SATURATED FATTY ACIDS 41 



Curran^^^ reported that the rate of fatty acid synthesis was slightly in- 

 creased in the biotin-deficient rat; the increased rate of synthesis was be- 

 lieved to be related to the inanition accompanying biotin deficiency rather 

 than to the deficiency itself. 



Because of the importance of pantothenic acid as a component of the 

 CoA molecule, it is obvious that a deficiency in this vitamin would have a 

 profound effect on fatty acid synthesis. In pantothenic acid deficiency 

 in ducks, CoA is present in the liver to the extent of only 40% of the normal 

 amount."^ Although definite effects of CoA deficiency have not been re- 

 ported, other intermediary reactions such as acetylation (see page 28) and 

 fat oxidation (see page 86) are markedly altered under such conditions. 



f. The Effect of Experimental Diabetes. Lipogenesis has been studied 

 in alloxan diabetes and in pancreatic diabetes. Stetten and Boxer^^* 

 first reported that the depression in lipogenesis was the major metabolic 

 defect in alloxan diabetes in the rat. Subsequently, Brady and Gurin^^^ 

 found that the synthesis of long-chain acids from acetate could not be 

 effected in the livers of rats with alloxan diabetes. According to Van 

 Bruggen et al.,^^^ a decrease in the incorporation of acetate in liver slices 

 from alloxan-diabetic rats occurs, comparable to that obtained on fasting. 

 After a fast lasting twenty hours, the decrease in hpogenesis was less in the 

 slices from diabetic rats than in those of normal rats. Cholesterol synthesis 

 was not similarly affected. 



The same failure in S3nithesis of acetate obtained in depancreatized 

 cats; however, the synthesis of cholesterol from acetate was not found to be 

 inhibited, except in prolonged and severe diabetes. The lipogenic action 

 could not be restored by the addition to the medium of insulin, glucose, 

 fructose-G-phosphate, oxaloacetate, or a-ketoglutarate. The accumula- 

 tion of fat in the liver in diabetes is therefore attributed mainly to increased 

 transport from extrahepatic tissues, rather than to an increased rate of 

 synthesis in situ. 



g. The Effect of Glycerol. Glycerol was found to stimulate the utiliza- 

 tion of acetate more than that of glucose. This throws open to question the 

 hypothesis that glycerol stimulates lipogenesis by removing fatty acids, in 

 the form of glycerides, from the site of synthesis. It also indicates that, 

 although the prolipogenic action of insulin is closely related to the utilization 

 of carbohydrate, it is doubtful whether or not this action is mediated 

 through the formation of glycerol from glucose.^" 



18^ G. L. Curran, Proc. Soc. Exptl. Biol. Med., 75, 496-498 (1950). 

 "5 R. O. Brady and S. Gurin, /. Biol. Chem., 187, 589-596 (1950). 

 186 J. T. Van Bruggen, T. T. Hutchens, and P. Yamada, Federation Proc, 12, 283 

 (1953). 



