466 IX, CAROTENOIDS AND VITAMINS A 



tributed this increase to the large amounts of vitamin A and carotene in the 

 diet of the diabetic patients. Peters and Van Slyke^^^ also questioned 

 whether or not carotenemia is a direct result of diabetes mellitus. There 

 is no experimental evidence that the destruction of carotene is associated 

 with the utilization of carbohydrate.^^* Although the reason why caroten- 

 emia occurs in diabetes mellitus must still be regarded as open to question, 

 one must incline to the explanation based upon dietarj^ changes as the 

 more probable one. 



Alloxan diabetes produces an abnormally low level of vitamin A in the 

 liver. Thus, Sobel and co-workers^^^ observed that rats with severe alloxan 

 diabetes (blood sugar over 150 mg./lOO ml.) stored a much smaller amount 

 of vitamin A in their livers after the administration of 2000 ng. of carotene 

 (dissolved in 0.2 ml. of cottonseed oil) than did normal rats; the compara- 

 tive vitamin A stores were 22 ± 20 ng. and 88 ± 25 ug. per liver, respec- 

 tively. When vitamin A itself was fed, the variations in hepatic vitamin 

 A were much less marked (90 ± 41 fig. as compared with 123 ± 30 ng.). 

 The most probable explanation for the failure of the alloxan-diabetic rats 

 to store more vitamin A after the administration of carotene is that the 

 transformation of carotene to vitamin A is depressed under these conditions. 

 That this is the case is indicated by the later results of Rosenberg and 

 Sobel, ^^^ who reported a decreased in vitro conversion of /3-carotene in the 

 gut of the alloxan-treated rat. Thus, when the excised intestine of rats, 

 killed immediately after carotene feeding, according to the procedure of 

 these investigators,^'** was incubated at 45°C. for two hours, an average of 

 only 0.76 /jig. of vitamin A was found to be present per entire intestinal 

 wall, as contrasted with a mean value of 4.25 /xg. in normal rats under 

 similar conditions. 



Mastitis is another condition which, it was formerly believed, involved 

 an abnormal carotene metabolism. Miller, Lease, and Anderson^^^ re- 

 ported that the milk carotenoid levels were considerably increased in ex- 

 perimentally-induced mastitis in the cow, but that the total daily output 

 of carotenoid was markedly lower than normal as a result of the decreased 

 yield of milk. Chanda^^'^ confirmed the fact that a concentration of caro- 

 tene occurs in the milk of cows infected with mastitis (Streptococcus agalac- 

 tiae contagiosae) , but he noted that nitrogen, chloride, and phosphatase 



^^* J. P. Peters and D. D. Van Sh'ke, Quantitative Clinical Chemistry, Vol. I, Inter- 

 pretations, 2nd ed. Williams & Wilkins, Baltimore, 1946, p. 514. 



^'^ A. E. Sobel, A. Rosenberg, and H. Adelson, Arch. Biochem. Biophys., 44, 176-180 

 (1953). 



336 p. G. Miller, E. J. Lease, and G. W. Anderson, J. Dairy Sci., 23, 573-574 (1940). 



3" R. Chanda, Biochem. J., 54, 68-77 (1953). 



