Wang et al 2008 Upper intestinal lipids trigger a gut-brain-liver axis to regulate glucose production Nature vol 452, 1012-1016
Thaler and Cummings 2008, Food Alert Nature vol 452, 941-42
Energy and glucose homeostasis are regulated by food intake and liver glucose production, respectively. The upper intestine has a critical role in nutrient digestion and absorption. Upper intestinal lipids inhibit food intake as well in rodents and humans by the activation of an intestine-brain axis..
Wang and her colleagues tested the hypothesis that upper intestinal lipids activate an intestine-brain-liver neural axis to regulate glucose homeostasis. Direct administration of lipids into the upper intestine increased upper intestinal long-chain fatty acyl-coenzyme A (LCFA-CoA) levels and suppressed glucose production
Co-infusion of the acyl-CoA synthase inhibitor triacsin C or the anaesthetic tetracaine with duodenal lipids abolished ihe inhibition of glucose production, indicating that upper intestinal LCFA-CoAs regulate glucose production in the preabsorptive state.
Subdiaphragmatic vagotomy interrupts the neural connection between the gut and the brain, and blocks the ability of upper intestinal lipids to inhibit glucose production.
Direct administration of the N-methyl-D-aspartate ion channel blocker MK-801 into the fourth ventricle or the nucleus of the solitary tract where gut sensory fibres terminate abolished the upper-intestinal-lipid-induced inhibition of glucose production.
Hepatic vagotomy negated the inhibitory effects of upper intestinal lipids on glucose production.
Upper intestinal lipids activate an intestine-brain-liver neural axis to inhibit glucose production, a pathway that regulates glucose homeostasis.

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