370 INOSITOLS 



encephalomalacia and exudative diathesis, two symptoms frequently en- 

 countered in chicks fed vitamin E-deficient diets, were prevented by adding 

 inositol to the diet. 



Hogan and Hamilton^^ found that the rate of growth of guinea pigs fed a 

 partially purified diet was increased by inositol supplementation. 



Cooperman et al.^'^ reported an increased rate of growth of hamsters 

 when inositol was added to a purified diet. Hamilton and Hogan,^^ however, 

 found that inositol supplementation did not increase the growth rate of 

 hamsters; but the vitamin did counteract reproductive difficulties in ham- 

 sters in which the young were born dead or as shapeless bloody masses and 

 where the mothers frequently failed to survive parturition. 



Mclntire^^ found that the addition of inositol to a purified diet almost 

 doubled the rate of growth of cotton rats. This increase in growth rate is 

 the greatest observed with any species fed a purified diet which was not 

 supplemented with a sulfonamide. 



There appears to be general agreement among investigators that inositol 

 is a lipotropic factor. Gavin and McHenry" found that the addition of 

 biotin to a purified diet caused a fatty liver in rats that could be prevented 

 by the further addition of inositol. The lipotropic action of inositol in 

 rats has been confirmed by Engel,^^ Forbes,''^ Handler,^" and McFarland 

 and McHenry.^i Gavin et al.*^ found that, when thiamine was the only 

 B-complex vitamin supplement added to a purified diet, the liver fat of 

 the rat could be maintained at a normal level by supplying one lipotropic 

 agent, choline. However, when other B vitamins were added to the ration, 

 the fatty livers responded to both inositol and choline. All the observations 

 of McFarland and McHenry^i indicate that a fatty liver, of the type pro- 

 duced by in vivo fat synthesis, is made resistant to choline and responsive 

 to inositol by increasing the intake of B vitamins, both in kind and in 

 quantity. Handler^" has suggested that a large increase in food intake, with 

 a surge in fatty acid synthesis, may be the factor causing choline resistance 

 and inositol responsiveness. However, McFarland and McHenry^^ reported 

 on paired feeding tests which showed that food consumption is a contri- 



33 A. G. Hogan and J. W. Hamilton, J. Nutrition 23, 533 (1942). 



3* J. M. Cooperman, H. A. Waisman, and C. A. Elvehjem, Proc. Soc. Exptl. Biol. 

 Med. 52,250 (1943). 



35 J. W. Hamilton and A. G. Hogan, /. Nutrition 27, 213 (1944). 



36 J. M. Mclntire, B. S. Schweigert, and C. A. Elvehjem, /. Nutrition 27, 1 (1944). 



37 G. Gavin and E. W. McHenry, J. Biol. Chem. 139, 485 (1941). 



38 R. W. Engel, J. Nxitrition 24, 175 (1942). 



39 J. C. Forbes, Proc. Soc. Exptl. Biol. Med. 54, 89 (1943). 

 " P. Handler, J. Biol. Chem. 162, 77 (1946). 



« M. L. McFarland and E. W. McHenry, J. Biol. Chem. 176, 1 (1948). 



42 G. Gavin, J. M. Patterson, and E. W. McHenry, J. Biol. Chem. 148, 275 (1943). 



