Abstract
Murlin and Kramer 1 have shown that alkali administered to depancreatized dogs reduces the glycosuria, often lowers the blood sugar, and, especially in partially depancreatized animals, assists in the combustion of glucose. It has been held generally that alkali administered to diabetic patients does not influence the glycosuria 2 or hyperglycemia. A critical study of several cases kept under perfect dietary control in the metabolism ward of the Sage Institute of Pathology in Bellevue Hospital during the past summer seems to show, however, that alkali (1 per cent. Na2CO3) administered by duodenal tube often reduces the glycosuria very materially and may likewise affect the hyperglycemia.
A preliminary study of the blood sugar and carbon dioxide combining power of the whole blood in six patients with diabetes and several normal persons exhibits a striking inverse relationship which is almost proportional.
Two patients among the eight studied exhibited features of special interest. One (Frank B.) had a normal blood sugar throughout but excreted from 25 to 39 gm. of sugar, regardless of the amount eaten. He is probably a case of renal glycosuria. The other (Harry H.) was sugar-free for two weeks on 15, 30 and 50 gm. carbohydrate but had no pancreatic digestion. When given pancreatic digestion with lactopeptine 3 (New York Pharmacal Ass'n) or Merck's pancreatin he excreted about 60 out of 100 gm. carbohydrate fed. Proof that such digestive powders do survive the stomach was established by recovery of them from the intestine by means of the duodenal tube. The utilization of carbohydrate under these circumstances was apparently increased by giving 0.3 per cent, sodium carbonate by duodenal tube.
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