Trypanosoma brucei brucei Induced Hypoglycaemia Depletes Hepatic Glycogen and Altered Hepatic Hexokinase and Glucokinase Activities in Infected Mice

Abstract

Little progress has been made in understanding the effect of Trypanosoma brucei brucei infection that was allowed to run its course without treatment on human and animal carbohydrate metabolism even though most of the symptoms associated with the disease can be clearly linked with interference with host energy generation. The present study therefore assessed the course of untreated Trypanosoma brucei brucei infection on hepatic glycogen, hepatic hexokinase and glucokinase activities. Mice were grouped into two: control and infected group. Trypanosomiasis was induced by intraperitoneal inoculation of 1 × 104 parasites/mice in 0.3ml of phosphate saline glucose. The infection was allowed to run its course until the first mortality was recorded with all the mice showing chronic symptoms of the second stage of the disease before the research was terminated. Blood and liver samples were collected from the mice in each group for the assessment of hepatic glycogen and total protein, hepatic hexokinase and glucokinase activities, liver biomarkers, blood glucose and protein with packed cell volume. The infection resulted in decrease in blood glucose, hepatic glycogen, liver protein, PCV, hepatic hexokinase and glucokinase activities, but increase in serum total protein and liver biomarkers. Trypanosomiasis negatively affects hepatic integrity, resulting in the depletion of hepatic glycogen content and suppression of both hepatic hexokinase and glucokinase activities. The suppression of hepatic hexokinase and glucokinase activities suggested that trypanosomiasis affected the oxidation of glucose and host energy generation via glycolysis. This probably denied the host of the needed energy which is likely the reason for early death in untreated African trypanosomiasis.