Abstract
The brain, especially the hypothalamus, can modulate hepatic glucose fluxes. The sympathetic system promotes glycogen breakdown. The parasympathetic system stimulates glycogen deposition. Central insulin signalling or hypothalamic long-chain fatty acid oxidation can both control insulin's suppression of endogenous glucose production. Intestinal gluconeogenesis initiates a portal glucose signal, transmitted to the brain via the gastrointestinal nervous system. This signal may modulate the sensation of hunger and satiety and insulin sensitivity of hepatic glucose fluxes as well, via the modulation of hypothalamic activity
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