The hereditary obese-hyperglycemic syndrome is a Mendelian recessive condition which has been intensively studied in the last few years. In particular, mice with this syndrome are grossly obese (weights up to 115 gm. have been recorded), hypercholesterolemic, show high blood glucose levels generally further increased by the administration of growth hormone, 1 an increased lipogenesis even when fasted, 2 increased glycogen turnover, 3 increased liver phosphorylase,* and a number of other nutritional, endocrine and behavioral idiosyncrasies. 5 Of particular interest from the etiological point of view is the fact that the islets of Langerhans are grossly hypertrophied, 6 " 8 that the insulin content of the pancreas is increased, 7 that the insulin-like activity of their serum is greater than that of the nonobese animals, 9 that diethyldithiocarbamate, which Kadota and Midorikawa found to be alphacytotoxic, 10 decreases blood sugar and eliminates the hyperglycemic reaction to growth hormone 11 and that the pancreatic glucagon content appears increased after growth hormone administration. 13 It has also been found that carbutamide did not correct the defects in carbohydrate metabolism 13 and in fat metabolism 14 found in these animals.It is obviously essential to the understanding of the syndrome to gather as accurate histologic data as possible. The lack of effect of carbutamide in a form of diabetes which is not due to a deficiency of insulin is of relevance to the formulation of a hypothesis concerning the mode of action of this substance and treated mice appeared worth including in this study. MATERIALS AND METHODSTwenty-one obese-hyperglycemic mice and twentyfour sibling controls were studied. The animals were either two or four months old at the beginning of the experiment (four or six months old when sacrificed).

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