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ROBERT L. NIELSEN, M.D.; HEIDI E. SWANSON, Ph.D.; DONALD C. TANNER, M.D.; ROBERT H. WILLIAMS, M.D.; MAUREEN O'CONNELL, B.S.

AMA Arch Intern Med. 1958;101(2):211-215.

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

It has long been known that some diguanidine compounds, such as Synthalin A and B, produce hypoglycemia in man ¹ and in laboratory animals.²,³ In a systematic search for orally effective hypoglycemic compounds, Ungar et al.⁴ found that phenethylformamidinyliminourea, a condensed diguanidine (or a diguanide), was effective. The compound has been called DBI by others,⁴,⁶ but since the diguanide group is presumably essential for the hypoglycemic action, we have used the term phenethyldiguanide (PEDG) (Fig. 1).

These studies are a part of our efforts to define and elucidate the actions of this compound. The effects of PEDG on blood sugar in intact and eviscerated animals, on the hepatic glucose output, and on the degradation of insulin I¹³¹ were investigated.

Experimental Studies

Synthalin A, even in very small doses, is toxic and produces histological changes in the liver, kidneys, and pancreas.³ A study of the toxicity of PEDG was done because . . . [Full Text PDF of this Article]

Author Affiliations
Seattle

From the University of Washington School of Medicine, Department of Medicine.

Footnotes
Submitted for publication Sept. 30, 1957.

Presented at the annual meeting of the Endocrine Society, June 1, 1957, New York.

Aided in part by grants from the Atomic Energy Commission, the U. S. Public Health Service, and the U. S. Vitamin Corporation.

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