PHOSPHOLIPIDS 61 



regards the incorporation of phosphate (which involves the phosphate- 

 glycerol and the phosphate-choline bonds) , but also in the incorporation of 

 fatty acids into the molecule (glycerol-fatty acid bonds). The importance 

 of ACTH in phospholipid synthesis in brain was noted by Torda.-" 



d. The Effect of Phlorhizin. Since the classical demonstration by von 

 Mering^"^ that the injection of the glycoside, phlorhizin, into a normal 

 animal is followed almost immediately by a profuse glycosuria, it has re- 

 peatedly been demonstrated that its action is exclusively renal. Thus, 

 Deuel et al}^'^ and Nash^"^ reported that this drug had no direct effect upon 

 the carbohydrate metabolism of nephrectomized dogs. 



The renal effect is now known to result from the inability of the glucose 

 to be reabsorbed in the kidney tubules. The absence of reabsorption has 

 been attributed to the fact that phosphorylation is required to bring about 

 absorption, and that phlorhizin prevents this.*"^ However, both Lunds- 

 gaard^'^'^ and Lambrechts^"^ reported that the concentration of phlorhizin 

 necessary to produce glycosuria is much less than that required to poison 

 phosphatases. 



On the other hand, Wilbrandt and Laszt^"^ reported that iodoacetate, 

 which is known to interfere with phosphorylation, also inhibits the absorp- 

 tion of glucose. Moreover, Beck^^° was able to confirm these findings in 

 regard to phosphorylation; he used phlorhizin, which is much less toxic 

 than is the iodoacetate. When animals received phlorhizin, absorption 

 of glucose from the gastrointestinal tract was decreased. Moreover, this 

 investigator demonstrated that the accumulation of hexose-phosphate in 

 the intestinal mucosa of rats which had received phlorhizin was not com- 

 parable to that observed in the normal animals. Thus, if phlorhizin in- 

 hibits phosphorylation of sugars, it would be expected that it might retard 

 the synthesis of phospholipids in a similar manner. 



However, Weissberger"^ did not observe any inhibition in the rate at 

 which P^2 was incorporated into phospholipids in the liver, kidney, or small 



3»3 J. von Mering, Verhandl. Kong. mn. Med., 5, Wiesbaden, 185-189 (April, 1886). 



SO" H. J. Deuel, Jr., H. E. C. Wilson, and A. T. Milhorat, /. Biol. Chem., 74, 265-298 

 (1927). 



305 T. P. Nash, Jr., /. Biol. Chem., 83, 139-155 (1929). 



^* J. P. Peters and D. D. Van Slyke, Quantitative Clinical Chemistry, 2nd ed., vol. I, 

 Williams & Wilkins, Baltimore, 1946, p. 256. 



»'E. Lundsgaard, Biochem. Z., 264, 209-220; 221-227 (1933); Skand. Arch. Physiol, 

 72, 265-270 (1935). 



308 A. Lambrechts, Compt. rend. soc. biol, 122, 468-471 (1936). 



309 W. Wilbrandt and L. Laszt, Biochem. Z., 250, 398-417 (1933). 



310 L. V. Beck, J. Biol. Chem., 143, 403-415 (1942). 



311 L. H. Weissberger J. Biol. Chem., 139, 543-550 (1941). 



