Malaria Pathophysiology as a Syndrome: Focus on Glucose Homeostasis in Severe Malaria and Phytotherapeutics Management of the Disease

Abstract

Severe malaria presents with varied pathophysiological manifestations to include derangement in glucose homeostasis. The changes in glucose management by the infected human host emanate from both Plasmodium parasitic and host factors and/or influences which are aimed at creating a proliferative advantage to the parasite. This also includes morphological changes that that take place to both infected and uninfected cells as structural alterations occur on the cell membranes to allow for increased nutrients (glucose) transportation into the cells. Without the availability, effective and efficient intervention there is a high cost incurred by the human host. Hyperglycaemia, hypoglycaemia and hyperinsulinemia are critical aspects displayed in severe malaria. Conventional treatment to malaria renders itself hostile to the host with negative glucose metabolism changes experiences in the young, pregnant women and malaria naïve individuals. In malaria, therefore, host effects, parasite imperatives and treatment regimens play a pivotal role in the return to wellness of the patient. Phytotherapeutics are emerging as treatment alternatives that ameliorate glucose homeostasis alternations as well as combat malaria parasitaemia. The phytochemicals e.g. triterpenes, have been shown to alleviate the "disease" and "parasitic" aspects of malaria pointing at key aspects in ameliorating malaria glucose homeostasis fallings-out that are experienced in malaria.

Malaria: biochemical, physiological, diagnostic, and therapeutic updates

“…The metabolic modifications brought on by parasites that prevent gluconeogenesis: Infection with P. falciparum causes the release of cytokines such as tumor necrosis factor (TNF), interleukin (IL)-1, and 6, which block the activity of phosphoenolpyruvate carboxykinase, a crucial enzyme in the gluconeogenetic pathway ( Mavondo et al, 2019 ).…”

“…Malaria-related increases in IL-1 and IL-6 release encourage islet cell hyperplasia resulting in an unregulated insulin response and subsequent reduction of the blood glucose level ( Mavondo et al, 2019 ).…”