When people with normal insulin sensitivity consume glucose, their sympathetic nervous system becomes more active; in people with insulin resistance, the same glucose intake does not produce this...
Mechanism
Synthesis from 3 studies
When you eat sugar, your body releases insulin, which tells your brain to turn on the stress response in your muscles. If your brain is sensitive to insulin, this works well. If you're resistant to insulin, your brain doesn't hear the signal properly, so the stress response stays weak—even when...
Most probable mechanism
When sugar is consumed, the body releases insulin, which signals the brain to activate the fight-or-flight system, increasing nerve activity in muscles. In people who respond well to insulin, this signal works strongly. In people with insulin resistance, the brain doesn't respond properly to insulin, so the fight-or-flight system doesn't turn on as much, even when insulin levels are high.
Oral glucose ingestion causes blood glucose levels to rise, triggering pancreatic beta-cells to secrete insulin.
Insulin crosses the blood-brain barrier and binds to receptors on hypothalamic neurons, activating intracellular signaling pathways including PI3K and MAPK.
Activated hypothalamic neurons increase efferent sympathetic outflow to skeletal muscle vasculature, elevating muscle sympathetic nerve activity and norepinephrine release.
Chronic hyperinsulinemia and elevated body fat impair insulin signaling in hypothalamic neurons, reducing the sensitivity of the sympathetic response to insulin.
Evidence from Studies
Supporting (3)
Community contributions welcome
Blunted sympathetic neural response to oral glucose in obese subjects with the insulin-resistant metabolic syndrome.
Influence of endurance training on central sympathetic outflow to skeletal muscle in response to a mixed meal.
Muscle Sympathetic Nerve Activity in Response to Glucose Ingestion: Impact of Plasma Insulin and Body Fat
Contradicting (0)
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