A clinical treatise on diabetes mellitus / by Marcel Labbé ; translated ... and edited by Charles Greene Cumston.

  • Marcel Labbé
Date:
1922
Catalogue details

Licence: Public Domain Mark

Credit: A clinical treatise on diabetes mellitus / by Marcel Labbé ; translated ... and edited by Charles Greene Cumston. Source: Wellcome Collection.

    16/400 page 4
    In the pathologic state things are different. As soon as a disturbance arises in the glycoregulator apparatus, the result of a morbid change in one of the organs composing this system, the CH metabolism no longer takes place with regu¬ larity, glucose is not carbonized completely by the tissues, and consequently accumulates in the blood and tissues. The syndrome ' of hyperglycemia and hyperglycistia ensues, and diabetes develops. From the physiopathological view-point, diabetes is charac¬ terized by the absence of combustion of the totality or a portion of the CH introduced into the body with the food or furnished by the organism itself. This theory of insufficiency of CH combustion, maintained by Bouchard and the majority of modern writers, can alone explain diabetes. The theory of superproduction of sugar cannot explain it, because the normal organism appears capable of burning an almost indefinite quantity of CH. But a more penetrating physiological analysis must be made in order to exactly understand the functional disturbance characterizing diabetes. The researches that I undertook with H. Labbé on the nutrition of diabetics led me to distinguish two great categories of diabetes: 1. Diabetes without denutrition, which is by far the most frequent. This corresponds to the fat diabetes of the older writers and the arthritic diabetes of the classic writers. The nitrogenous equilibrium is preserved in these cases, therefore there is no denutrition. The physiological dis¬ turbance only involves metabolism of the CH introduced with food; the patient can tolerate a certain amount; the glycosuria originates from the CH in the food. 2. Diabetes with denutrition is less common, but the process is more serious, This form corresponds to the thin diabetes of the older writers and to pancreatic diabetes of the classic authors. In this case the nitrogenous equilibrium is broken, the patient destroys his own tissues, and therefore emaciates. He cannot tolerate even the minutest quantity of CH, and even when these have been cut out of his diet the glycosuria never¬ theless continues. It is always abundant and its origin com-
    digitised image 1
    digitised image 2
    digitised image 3