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This manuscript elucidates the intricate roles of lactate in Diabetic Cognitive Dysfunction (DCD), extending beyond its conventional role as an energy substrate. The investigation centers on the participation of lactate in energy metabolism and epigenetic modulation, with a particular emphasis on its influence on cognitive faculties through histone lactylation. The discourse scrutinizes lactate's part in the metabolic equilibrium of the central nervous system, encompassing its fluctuating concentrations under various conditions and its pivotal function within the Astrocyte-Neuron Lactate Shuttle (ANLS) mechanism as an energy conduit. The involvement of lactate in DCD is multilayered, encompassing metabolic pathways, cellular signaling cascades, and the regulation of gene expression. Dysregulation in lactate metabolism and the histone lactylation process may modulate neuronal functionality by impacting genes integral to neuroplasticity and cognitive capabilities. These revelations offer novel insights into the molecular underpinnings of DCD and lay the groundwork for the discovery of potential therapeutic targets. Subsequent scholarly endeavors are poised to dissect the nuanced mechanisms by which lactate and its lactylation exert influence in DCD, pinpointing the critical genes modulated by lactylation and assessing their ramifications on neuronal function and signal transduction pathways. Given the intricate regulatory dynamics of lactate, contingent upon concentration, temporal factors, and disease etiology, a more profound elucidation of lactate's role in DCD necessitates an augmented cadre of animal experimentation and clinical observational research. Such investigative pursuits are anticipated to yield innovative approaches and methodologies for the comprehensive management of DCD, spanning prevention, diagnosis, and therapeutic intervention.
Yin et al. (Wed,) studied this question.