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S. SOSKIN, M.D.; M. D. ALLWEISS, M.D.; I. A. MIRSKY, M.D.

Arch Intern Med. 1935;56(5):927-934.

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

The decreased tolerance for carbohydrate which occurs in patients with acute infectious diseases has been confirmed recently by Williams and Dick,¹ whose paper contains an excellent review of the previous literature. A similar disturbance in carbohydrate metabolism has been demonstrated in experimentally induced toxemias in animals.² The "diabetic" type of dextrose tolerance curve obtained in the conditions mentioned has been interpreted by some as being due to a lack of endogenous insulin, consequent to the functional impairment of the islands of Langerhans.³ Others have ascribed the phenomenon to an interference with the action of the available insulin, whether of endogenous or of exogenous origin.⁴

The former interpretation is based on the belief that the normal dextrose tolerance curve is dependent on an increase in the circulating insulin consequent to pancreatic stimulation by the administered dextrose. We have shown recently, however, that a normal dextrose tolerance curve . . . [Full Text PDF of this Article]

Author Affiliations
CHICAGO

From the Metabolic Laboratory of the Department of Physiology, Michael Reese Hospital, and the Department of Physiology, LTniversity of Chicago.

Footnotes
This study was aided by the Max Pam Fund for Metabolic Research. Presented in preliminary form before the Central Society for Clinical Research, Nov. 2, 1934.

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