Experimental studies on the liver injury in diabetes mellitus

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The following experimental studies were undertaken to investigate on alloxan induced diabetic rats how recovery or progression of the liver injury might be influenced by the addition of certain hepatotoxic agents to the diabetic animals. 1) Seven alloxan diabetic male rats were maintained for 9N12 months on basal diet containing casein of 18 percent, and no cirrhotic or fibrotic changes were observed histologically in the liver. 2) Carbon tetrachloride was given to alloxan diabetic and normal rats to produce liver injuries. Rats were given intraperi toneal injections of carbon tetrachloride as a 10 percent solution in olive oil. In acute exper iments (a large single dose of 0.5 ml per 100g weight), the serum transaminase activities were measured as an index of recovery of the liver injury, and the results clearly showed the prolongation of recovery of serum transaminase activities in diabetic groups. In long-term exper iments (0.3 ml per 100 g weight bi-weekly, totalling 20 times), alloxan diabetic female rats showed histologically the finding of liver cirrhosis or liver fibrosis in all 6 cases, while the control rats showed only the findings of liver necrosis and fat ty deposits in 6 out of 7 rats. 3) Ethylalcohol was administered perorally to alloxan diabetic and normal male rats. In acute experiments (by s tomach tube, a large single dose of 0.75 ml per 100 g weight), the serum transaminase activities were measured af ter 12, 24, and 48 hours respectively, and the elevation of serum transaminase activities were not observed. In prolonged alcohol-feeding exper iments (maintained for over 100 days by basal diet mixed with alcohol), the elevation of serum transaminase activities were also not observed, and, in addition, no difference was observed between both rats in the contents of cholesterol, tr iglyceride and phospholipid of the liver. 4) The above-mentioned experimental results suggest that diabetes mellitus alone can scarcely induce liver cirrhosis and that if the former may induce the latter, the addition of some factors producing liver injury may be needed. But we could not obtain the result as to alcohol that alcohol was a factor producing or exacerbat ing the li~r injury in the diabetic rats.