Brain and Hepatic Glucose Utilization in Malarial Infection Does Not Depend on Cerebral Symptoms of the Disease

Soumita Ghosh,Haripalsingh M Sonawat,Arjun Sengupta,Shobhona Sharma

doi:10.1155/2019/3542393

Abstract

Cerebral malaria causes several deaths every year. Global metabolic alteration, specifically hypoglycemia and lactic acidosis are hallmarks of severe malaria. Glucose being the major fuel source for the brain, it is important to understand cerebral glucose utilization in the host during cerebral complications of the disease that may have a significant role in cerebral pathogenesis. We have used13C NMR spectroscopy to understand glucose utilization in the brain and liver of mice with cerebral malaria (CM), noncerebral malaria (NCM), and in control mice. Animals were challenged with intravenous glucose bolus followed by metabolic profiling of brain and liver extracts. Our result suggests a differential glucose utilization in the malaria group with respect to that of controls, while no difference between CM and NCM.

Highlights

Malaria is a global threat that is caused by intraerythrocytic stages of parasites of Plasmodium sp. [1]. e parasitized RBCs consume more glucose than the normal RBCs [2]. e rate of glucose utilization by these cells is higher than the normal RBCs [3, 4]
Out of 15 mice, 14 mice survived till day 9, while 1 mouse died during experiment. 7 mice developed cerebral malaria (CM) symptoms and exhibited rectal temperature
The parasite used in that study was P. berghei K173 for NCM. us, this study suggests that glucose utilization is dependent on the nature of parasites used for the study

Summary

Introduction

Malaria is a global threat that is caused by intraerythrocytic stages of parasites of Plasmodium sp. [1]. e parasitized RBCs consume more glucose than the normal RBCs [2]. e rate of glucose utilization by these cells is higher than the normal RBCs [3, 4]. Intraerythrocytic Plasmodium parasites lack gluconeogenic enzyme, fructose 1,6 biphosphatase [5] and glycogenolytic enzymes [6], relying on host RBCs to meet for glucose requirements [7]. Both glycolysis and TCA cycle operate in Plasmodium sp. Occurrence of pathophysiological features such as hypoglycemia and lactic-acidosis appears to be a function of disease severity and not cerebral complications [12,13,14,15,16,17] It is unknown if glucose utilization in a major metabolic tissue such as liver and brain operate di erentially under CM and NCM conditions. While such approaches are useful to delineate biomarkers and ngerprints of the tissues under certain perturbed conditions, they do not provide speci c pathway level

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Conclusion