1950
DOI: 10.1172/jci102293
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The Metabolism of Glucose and Electrolytes in Diabetic Acidosis 1

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1951
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Cited by 79 publications
(25 citation statements)
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References 34 publications
(39 reference statements)
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“…This does not, of course, imply that there is no intrinsic tubular mechanism for sodium transport which may be influenced by the character and flow of tubular urine, as has been pointed out (22,24). However, such observations as the failure of a sulfate diuresis to sweep out sodium chloride (25,26), the variable response to urea loads (1,2,6,23), and the cutback in sodium excretion in some diabetic patients despite continued massive glycosuria (18,27,28), suggest that the osmotic influence of the injected solute within the renal tubule may be only one of several determinants. This view is, on the whole, consonant with that expressed in greater detail by Wolf (29).…”
Section: Methodsmentioning
confidence: 97%
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“…This does not, of course, imply that there is no intrinsic tubular mechanism for sodium transport which may be influenced by the character and flow of tubular urine, as has been pointed out (22,24). However, such observations as the failure of a sulfate diuresis to sweep out sodium chloride (25,26), the variable response to urea loads (1,2,6,23), and the cutback in sodium excretion in some diabetic patients despite continued massive glycosuria (18,27,28), suggest that the osmotic influence of the injected solute within the renal tubule may be only one of several determinants. This view is, on the whole, consonant with that expressed in greater detail by Wolf (29).…”
Section: Methodsmentioning
confidence: 97%
“…Moreover, antecedent saltfree diets do not, in normal subjects, prevent the diuresis of salt (17). And finally, marked augmentation of salt excretion is observed during diabetic acidosis when analogous glucose loads are present in patients who are free of edema, but whose intake of salt has necessarily been curtailed (18). Nevertheless, the data suggest that the renal response to administered glucose is not necessarily a function of the filtered glucose or sodium, but varies with those influences in the internal environment which condition tubular activity (19,20).…”
Section: Methodsmentioning
confidence: 99%
“…The derangements of body water and electrolytes in severe diabetic ketosis have been reviewed by several authors (7,21,(23)(24)(25). As a result of hyperglycemia and glycosuria, hyperventilation, and the vomiting which frequently occurs in diabetic ketoacidosis, there is usually a loss of large quantities of intracellular and extracellular water and electrolytes.…”
Section: Discussionmentioning
confidence: 99%
“…Up to the present, it has been recommended because none better was available. Glucose administered early in the course of treatment of diabetic ketosis either increases the blood glucose or delays its return to normal (21,26). The data presented here show that fructose disappears from the blood, even in severe diabetic ketosis, and that the blood total hexose decreases if adequate amounts of insulin are given.…”
Section: Discussionmentioning
confidence: 99%
“…A gain in extracellular glucose content, without any change in body water or monovalent cations, causes hypertonicity [9]. An increase in serum glucose concentration leads to osmotic transfer of intracellular water into the extracellular compartment resulting in dilution of extracellular solutes and hyponatremia [16]. An approximation of serum tonicity at hyperglycemia is provided by formula 1 in Table 2 [17].…”
Section: Changes In Serum Tonicity In Hyperglycemic Syndromes From Gamentioning
confidence: 99%