Activation of fluoroacetate by neoplastic and normal pituitary tissue.
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The opinion is incorrect that the monofluor carbon-induced hyperglucosaemia which in literature is cited under the term fluor acetate diabetes is caused by insulin deficiency due to lesion of the pancreatic beta-cells. The cause of the fluor acetate diabetes is a disturbance of the glucose degradation by inhibition of the enzyme phosphofructokinase. Insulin applications have no causal influence on the monofluor carbon intoxications and no symptomatic influence on the fluor acetate diabetes.
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