Abstract
Background: Gluconeogenesis is stimulated by low blood glucose to maintain the glucose level; it involves lipolysis (breaking down of triglycerides), release of cortisol, and production of glycerol which can be converted into glucose. Hypoglycemia is associated with Plasmodium infection in children. Glucose homeostasis also involves glycogenolysis. This work was designed to determine the possible evidence of gluconeogenesis in Plasmodium-infected children in relationship with the parasite density to provide the information for useful direction in the management of Plasmodium infection in children. Methods: Thirty-five (2–5 years; female – 14, male – 11) Plasmodium-infected children were recruited as test patients, while fifty (n = 50; female – 25, male – 23) age-matched children (Plasmodium-noninfected children) were recruited from the same environment as controls. Plasma cortisol and cortisol-binding globulin were measured by the ELISA; total bile acid, glycerol by spectrophotometry, glucose, and total triglycerides were measured using Cobas C111, while Plasmodium identification and density were carried out by Leishman's thin blood film technique. Results: The results obtained showed a significant increase in plasma cortisol, cortisol-binding globulin, total bile acid, and glycerol with increase in parasite density and in children with the parasite densities of 512 ± 4.0 and 1014 ± 6.0 than the control children (P
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