[1] In some animal models of afterload-induced heart failure greater dietary fat intake improves function. [2] Even in acute ischemia, shifting metabolism towards greater glucose has not uniformly improved outcome. [3] It is possible that excess glucose might be directed towards aberrant metabolic pathways. One such pathway is that mediated by aldose reductase (AR). In this context we and others have demonstrated that glucose flux via AR is enhanced under conditions of ischemia-reperfusion [4], [5], [6] and diabetes. [7]. This evidence concerns the gene AR and diabetes mellitus.