LIPEMIA 417 



elusion of the vessels unless they conibine to form large droplets. 

 Fischer doubts if the droplets ever fuse together enough to cause em- 

 bolism, supporting his contention both by experiments and clinical 

 records, but cases have been reported as fat emboUsm from diabetic 

 lipemia.'^^ 



The cause of lipemia has not yet been satisfactorily determined. 

 In alcohohsm it is commonly ascribed to a failure to burn fat, because 

 of the presence of the more readily oxidized alcohol, and the common 

 coexistence of diabetes and hpemia suggests for both a common cause; 

 i. €., lack of oxidation of fat and sugar. In corroboration may be 

 cited the occurrence of lipemia in other conditions associated with 

 defective oxidation; i. e., pneumonia, anemia,^'-* phosphorus-poisoning. 

 As we are still unfamiliar with the essential factors and steps in the 

 oxidation of fat, it would be mere speculation to attempt to explain 

 further the reason for the failure of destruction of the fat. The origin 

 of the fat in hpemia is likewise undetermined. Ebstein considers 

 that it arises partly from the food, partly from fatty degeneration of 

 the cells of the blood, the vessel-walls, and the viscera. Neisser and 

 Derlin consider it as merely food fat coming from the chyle and 

 accumulated in the blood. Fischer beheves that it is largely derived 

 from the fat depots, and that because of loss of the Hpolytic power 

 of the blood it cannot be rendered diffusible, and hence it cannot enter 

 the tissues where it is normally consumed. Sakai^" also found a low 

 lipase content in the blood and suggests that fat entering the blood is 

 unable to leave it because of defective hpolysis. Klemperer and Um- 

 ber hold that it comes from disintegration of tissue cells, but are 

 unable to determine the cells concerned. Ervin^^ attributes diabetic 

 hpemia to the glycogen deficiency of the cells, assuming that glycogen 

 acts as a protective colloid which holds the intracellular fats in 

 emulsion. 



Bloor's studies^- support strongly the view that the fats come 

 from the food, for he found hpemia only in diabetics receiving fat in 

 their food, and under fasting an existing hpemia disappears. Choles- 

 terol increases parallel with the fat, while lecithin is relatively little 

 increased. Verse^^ says that a lasting lipemia can be produced 

 by feeding rabbits mixed cholesterol and oil, but not with either of 

 these alone. In severe diabetes without hpemia the hpins are all much 

 increased in the plasma, but with the relative proportions about as in 

 normal individuals, although with a tendency for the fats to accumu- 

 late in excess. The facts that fat oxidation depends upon carbohy- 

 drate oxidation, and also that in diabetics excessive fat feeding is 



"8 Hedren, Svenska Liik. Handl., 1916 (42), 933. 



" See Boggs and Morris (Jour. Exper. Med., 1909 (11), 553), who produced 

 lipemia bv repeatedly bleeding rabbits. 

 8" Biochem. Zeit., 1914 (62), 387. 

 " Jour. Lab. Clin. Med., 1919 (5), 146. 

 " Jour. Biol. Chem., 1916 (26), 417; 1917 (31), 575. 

 83 Miinch med. Woch., 1916 (63), 1074. 



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