The specialized field of study and clinical practice that investigates the profound and bidirectional relationship between the brain’s sensitivity to insulin and overall neurological function. This concept highlights that insulin acts as a crucial neurotrophic factor in the central nervous system, influencing neuronal energy metabolism, synaptic plasticity, and the clearance of pathological protein aggregates. Impaired brain insulin signaling is now recognized as a key molecular component of age-related cognitive decline.
Origin
This intersectional term emerged from the convergence of endocrinology, metabolism, and neuroscience, particularly after research definitively revealed that the brain expresses insulin receptors and utilizes insulin signaling for critical, non-metabolic functions. The clinical term emphasizes the neurological consequences of peripheral metabolic dysfunction, recognizing the brain as a highly metabolically active and uniquely insulin-responsive organ.
Mechanism
Insulin binding to neuronal receptors activates intracellular signaling pathways that promote efficient glucose uptake for energy, regulate the release of various neurotransmitters, and support synaptic maintenance and growth. Enhanced insulin sensitivity in the brain facilitates efficient glucose utilization by both neurons and glia, supporting high-demand cognitive processes like memory formation. Furthermore, proper insulin signaling is essential for the hypothalamic regulation of peripheral energy balance and precise appetite control.
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