Brain Insulin Sensitivity refers to the capacity of neurons and glial cells within the central nervous system to appropriately respond to the binding of insulin, a key metabolic hormone. Optimal sensitivity is vital for regulating energy homeostasis, modulating appetite, and supporting cognitive function, including memory and learning processes. Impaired brain insulin signaling, known as brain insulin resistance, is clinically implicated in neurodegenerative conditions and metabolic disorders. Maintaining this sensitivity is a crucial component of metabolic and cognitive health.
Origin
The recognition of insulin’s role beyond peripheral glucose regulation, extending into the central nervous system, is a relatively recent development in neuroendocrinology. The concept emerged as research demonstrated the presence of insulin receptors throughout the brain, particularly in the hypothalamus and hippocampus. This expanded understanding shifted the focus from the pancreas-periphery axis to the intricate brain-metabolism connection.
Mechanism
Insulin, transported across the blood-brain barrier, binds to specific insulin receptors on neuronal and glial cell surfaces, initiating intracellular signaling cascades. This binding facilitates the uptake of glucose, modulates the release of neurotransmitters, and influences gene expression related to synaptic plasticity and survival. Insulin resistance disrupts this intricate signaling, leading to impaired glucose utilization and increased neuroinflammation within the brain parenchyma.
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