448 V. BLOOD LIPIDS 



cases. He believes that hyperglycemia is a more sensitive index of the 

 severity of diabetes than is the hyperlipemia. 



(&') The Cause of the Hyperlipemia. — A number of suggestions have 

 been advanced as to the cause of the hyperlipemia which occurs in diabetes. 

 Such leaders in the field of diabetes research as Allen et a/., 598 Joslin and 

 associates, 599 and Bloor 196 concluded that some defect in transportation, 

 disposal, or metabolism of fat accounts for the hyperlipemia in diabetes. 

 For this reason, the use of appreciable amounts of fat in diabetic diets has 

 been discouraged. 



However, Blix, 255 Blatherwick, 600 Marsh and Waller, 601 and Freyberg 

 et aZ. 602 found that hyperlipemia in diabetes bears little relation to the level 

 of dietary fat. In fact, Bloor, Gillette, and James 225 noted that a fall in 

 the level of blood lipids frequently obtained in their diabetic dogs when fat 

 was fed. In the pre-insulin days, Newburgh and Marsh 603-605 employed 

 diets containing as much as 200 g. of fat daily, with beneficial effects, in 

 cases of diabetes. When the patients improved on these diets, blood fats 

 decreased. 600,601 According to Peters and Van Slyke, 202 when a diabetic 

 is enabled by diet or by insulin to utilize an adequate amount of carbohy- 

 drate, the metabolism of the lipids is normal, and the pattern and concen- 

 tration of the serum lipids are also normal. 606 ' 607 



In spite of the several reports that dietary fat is of little importance in 

 the causation of diabetic hyperlipemia, Cochrane, Michaels, and Kinsell 608 

 found that the substitution of vegetable fat for "animal fat" in the high- 

 protein, high-fat diabetic diets resulted in a major fall in the levels of plasma 

 cholesterol and phospholipids. It is suggested that this reduction in hy- 

 perlipemia is not to be explained merely by the absence of dietary choles- 

 terol. Felch and Dotti 609 reported that inositol is an effective agent in 



598 F. M. Allen, E. Stillman, and R. Fitz, Total Dietary Regulation in the Treatment of 

 Diabetes, Monograph, Rockefeller Inst. Med. Research, New York, No. 11, October, 

 1919. 



* 99 E. P. Joslin, W. R. Bloor, and H. Gray, J. Am. Med. Assoc, 69, 375-378 (1917). 



600 N. R. Blatherwick, /. Biol. Chem., 49, 193-199 (1921). 



601 P. L. Marsh and H.'G. Waller, Arch. Internal Med., 31, 63-75 (1923). 



602 R. H. Freyberg, L. H. Newburgh, and W. A. Murrill, Arch. Internal Med., 58, 589- 

 597(1936). 



603 L. H. Newburgh and P. L. Marsh, Arch. Internal Med., 26, 647-662 (1920). 



604 L. H. Newburgh and P. L. Marsh, Arch. Internal Med., 27, 699-705 (1921). 



605 L. H. Newburgh and P. L. Marsh, Arch. Internal Med., 31, 455-490 (1923). 



606 1. L. Chaikoff, F. S. Smyth, and G. E. Gibbs, J. Clin. Invest., 15, 627-631 (1936). 



607 E. B. Man and J. P. Peters, /. Clin. Invest., 14, 579-594 (1935). 



608 G. C. Cochrane, G. D. Michaels, and L. W. Kinsell, J. Clin. Nutrition, 1, 295-298 

 (1953). 



609 W. C. Felch and L. B. Dotti, Proc. Soc. Exptl. Biol. Med., 72, 376-378 (1949). 



