Study About Gut Derived Serotonin's Effect On Metabolism

[Swandattur]

http://www.ncbi.nlm.nih.gov/pubmed/23085101
This study would seem to agree with what Ray Peat says about serotonin being a problem at least as far as glucose metabolism.

 

[Swandattur]

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Cell Metab. 2012 Nov 7;16(5):588-600. doi: 10.1016/j.cmet.2012.09.014. Epub 2012 Oct 18.
Gut-derived serotonin is a multifunctional determinant to fasting adaptation.
Sumara G, Sumara O, Kim JK, Karsenty G.
Source
Department of Genetics and Development, Columbia University Medical Center, New York, NY 10032, USA.
Abstract
Energy release from cellular storage is mandatory for survival during fasting. This is achieved through lipolysis and liver gluconeogenesis. We show here that in the mouse, gut-derived serotonin (GDS) is upregulated during fasting and that it favors both mechanisms. In adipocytes, GDS signals through the Htr2b receptor to favor lipolysis by increasing phosphorylation and activity of hormone-sensitive lipase. In hepatocytes, GDS signaling through Htr2b promotes gluconeogenesis by enhancing activity of two rate-limiting gluconeogenic enzymes, FBPase and G6Pase. In addition, GDS signaling in hepatocytes prevents glucose uptake in a Glut2-dependent manner, thereby further favoring maintenance of blood glucose levels. As a result, inhibition of GDS synthesis can improve glucose intolerance caused by high-fat diet. Hence, GDS opposes deleterious consequences of food deprivation by favoring lipolysis and liver gluconeogenesis while preventing glucose uptake by hepatocytes. As a result, pharmacological inhibition of its synthesis may contribute to improve type 2 diabetes.
Copyright © 2012 Elsevier Inc. All rights reserved.
PMID: 23085101 [PubMed - indexed for MEDLINE]
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