In overweight men, higher levels of the inflammatory marker IL-6 above 4 pg/mL are linked to lower self-reported hunger, and higher levels of the hormone PYY above 67.89 pg/mL are linked to an even...
Mechanism
Synthesis from 1 study
High levels of an inflammation signal and a fullness hormone together turn down the brain's hunger signals. The inflammation signal makes the brain less responsive to hunger, and the fullness hormone makes it even more responsive to feeling full. When both are high, hunger drops sharply.
Most probable mechanism
When inflammation signals rise in the blood, they reach the brain and tell the appetite center to reduce hunger. At the same time, a fullness hormone increases and strengthens this signal. Together, they shut down the brain's drive to eat, even when the body has stored excess fat.
Plasma IL-6 concentration exceeds 4 pg/mL, triggering direct signaling to hypothalamic neurons through blood-brain barrier transport or vagal afferent pathways
Elevated IL-6 activates pro-inflammatory signaling in the hypothalamus, suppressing neuropeptide Y and agouti-related peptide neurons that drive hunger
Plasma PYY concentration exceeds 67.89 pg/mL, binding to Y2 receptors on arcuate nucleus neurons to inhibit orexigenic signaling and enhance satiety
IL-6 and PYY act synergistically to amplify suppression of appetite perception, overriding concurrent orexigenic signals from TNF-alpha when IL-6 is elevated
A low IL-10/IL-1β ratio establishes a pro-inflammatory state in the hypothalamus that enhances the appetite-suppressing effects of IL-6 and PYY
Less supported by current evidence, but not ruled out
Physical activity alone increases a different inflammation signal that improves the brain's sensitivity to fullness hormones, reducing hunger without requiring high IL-6 or PYY levels.
Sprint exercise triggers skeletal muscle release of IL-6, which stimulates hepatic and adipose production of IL-10
Elevated IL-10 enhances hypothalamic sensitivity to leptin and insulin, reducing orexigenic drive
Reduced inflammatory tone in the hypothalamus increases responsiveness to satiety signals like CCK and PYY, even when their absolute concentrations are unchanged
Evidence from Studies
Supporting (1)
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Contradicting (0)
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