EXPERIMENTAL DIABETES PRODUCED BY THE ADMINISTRATION OF GLUCOSE

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Abstract
Hydropic degeneration of the [BETA]-cells of the islands of Langerhans was produced in 10 cats by intraperit, injns. of 20% glucose in 0.9% NaCl soln. Injns. were given 3 times a day for 14 to 104 days, the total daily dose varying from 50 to 420 ml. Five cats had approx. one half the pancreas removed prior to injn. The other 5 were normal. One of the normal cats was made permanently diabetic. It was sacrificed while in severe diabetic acidosis 22 days after the last injn. of glucose. Two of the partially depancreatized cats also developed persistent post-injn diabetes. A period of hyperglycemia of 9 days or more preceded the finding of hydropic degeneration. Twenty-five cats injected 3-21 days but exhibiting hyperglycemia on 8 days or less failed to develop hydropic degeneration of the islets. Many of the cats developed an unexplained syndrome of weakness, ataxia, occasionally convulsions, and death. Evidence for adrenocorticotropbic activity was sought. Adrenal wts. during glucose injns. were not significantly increased. However, the adrenal ascorbic acid and adrenal cholesterol concn. was decreased by intraperit. injns. of glucose, thus indicating some increased adrenocorticotrophic activity. The local effect of intraperit. glucose upon the pancreas was apparently minor because of the wide distribution of the hydropic islands, the absence of damage to other retroperitoneal organs and the similarity of pancreatic glucose concn. following intraperit. and intraven. glucose injns. The islet injury seems to be most clearly associated with the degree and particularly the duration of hyperglycemia. The events suggest that an excessive functional demand leads to the pathologic changes. However, hyperglycemia is so complex a situation that other mechanisms must still be considered.