , New York 1959). p. l. [9J Documenta Geigy, Scientific Tables, 5th Ed. (New York 1959), p. 469. [10J R. J. WINZLER, J. Cell. Compo Physiol. 21 (1943),229. [l1J D. W. WOOLLEY, in Progress in Drug Research, Vol. 2, Ed. by E. Jucker (Birkhauser Verlag, Basel 1960), p. 613. [12J A. , New York 1960), p. 103. [13J D. D. WOODS, Brit. J. Exp. Path. 21 (1940), 74. [14J A. , New York 1960), p. 50. [15J J. N. STANNARD, Am. J. Physiol.
These investigators examined adipose tissue cells that had been exposed to insulin in vitro and compared them with similar cells to which no insulin was added. The physiological effect of insulin~in this case, an increased production of gas, presumably carbon dioxide, which occurs during the synthesis of fat from glucose~was demonstrated manometrically before the tissue was fixed in osmium tetroxide for sectioning and electron microscopy. The electron micrographs clearly show that the plasma membranes of adipose cells incubated with insulin become invaginated at many sites to form minute finger-like indentations.
In addition, PAULING noted that, in contrast to other theories of anesthesia, the clathrate formation theory is not concerned with the lipids of the brain but rather involves the aqueous phase which is the predominant constituent of brain and other tissues. Of course, all tissues of the body would be similarly affected by anesthetic agents, but it is reasonable to assume that the effect on consciousness is related to an effect on brain and nerve. Although this theory is in agreement with the known pharmacological, physical, and chemical properties of anesthetic agents, there is as yet no proof that anesthesia is due to some type of clathrate formation or even that gas hydrates exist in the body.