Thyroid Factor in Diabete Gras 



213 



103 (2063) 



The thyroid factor in diabete gras. 

 By G. A. FRIEDMAN and J. GOTTESMAN. 



[From the Department of Clinical Pathology, College of Physicians 

 and Surgeons, Columbia University, New York City.] 



The fact that diabete gras can be produced by suppressing 

 thyroid function through almost complete removal of the thyroid, 

 points to the share of thyroid deficiency in mild diabetes. This 

 assumption is strengthened by the fact that all thyroids in the 

 dogs after partial duct ligation showed marked atrophic areas 

 on microscopical examination. 



It seems then that obesity does not predispose to diabetes as it 

 is generally believed, but that obesity results from mild diabetes, 

 as in middle aged patients. If general adiposity would be the 

 predisposing factor in diabetes, one cannot see why it should af- 

 fect the Langerhans islands, leaving intact the secreting acini of 

 the pancreas. Since the external secretory apparatus must also 

 become affected by the fat deposit, symptoms or signs of a dis- 

 turbance in the digestive pancreatic apparatus must establish 

 itself in genuine diabetes. It is a fact that pancreatic acini remain 

 intact in diabetes mellitus. The clinician at least is not aware of 

 a disturbance in the latter. 



Another argument: If obesity predisposes to diabetes, a low- 

 ered glucose tolerance should frequently be found in obese per- 

 sons. Paullin 1 made glucose tolerance tests in 26 cases of obesity 

 without renal disorders. Five of these patients showed a lowered 

 sugar tolerance and two of them later actually developed gly- 

 cosuria. 



That mildness of diabetes varies directly with thyroid dysfunc- 

 tion may be concluded from the experiments of Wilder 2 and his 

 coworkers. Throughout these experiments in human diabetes the 

 glucose tolerance varied inversely with the basal metabolism. 

 The tolerance rose when the metabolic rate fell and fell when the 



1 Paullin, J. E., J. Am. Med. Assn., 1921, lxxyii, 1996. 



2 Wilder, R., Boothbv, W. M., and Beeler, C, J. Biol. Chemist., 1922, li, 311. 



