The occurrence of diabetes in connection with acute inflammations of the liver and passive hepatic congestion secondary to advanced cardiac disease favours the hypothesis that glycosuria may be developed by an increase in the amount of blood flowing through the liver, which is thereby stimulated to an active conversion of its glycogen into sugar, or else the blood passes so rapidly through the liver that the sugar absorbed from the food by the branches of the portal vein does not have time to be converted into glycogen, but goes through the liver into the general circulation unaltered. Thus, whether the glycogenic function be increased or diminished in glycosuria, either condition would demand altered activity of the portal circulation.