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JEROME W. CONN, M.D.; L. H. NEWBURGH, M.D.; MARGARET W. JOHNSTON, Ph.D.; JOHN M. SHELDON, M.D.

Arch Intern Med. 1938;62(5):765-782.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Hypoglycemia has been the outstanding and most constant result of the disturbed carbohydrate metabolism observed when severe injury of the liver has been found clinically or produced experimentally. It appears to have been established that in the normal organism the presence of the liver is necessary for the maintenance of a normal glycemic level.¹ It has been shown that the liver has at least three separate functions directly concerned with the metabolism of dextrose. These functions are (1) glycogenesis, (2) glycogenolysis and (3) the production of dextrose and the deposition of glycogen from noncarbohydrate precursors (glycogenic amino acids and glycerol fraction of fats). The balance between glycogenesis and glycogenolysis allows the liver to function as a storehouse of readily available dextrose to be delivered into the blood stream in times of need.

From these facts it is apparent that there are several possible explanations for the hypoglycemia observed in . . . [Full Text PDF of this Article]

Author Affiliations
ANN ARBOR, MICH.

From the Department of Internal Medicine, University of Michigan Medical School.

Footnotes
The expense of this study was defrayed in part by a grant from the Horace H. Rackham and Mary A. Rackham Foundation.

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