Since Rosenbaum,1 in 1882, called attention to the depletion of hepatic glycogen following chloroform narcosis, arsenic or phosphorus poisoning and excessive administration of morphine, there has been adequate confirmation of the fact that a damaged liver contains little glycogen.2 Concomitant with the loss of glycogen, fatty changes appear in the liver after exposure to these hepatotoxic agents. Rosenfeld3 observed that animals fed carbohydrate are, in general, less susceptible to any drug which produces accumulations of fat in the liver. Furthermore, after such poisonings the feeding of dextrose aids recovery of the animal. Since the early reports of Whipple and Sperry,4 Opie and Alford5 and Graham6 on the resistance to chloroform or phosphorus poisoning of animals fed large amounts of carbohydrate or animals with livers containing large stores of glycogen, there have been many similar observations.7 The protective action of high carbohydrate intake has also been noted in the prevention of
SOSKIN S, HYMAN M. PHYSIOLOGIC BASIS OF INTRAVENOUS DEXTROSE THERAPY FOR DISEASES OF THE LIVER. Arch Intern Med (Chic). 1939;64(6):1265–1270. doi:10.1001/archinte.1939.00190060134009
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