Abstract
Investigation of glucose utilization during an infection is central to the study of energy metabolism. The heavy utilization of glucose by the malaria parasite, and the consequences of this process, have been investigated extensively. However, host glucose utilization during early infection has not been explored to date. In a first attempt, this article investigates the changes in the host glucose utilization in Balb/c mice infected with Plasmodium berghei ANKA using 13C-labeled glucose infusion followed by NMR spectroscopy. The results suggested significant alterations of liver, brain and red blood cell (RBC) glucose utilization during early infection when the parasitemia was <1%. At the pathway level, we observed a decrease in the shunt metabolite 2,3-bisphosphoglycerate in the RBCs. Glycolysis and pathways associated with it, along with fatty acid unsaturation, were altered in the liver. Significant changes were observed in the central carbon metabolic pathways in the brain. These results have implications in understanding the host physiology during early infection and pave the way for detailed flux analysis of the proposed perturbed pathways.
Highlights
Alteration of the metabolic network during severe infection by malarial parasites has long been known
In red blood cell (RBC) cultures at ~5% parasitemia, significant alterations in glucose utilization have been observed [14,27], and it was of interest to study whether glucose utilization will be affected in the RBCs, liver, and brain of the host during this early stage of malarial infection
NMR spectroscopy was performed on the hydrophobic and hydrophilic extracts of the liver, brain, and RBCs to assess the labeled metabolite pool after 30 min of injection of the labeled glucose
Summary
Alteration of the metabolic network during severe infection by malarial parasites has long been known. This has been attributed to the different tissues affected by the parasite [1,2]. In severe cases of Plasmodium falciparum infection, the parasitized red blood cells exhibit sequestration in the blood vessels. This, in turn, affects the microvasculature of several tissue types, perturbing the physiology of tissues/organs such as the liver, heart, kidney, lungs, adipose tissue, retina, etc. As the disease approaches its late stage, the inflammatory immune responses generated by the infection lead to severe complications such as liver damage, renal malfunction, cerebral malaria, hypoglycemia, and acidosis, which are often causes of death [6,7,8]
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