Suppression of carcass weight loss in cachexia in rats bearing Leydig cell tumor by the novel compound NO-1886, a lipoprotein lipase activator.

The Leydig cell tumor has been reported to produce tumor necrosis factor (TNF) and induce cachexia in rats. TNF is thought to reduce lipoprotein lipase (LPL) activity, decrease fat deposits, induce emaciation, and worsen cachexia. Therefore, we thought emaciation might be prevented and thus cachexia improved by increasing LPL activity. We administered NO-1886, a lipoprotein lipase activator, to rats bearing Leydig cell tumor and observed its effect on improving the cachexia induced by the tumor. In Leydig cell tumor-bearing rats, the emaciation progressed after tumor inoculation and the general condition worsened daily. Plasma levels of total protein, albumin, and glucose, which are biological parameters of malnutrition, were found to decrease soon after tumor inoculation in tumor-bearing rats. In contrast, rats given NO-1886 showed less malnutrition than tumor-bearing rats. LPL activity of rat adipose tissue was decreased, the weight of adipose tissue was decreased, carcass weight was reduced, and food consumption was decreased after Leydig cell tumor inoculation. NO-1886 increased adipose tissue LPL activity and suppressed the decrease in the weight of adipose tissue, carcass weight, and food consumption due to cachexia without influencing tumor growth. The present results suggest that the novel compound NO-1886 may suppress carcass weight loss in rats bearing Leydig cell tumor by suppressing the decrease in food consumption and LPL activity.