Abstract:
Malaria and diabetes continue to affect millions of people globally. Although global malaria burden is declining
gradually, that of diabetes seems to be increasing. Sub-Saharan Africa with the greatest burden of malaria is
predicted to house the greatest proportion of incidence of diabetes by 2030. This prediction though hinges on
expected increase in prevalence of obesity, the possible impact of infection in general and Plasmodium infection in
particular cannot be overlooked. This review focuses on the effect of Plasmodium infection on circulating glucose
level in humans and discusses possible mechanisms by which malaria could be linked to the pathogenesis of
type 2 diabetes mellitus (T2DM). Malaria causes inflammation and oxidative stress which could lead to insulin
resistance and eventually impact negatively on glucose homeostasis. The nature of malaria-induced inflammation
and oxidative stress appears similar to that observed in diabetes and obesity. At the pharmacological level,
anti-malarials and anti-diabetics can be synthesized from a common ’biguanides’ with possible cross reactivities.
At the molecular level, artimisins, a potent class of antimalarials, appear to have capability to transform α-cells
in the islets into insulin-secreting β -cells through enhanced gamma amino-butyric acid (GABA) signaling, to
improve glucose homeostasis in different models of mammalian cells. Putting together, these various levels of
evidence suggest a greater potential for a link between malaria and diabetes. However, more research work is
needed for improved understanding of the mechanistic link of malaria to T2DM to properly define the contribution
of malaria to the predicted increase in incidence of T2DM in malaria-endemic regions.
