KBs (
ketone bodies), i.e.,
acetoacetate,
acetone, and (R)-3-Hydroxybutanoate, constitute the intermediate products of the incomplete oxidative degradation of
fatty acids. These KBs are used as a source of energy in the hosts' brain, skeletal muscles, and heart. Additionally, they regulate
inflammation and oxidative stress of the host by acting as signaling mediators.
Parasitic infection is known to result in abnormal physiological and biochemical metabolism,
ketoacidosis, and other damage to the host. In this study, we investigated the effects of Trypanosoma evansi and Toxoplasma gondii on
ketone body metabolism in mice, as well as the KB levels in the brain, liver, and peripheral blood. T. gondii was found to significantly increase the KB levels, resulting in
ketonemia; T. evansi was found to stabilize KB levels in mice. Further investigations showed that T. evansi downregulated the expression of genes encoding
enzymes involved in KBs synthesizing pathway and enhanced KBs synthesizing to eliminate
ketonemia. Conversely, T. gondii significantly increased the expression of genes encoding
enzymes involved in KBs synthesizing pathway and decreased KBs metabolism pathway ones and resulting in increased KBs levels in peripheral blood, culminating in
ketonemia. These findings elucidate the differences in the KBs metabolism resulting from
infection with T. evansi and T. gondii.