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Gut carbohydrate inhibits GIP secretion via a microbiota/SCFA/FFAR3 pathway.

J. Endocrinol.2018 Dec 01;239(3):267-276
Eun-Young Lee 1 , Xilin Zhang 1 , Junki Miyamoto 2 , Ikuo Kimura 2 , Tomoaki Taknaka 3 , Kenichi Furusawa 4 , Takahito Jomori 4 , Kosuke Fujimoto 5 , Satoshi Uematsu 5 , Takashi Miki 1
Eun-Young Lee 1 , Xilin Zhang 1 , Junki Miyamoto 2 , Ikuo Kimura 2 , Tomoaki Taknaka 3 , Kenichi Furusawa 4 , Takahito Jomori 4 , Kosuke Fujimoto 5 , Satoshi Uematsu 5 , Takashi Miki 1
+ et al

[No authors listed]

Author information
  • 1 Department of Medical Physiology, Chiba University, Graduate School of Medicine, Chiba, Japan.
  • 2 Department of Applied Biological Science, Graduate School of Agriculture, Tokyo University of Agriculture and Technology, Fuchu, Japan.
  • 3 Department of Molecular Diagnosis, Chiba University, Graduate School of Medicine, Chiba, Japan.
  • 4 Drug Fostering and Evolution Coordinating Center, Sanwa Kagaku Kenkyusho Co., Ltd., Nagoya, Japan.
  • 5 Division of Innate Immune Regulation, International Research and Development Center for Mucosal Vaccines, Institute of Medical Science, The University of Tokyo, Minato-ku, Japan.

摘要


Mechanisms of carbohydrate-induced secretion of the two incretins namely glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are considered to be mostly similar. However, we found that mice exhibit opposite secretory responses in response to co-administration of maltose plus an α-glucosidase inhibitor miglitol (maltose/miglitol), stimulatory for GLP-1, as reported previously, but inhibitory for GIP. Gut microbiota was shown to be involved in maltose/miglitol-induced GIP suppression, as the suppression was attenuated in antibiotics (Abs)-treated mice and abolished in germ-free mice. In addition, maltose/miglitol administration increased plasma levels of short-chain fatty acids (SCFAs), carbohydrate-derived metabolites, in the portal vein. GIP suppression by maltose/miglitol was not observed in mice lacking a SCFA receptor Ffar3, but it was normally seen in Ffar2-deficient mice. Similar to maltose/miglitol administration, co-administration of glucose plus a sodium glucose transporter inhibitor phloridzin (glucose/phloridzin) induced GIP suppression, which was again cancelled by Abs treatment. In conclusion, oral administration of carbohydrates with α-glucosidase inhibitors suppresses GIP secretion through a microbiota/SCFA/FFAR3 pathway.

KEYWORDS: FFAR3, GIP secretion, SCFA (short chain fatty acid), microbiota, α-glucosidase