614 VI. OCCURRENCE OF LIPIDS IN THE ANIMAL 



Thus, Clement 439 reported that section of the nerve supply to the inter- 

 scapular fat body or to the perinephric fat depot abolished the fat-mobiliz- 

 ing action of pituitary extracts. 



The relation of the pituitary gland to fat mobilization has also been 

 followed by the use of hypophysectomized animals. Thus, Lee and Ayres 440 

 reported that hypophysectomized rats kept on a suboptimal diet lost less 

 depot fat than did control animals on the same diet. On the other hand, 

 forced feeding of hypophysectomized rats was shown to lead to excessive 

 adiposity. 441-4 " 



b'. The Regulation by the Adrenal Cortex and Medulla: Cortical hor- 

 mones are of importance in both the mobilization and the deposition of 

 adipose tissue. The original observation of Verzar and Laszt 444 that fatty 

 livers cannot be produced in adrenalectomized animals has been confirmed 

 by a number of workers. 445-448 In fact, Hartman and co-workers 449 re- 

 ported the isolation of a new cortical factor, distinct from the sodium and 

 carbohydrate factors, which causes the deposition of fat in the livers of fast- 

 ing adrenalectomized animals. 



However, the inability to elicit fatty livers in adrenalectomized animals 

 cannot be attributed solely to an inadequate fat mobilization from the de- 

 pots. If this were the only defect after extirpation of the adrenals, the 

 adipose tissues should be fully charged. Tuerkischer and Wertheimer 120 

 reported that the opposite condition obtained, and that the fat depots of 

 such adrenalectomized animals were largely depleted. The low level of 

 storage could not be caused by an inadequate intake of food, since fat 

 levels in adrenalectomized rats were always lower than those in pair-fed 

 normal controls. 450 When deoxycorticosterone acetate or adrenal cortical 

 extracts were injected into adrenalectomized animals, normal fat storage 

 was restored. The adrenocortical extract was the less effective of the two. 



Further experiments in support of this hypothesis have been reported by 



439 G. Clement, Compt. rend. soc. biol, 141, 317-320 (1947). 



440 M. Lee and G. B. Ayres, Endocrinology, 20, 489-495 (1936). 



441 L. T. Samuels, R. M. Reinecke, and H. A. Ball, Endocrinology, 31, 35-41 (1942). 



442 L. T. Samuels, R. M. Reinecke, and K. L. Bauman, Endocrinology, 33, 87-95 

 (1943). 



443 L. Levin, Am. J. Physiol., 141, 143-150 (1944). 



444 F. Verzar and L. Laszt, Biochem. Z., 288, 356-358 (1936). 



446 E. M. MacKay and R. H. Barnes, Am. J. Physiol, 118, 525-527 (1937). 



446 E. M. MacKay, Am. J. Physiol, 120, 361-364 (1937). 



447 E. G. Frv, Endocrinology, 21, 283-291 (1937). 



448 D. J. Ingle, J. Clin. Endocrinol, 3, 603-612 (1943). 



449 F. A. Hartman, K. A. Brownell, and J. S. Thatcher, Endocrinology, 40, 450 (1947). 

 «° F. Schiffer and E. Wertheimer, /. Endocrinol, 5, 147-151 (1947). 



