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

PURPOSE: 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. METHODS: Mice were grouped into two: control and infected group. Trypanosomiasis was induced by intraperitoneal inoculation of 1 × 104 parasites/mice in 0.3 ml 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. RESULTS: 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. CONCLUSION: 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.

Comprehensive analysis of oral administration of Vitamin E on the early stage of Trypanosoma brucei brucei infection.

Reinforcement of the body with exogenous antioxidants have been shown to mitigate the negative effects of African trypanosomiasis on the host and contribute greatly to their survival. This study was therefore conducted to evaluate the effects of oral administration of Vitamin E on the early stage of Trypanosoma brucei brucei infection. To achieve this, parasite free healthy rats were acclimatized for 2 weeks before they were divided into three groups. Two of the groups were infected by intraperitoneal inoculation of 1 × 104 parasites/rat and monitored for the presence of Trypanosoma brucei brucei. Blood samples were collected from the infected rats from the second day post infection to detect the presence of parasites. Vitamin E treatment started day 4 post infection at the onset of parasitaemia. Parasites were monitored till the end of the study. The blood glucose level was determined using a glucometer; the lipid profile, liver and kidney biomarkers, electrolytes and protein were determined by colorimetric method using commercial kits. Haematological parameters were analysed using a sysmex haematology analyser. The results of this study showed that the infection adversely affected the biomarkers examined showing its negative effect on liver, kidney, haematological parameters and host electrolyte balance. Treatments with Vitamin E was however able to mitigate the negative effect of this infection. In conclusion, the treatment was able to ameliorate the anaemia and organ damage caused by Trypanosoma brucei brucei, extend the life span of the treated rats and greatly delay the time taken to get to the second stage of the infection.