The toxic potential of widely used commercial-grade organophosphorus insecticides namely, fenitrothion and ethion, as a function of gycogen metabolism of hemolymph and fat body on days 1, 3, 5, and 7 of the fifth-instar silkworm, Bombyx mori were studied. Results showed that both lethal and sublethal doses of fenitrothion and ethion registered significant depletion in fat body glycogen reserves followed by concomitant increases in fat body phosphorylase and trehalase activities. Increase in glycogen phosphorylase activity and decrease in glycogen content indicated increased glycogenolysis at tissue level. Increase in trehalase activity may be attributed to the failure of homeostatic mechanism in silkworms on exposure to insecticides. In contrast, both insecticides produced a significant hyper and hypo-trehalosemia, hyper and hypo-glycaemia in hemolymph, and fat body, respectively, suggesting mobilization of trehalose and glucose from fat body to hemolymph to counteract the induced insecticides toxicity. The magnitude of these changes increased with time on exposure (1<3<5<7). These changes clearly indicated that there was a breakdown of homeostatic mechanism coupled with glycogenolysis to meet the required energy demands of the silkworms under insecticides toxicity. Food consumption and faeces defecated during the fifth-instar decreased significantly at lethal dose, while it increased marginally at sublethal doses of fenitrothion and ethion. The potential effects of fenitrothion and ethion on glycogen metabolism of hemolymph and fat body of the silkworms were dose dependent. These effects were more pronounced on exposure to lethal dose than sublethal dose of both insecticides and in general, the changes induced by ethion were more striking than those caused by fenitrothion.