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The following study is concerned with the effort to demonstrate the main factors which influence the duration of hyperglycemia after a glucose meal. More than 200 cases have been studied critically. There is extensive literature on the subject of blood sugar curves after various sorts of carbohydrate meals. In some studies standardized meals were given, in others not. Many clinicians have assigned diagnostic importance to an increased hyperglycemia following glucose ingestion.The interpretation of the value of sugar curves depends on the following factors: (1) The technic of the administration of the glucose meal; (2) the collection of blood samples; (3) the method of doing the blood sugar determination, and (4) the wide application of the test so as to learn the many factors which influence these curves.We believe it necessary, in order to support our conclusions, to discuss the first three of these points in detail. STANDARDIZED GLUCOSE

The discoverers of insulin have made fundamental observations1 on its clinical application to the treatment of diabetes. The observations may be thus summarized:Blood sugar is reduced and glycosuria disappears.Glycogen is stored in diabetic animals, and the respiratory quotients are raised, showing the burning of sugar.Ketonuria rapidly disappears, and patients in coma may be successfully restored to consciousness and life.An overdose of insulin in animals produces violent symptoms of a convulsive nature, followed by coma and death. The antidote for this state is glucose.Of the mass of invaluable physiologic data presented by the Toronto workers, these are the main facts of direct clinical bearing.Through the courtesy of Professor Shaffer of the department of biologic chemistry, insulin2 produced by his laboratory became available for clinical use, Oct. 1, 1922. The observations here recorded have been made from work on more than forty patients. Effort

In cultures, bacteria break down sugar into fatty acids, alcohol, lactic acid, methane, hydrogen and carbon dioxide. We have determined the amounts of the fatty acids occurring in human stools with various diets and under the conditions of constipation or catharsis.1Since lactic acid is produced in cultures in large amounts, this work was undertaken to answer the question whether lactic acid is present in stools in amounts comparable to those found for volatile fatty acids.The isolation of lactic acid from stools could be carried out by extracting with ether or if a suitable precipitant were found which would free the filtrate from interfering substances, the filtrate might be directly oxidized. By means of the mercuric sulphate precipitation of West,2one can obtain from stool water clear filtrates practieally free from nitrogen and almost free from interfering substances.3The filtrate from the mercury precipitation must be further treated by the usual copper sulphate and lime precipitation. Applying the method of Friedemann, Cotonio and Shaffer,3we found that the amounts of oxidizable material in such filtrates is small as shown by the fact that 100 cc. of filtrate, representing from 5 to 10 gm. of stool, require in the lactic acid apparatus less than 50 cc. of 0.01 N potassium permanganate to show a permanent excess of permanganate. As a matter of fact, there was obtained only 0.2 to 0.5 mg. of sulphite binding substance from the above mentioned amount of material.To obtain filtrates that do not give a biuret test, we found it necessary to use 2 volumes of a 30% mercuric sulphate solution in 10% sulphuric acid to one volume of stool.

Gallbladder and bile duct disease has long been recognized as a cause for pancreatitis. Judd1 says, "Cholecystitis is nearly always associated with a certain grade of hepatitis or pancreatitis, or both," and Deaver and Sweet2 say, "The most frequent forerunner of disease of the pancreas is some affection of the gallbladder or the bile passages which is frequently but not always associated with calculi." Mayo-Robson believes that there is evidence of chronic pancreatitis in 60 per cent of patients in whom operation has shown the presence of stone in the common bile duct. This being a common observation of surgeons, the association of chcolecystitis and diabetes mellitus has been sought. From a statistical standpoint, there are those who could find no relationship between the incidence of biliary tract diseases and diabetes, 3 while others are convinced that there is such a relationship.4It seemed, therefore, worth while