Upper intestinal lipids trigger a gut–brain–liver axis to regulate glucose production

Penny Y. T. Wang, Liora Caspi, Carol K. L. Lam, Madhu Chari, Xiaosong Li, Peter E. Light, Roger Gutierrez-Juarez, Michelle Ang, Gary J. Schwartz and Tony K. T. Lam ()
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Penny Y. T. Wang: Toronto General Hospital Research Institute, University Health Network
Liora Caspi: Toronto General Hospital Research Institute, University Health Network
Carol K. L. Lam: Toronto General Hospital Research Institute, University Health Network
Madhu Chari: Toronto General Hospital Research Institute, University Health Network
Xiaosong Li: Albert Einstein College of Medicine, Bronx, New York 10461, USA
Peter E. Light: University of Alberta
Roger Gutierrez-Juarez: Albert Einstein College of Medicine, Bronx, New York 10461, USA
Michelle Ang: Toronto General Hospital Research Institute, University Health Network
Gary J. Schwartz: Albert Einstein College of Medicine, Bronx, New York 10461, USA
Tony K. T. Lam: Toronto General Hospital Research Institute, University Health Network

Nature, 2008, vol. 452, issue 7190, 1012-1016

Abstract: Blood glucose regulation The mere presence of lipids in the intestine is known to reduce nutrient intake in both rodents and humans by activating the intestine–brain neural axis. More recently, studies have indicated that the brain senses blood lipids directly to inhibit glucose production and maintain glucose homeostasis in rodents through a brain–liver neural axis. Now comes the first demonstration that upper intestinal lipids rapidly inhibit glucose production through an intestine–brain–liver neurocircuit. Work in rats shows that the lipids or fats which enter the small intestine trigger the afferent neuronal signal to the brain, which then sends signals to the liver to lower glucose production and blood glucose levels in as little as fifteen minutes. But eating a high-fat diet for just three days can interfere with this signal, disabling it so that it does not signal the other organs to lower blood glucose levels. This holds out the prospect that novel sites and targets may be revealed to lower glucose or blood sugar levels in those who are obese or have diabetes.

Date: 2008
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DOI: 10.1038/nature06852

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