FACTORS ALTERING CONCENTRATION OF BLOOD LIPIDS 441 



plete removal of the hypophysis. It is believed that the hyperlipemia and 

 the hypercholesterolemia which are frequently found in acromegaly (over- 

 production of the growth hormone of the anterior pituitary gland) are 

 not related to the pituitary hormone, but rather to the diabetes or other 

 disorders usually associated with this disease. 533 Normal values for serum 

 lipids obtain in pituitary basophilism. 533 



(c) Variations Primarily Related to the Adrenal Glands. Since the adrenal 

 cortex plays such an important role in the manufacture of steroid hormones, 

 it is natural to suppose that it would exert some control over the cholesterol 

 content of the blood. In fact, in the report of Ingle, 534 a direct or secondary 

 control of fat metabolism by the adrenal cortex is implied. 



A number of investigators 535-537 failed to demonstrate any change in the 

 serum cholesterol level after adrenalectomy. However, Medvei 538 ob- 

 served that blood cholesterol is somewhat elevated in Addison's disease, 

 which primarily affects the adrenal cortex. 



Hoffmeyer 539 reported an increase in the blood cholesterol of rabbits fol- 

 lowing the transplantation of adrenals or the injection of adrenal cortical 

 extract. Adrenalectomy did not result in any definite alterations in the 

 serum cholesterol. According to other sources, some decreases in serum 

 cholesterol may occur after the injection of cortical extracts. 538>540,541 

 However, the action of desoxycorticosterone acetate (DCA) and that of 

 corticosteroid are markedly different. Thus Zilversmit et a/. 542 reported 

 a marked decrease in plasma phospholipid concentration, as well as in total 

 circulating plasma phospholipids, in bilaterally adrenalectomized dogs 

 maintained on DCA. In a later report, 543 it was shown that the plasma 

 cholesterol was likewise reduced in DCA-maintained adrenalectomized 

 dogs. After four weeks of DCA therapy, the concentration of these lipids 

 was lowered 30 to 50% below the original value, without alteration of the 

 cholesterol : phospholipid ratio. The decrease in phospholipid concentra- 

 tion cannot be ascribed to dilution or to increased utilization of phospho- 



533 E. B. Man, Unpublished observation; cited by J. P. Peters and D. D. Van Slyke, 

 Quantitative Clinical Chemistry, 2nd ed., Vol. I, Williams & Wilkins, Baltimore, 1946. 



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



635 E. J. Baumann and O. M. Holly, J. Biol. Chem., 55, 457-475 (1923). 



536 F. S. Randies and A. Knudson, J. Biol. Chem. 76, 89-93 (1928). 



537 C. Reid, J. Physiol, 75, 34P-35P (1932). 



538 C. V. Medvei, Z. klin. Med., 128, 58-68 (1935). 



639 J. Hoffmeyer, Acta Physiol. Scand., 10, 31-41 (1945). 

 540 J. Bauer and A. Buttu, Z. klin. Med., 122, 601-606 (1932). 



641 S. Thaddeaand W. Fasshauer, Arch, exptl. Pathol Pharmakol Naum/n-Schmiede- 

 berg's, 182, 477-498 (1936). 



542 D. B. Zilversmit, T. N. Stern, and R. R. Overman, Am. J. Physiol, 164, 31-34 

 (1951). 



543 N. R. Di Luzio, M. L. Shore, and D. B. Zilversmit, Federation Proc, 12, 197 (1953). 



