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94 reviewsSUMMARYMetabolic disorders are closely linked to increased risk of cognitive decline, with Western-style high-fat diets(HFDs) emerging as key contributors. However, the underlying cellular and molecular mechanisms remainunclear. Here, we demonstrate that short-term HFD (stHFD) consumption disrupts memory processing byinducing hyperactivity in dentate gyrus (DG) cholecystokinin-expressing interneurons (CCK-INs). We identifyDG CCK-INs as glucose-inhibited neurons that become hyperactive in response to stHFD-induced reductions in DG glucose availability, coinciding with increased phosphorylation of the glycolytic enzyme pyruvatekinase M2 (PKM2). Restoring glucose availability, reducing PKM2 expression, or inhibiting PKM2 activity normalizes CCK-IN activity and rescues memory deficits. Furthermore, interventions preventing CCK-IN hyperactivity or PKM2 phosphorylation protect against long-term cognitive impairments in a diet-induced obesitymouse model. These findings reveal a previously unrecognized mechanism by which dietary metabolic stressdisrupts hippocampal function and highlight DG CCK-INs and PKM2 as promising therapeutic targets forpreventing cognitive decline associated with metabolic disorders.
