Key result
Attenuating rodent hippocampal LPL increases weight gain via decreased energy expenditure, preventable by inhibiting ceramide synthesis.
Hippocampal lipid sensing via lipoprotein lipase regulates energy homeostasis through de novo ceramide synthesis in rodents.
Rodent findings warrant no clinical change in obesity management; leaves open hippocampal ceramide pathways as human energy-balance targets.
Brain lipid sensing is necessary to regulate energy balance. Lipoprotein lipase (LPL) may play a role in this process. We tested if hippocampal LPL regulated energy homeostasis in rodents by specifically attenuating LPL activity in the hippocampus of rats and mice, either by infusing a pharmacological inhibitor (tyloxapol), or using a genetic approach (adeno-associated virus expressing Cre-GFP injected into Lpl (lox/lox) mice). Decreased LPL activity by either method led to increased body weight gain due to decreased locomotor activity and energy expenditure, concomitant with increased parasympathetic tone (unchanged food intake). Decreased LPL activity in both models was associated with increased de novo ceramide synthesis and neurogenesis in the hippocampus, while intrahippocampal infusion of de novo ceramide synthesis inhibitor myriocin completely prevented body weight gain. We conclude that hippocampal lipid sensing might represent a core mechanism for energy homeostasis regulation through de novo ceramide synthesis.
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Picard et al. (2013) studied Energy balance regulation. Attenuation of hippocampal LPL activity (pharmacological or genetic) was evaluated on Body weight gain and energy expenditure. Attenuating hippocampal LPL activity in rodents increased body weight gain due to decreased energy expenditure, a process prevented by inhibiting de novo ceramide synthesis.
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