Commentary Cellscience Reviews Vol 5 No 1 ISSN 1742-8130

How do intestinal lipids control glucose homeostasis?

Dietary lipids control appetite, gut motility and hormones. Wang et al. recently showed that acute infusion of a lipid emulsion into the duodenum of rats generated long-chain fatty acyl-coenzyme A (LCFACoA) locally, increased insulin sensitivity and suppressed glucose production from the liver. The critical role of LCFACoAs in the upper intestine was confirmed by the co-infusion of triascin C, an acyl-CoA synthase inhibitor, which prevented the suppression of glucose production. Next, the authors explored the neuronal basis of glucose regulation by intestinal LCFACoAs. Chemical disruption of the vagal sensory innervation from the gut via injection of MK-801, an N-methyl-D-aspartate ion channel inhibitor, into the nucleus of the tractus solitarius in the brain stem abolished the effect of intraduodenal LCFACoAs on glucose. Furthermore, surgical removal of vagal innervation from the upper intestine or liver blocked the insulin sensitizing action of intestinal lipids. These findings reveal a novel mechanism by which dietary lipids activate unique neuronal connections to the brain and liver to control glucose metabolism.

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