Fig. 5: Inhibition of lipolysis in the brain induces torpor.
From: Triglycerides are an important fuel reserve for synapse function in the brain
a, Schematic representation of the experimental paradigm illustrating induction of torpor following intraperitoneal injection of etomoxir or KLH45. Environmentally acclimated (≥3 days) and individually housed mice were placed on food restriction for 3 h. The mice were injected with etomoxir or KLH45 and returned to their cages without food. Core body temperature (Tb) was measured at regular intervals up to 3 h. b, Tb at 0, 0.5, 1 and 3 h after etomoxir injection. Mice injected with vehicle for etomoxir (PBS) were used as controls. Data are presented as means; error bars, s.e.m. P values (†P = 0.027; #P = 0.0129; *P = 0.0216) were determined using an unpaired samples two-tailed t-test for n = 3 in both control (PBS) and etomoxir conditions. c, Tb at 0, 0.5, 1 and 3 h after KLH45 injection. Mice injected with vehicle for KLH45 (18:1:1 saline/ethanol/polyethylene glycol monooleyl ether) were used as controls. Data are presented as means; error bars, s.e.m. P value (*P = 0.0187) was determined using an unpaired samples two-tailed t-test for n = 3 in both control (vehicle) and KLH45 conditions. Mice injected with etomoxir or KLH45 (red) exhibited a significant drop in their core body temperature compared to controls (blue). d, Schematic summary of the mechanism of DDHD2-dependent FA fuelling of synaptic function to prevent a torpor-like state. Asterisk (*), hash (#) and dagger (†) symbols are used to distinguish between different groups of statistically significant comparison. Created in BioRender.com.
