LIPID STORAGE UNDER ABNORMAL CONDITIONS 685 



of lipid from the liver during the recovery phase. However, Campbell 454 

 reported that insulin partially prevents the increase in liver fat, in fasting 

 mice, rats, and guinea pigs, which occurs after the administration of ante- 

 rior pituitary extracts. After labeling body fats with deuterium, Stetten 

 and Salcedo 433 were able to prove that the fatty infiltration following the 

 injection of the anterior pituitary substance is produced by the increase in 

 the rate of fat transfer from the fat depots to the liver. Conversely, when 

 no ketogenic hormone is available, as occurs after hypophysectomy, fat 

 transfer to the liver is inhibited, even when such powerful stimuli as the 

 liver poisons, phosphorus and carbon tetrachloride, are administered. 868 

 Weil and Stetten 435 gave the name adipokinin to this fat-mobilizing agent of 

 the anterior lobe of the pituitary. 



(b') Growth Hormone. — In addition to the ketogenic hormone of the 

 anterior lobe of the pituitary gland, growth hormone also causes a rapid 

 mobilization of lipid to the liver; the peak of mobilization occurs within six 

 hours after treatment with the hormone, and the blood lipids return to 

 normal within twenty-four hours. 869 According to Greenbaum and Mc- 

 Lean, 869 the changes are mainly reflected in the neutral fat fraction. The 

 synthesis of phospholipids in the liver is likewise stimulated. These com- 

 pounds are then released to the plasma. When the purified growth hor- 

 mone was continuously injected into adult female rats, a progressive de- 

 crease in the fat content of the carcass occurred. Greenbaum 870 suggests 

 that one of the primary effects of the growth hormone is in the catabolism of 

 fats. 



c'. Adrenal Hormones: The injection of adrenocortical extracts has been 

 shown to cause an increase in the fat content of the liver 281 ' 871 ; on the other 

 hand, the animal loses its ability to transport fat to the liver following ad- 

 renalectomy. Thus, LeBlond and co-workers 872 reported that fatty livers 

 could not be produced after extirpation of the adrenal glands, while Verzar 

 and Laszt 444 found that even the powerful hepatic poison, phosphorus, was 

 unable to elicit fat mobilization in the liver under such circumstances. 

 Barnes, Miller, and Burr 281 likewise found that adrenalectomized animals 

 which had been maintained in good physical condition by the administra- 

 tion of salt had an impaired ability to deposit absorbed fat in the neutral fat 

 stores in the liver. 



868 B. v. Issekutz and F. Verzar, Arch. ges. Physiol. (Pfliiger's), 240, 624-635 (1938). 



869 A. L. Greenbaum and P. McLean, Biochem. J., 54, 407-413 (1953). 



870 A. L. Greenbaum, Biochem. J., 54, 400-407 (1953). 



871 C. H. Li, M. E. Simpson, and H. M. Evans, Arch. Biochem., 28, 51-54 (1949). 



872 C. P. LeBlond, N. Van Thoai, and G. Segal, Compt. rend. soc. biol, 130, 1557-1559 

 (1939). 



