Insulin Sensitivity Brain refers to the efficiency with which neuronal tissue utilizes glucose, mediated by insulin signaling pathways within the central nervous system. Optimal sensitivity is critical for sustained cognitive energy supply and preventing neurodegenerative processes linked to chronic hyperglycemia. Impaired sensitivity, sometimes termed brain insulin resistance, directly compromises memory consolidation and plasticity. We assess this functional relationship closely in advanced metabolic evaluations.
Origin
This term connects “Insulin Sensitivity,” a core concept in metabolic endocrinology, with the “Brain,” the primary consumer of glucose energy. The origin acknowledges that the brain possesses specific insulin receptors whose function directly impacts neural signaling fidelity. It recognizes insulin’s non-metabolic, neurotrophic roles.
Mechanism
Insulin acts as a neurotrophic factor in the brain, promoting synaptic plasticity via the PI3K/Akt pathway, which is distinct from its peripheral glucose uptake role. When sensitivity is high, this pathway functions effectively, supporting learning and memory encoding. Conversely, chronic inflammation or elevated cortisol can induce insulin receptor downregulation, impeding these vital cognitive support functions.
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