148 III. OXIDATION AND METABOLISM 



There appears to be general agreement that spontaneous or clinical 

 ketosis of cows and also of ewes is associated with hypoglycemia. Thus, it 

 has been reported that an mverse relationship exists between the levels of 

 total ketone bodies and glucose in the blood of ruminants suffering from 

 ketosis. "^"^"^"^ The average ketonemia and blood sugar of nine healthy 

 cows were found to be 2.21 mg. % (0 to 7.07) and 48.2 mg. % (36.2 to 59.9), 

 respectively, as contrasted with mean values of 55.8 mg. % (22.0 to 176.1) 

 and 28.5 mg. % (18.1 to 44.1), respectively, in the case of nine cows suffer- 

 ing from ketosis. ^^^ The symptoms of the ketosis resulting from hypo- 

 glycemia are believed to be due to the hypoglycemia itself, while the ace- 

 tonemia is attributed to the failure of carbohydrate oxidation. According 

 to Kruse (cited by Hupka)*""-*"^ typical symptoms of acetonemia in cows 

 were produced in healthy animals by the administration of large doses of 

 insulin. However, clinical ketosis has likewise been reported in cows hav- 

 ing a fairly normal blood sugar level. ^^^"^"^ Recovery of normal appetite 

 and milk flow does not occur until ketonemia has been dissipated.*"^ More- 

 over, Shaw*^" was unable to prevent the incidence of ketosis in one herd 

 of high-producing Holstein cattle by feeding molasses for several weeks 

 prior to parturition. It was, however, recognized that a close relationship 

 exists between the amount of hver glycogen and the development of ketosis. 

 Although most workers have reported that ehnical ketosis in dairy cattle 

 usually occurs from one to six weeks after parturition, ^^^'^^^'^^^ Knodt 

 et al^^^ state that factors such as gestation, parturition, stage of lactation, 

 and sudden cessation of milking do not ordinarily exert much influence on 

 the concentrations of acetone bodies in the blood and urine. 



Acetonemia in cattle has been related to vitamin Bi deficiency,*^' but 

 this appears questionable, inasmuch as the mature ruminant is able to 



«3 J. Sampson and C. E. Hayden, Cornell Vet., 26, 183-199 (1936). 



^°* J. W. Groenewald, H. Graf, and R. Clark Onderstepoort J. Vet. Set. Animal Ind., 17, 

 225-244 (1941); J. W. Groenewald, H. Graf, P. M. Becker, J. R. Malan, and R. Clark, 

 76zd., 245-296 (1941). 



«5 M. H. Roepke, J. Am. Vet. Med. Assoc, 100, 411-415 (1942). 



*'^ Kruse, Beitrag ziir Aetiologie der Gebdrparese, Inaug. Diss., Hannover, 1927; cited 

 by E. Hupka, Deut. tierarztl. Wochschr., 36, Special No., 98-101 (1928), p. 101. 



«U. Sampson, A. C. Gonzaga, and C. E. Hayden, Cornell Vet., 23, 184-207 (1933). 



«8 G. F. Boddie, Vet. Record, 15, 1539-1546 (1935); Chem. Abst., 30, 6054 (1936). 



*o3 J. Sampson and L. E. Boley, Am. J. Vet. Research, 2, 327-332 (1941). 



*i» J. C. Shaw, J. Dairy Sci., 26, 1079-1090 (1943). 



^11 C. W. Duncan, C. F. Huffman, and H. A. Tobin, /. Am. Vet. Med. Assoc, 95, 

 690-700(1939). 



412 C. B. Knodt, J. C. Shaw, and G. C. White, /. Dairy Sci., 25, 851-860 (1942). 



41^ B. Carlstrom, K. Myrback, N. Holmin, and A. Larsson, Skand. Vet. Tidskr., 29, 

 403-444, 589-597 (1939); Ahst. Vet. Bull, 11, 470-472 (1941); Acta Med. Scand., 102, 

 175-213 (1939). 



