Tóm tắt
Adult desert locusts were experimentally infected with 50 Mermis nigrescens ova and changes in the fat body carbohydrate levels and glycogen phosphorylase activities recorded. At both 2 and 3 weeks after infection, the parasitism caused a significant reduction in the level of glycogen and non-glycogen carbohydrates in the host fat body, together with a progressive depletion of active and inactive glycogen phosphorylases. By feeding extensively upon the blood carbohydrates of the host, the developing nematode deprives the fat body of carbohydrates and thereby effects a reduction in glycogenesis by the host fat body. Increased catabolism (and (or) decreased anabolism) of the fat body phosphorylases, together with a possible suppression of the host "hyperglycaemic factor" by the nematode, prevent further glycogenolysis by the fat bodies of mermithid-infected locusts and allow a low, constant level of fat body glycogen to be maintained in these insects.
