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The provision of the fermentable fibers soy polysaccharides and fructooligosaccharides increases short‐chain fatty acid transporter abundance in healthy piglets
Author(s) -
Woodard Jennifer,
CorreaMatos Nancy J,
Tappenden Kelly A
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.102.1
Subject(s) - ileum , short chain fatty acid , fermentation , transporter , chemistry , fatty acid , in vivo , polysaccharide , biochemistry , in vitro , food science , biology , butyrate , microbiology and biotechnology , gene
Glucagon‐like peptide 2 (GLP‐2) is an intestinotrophic hormone released from the distal ileum and colon shown to be stimulated by short‐chain fatty acids (SCFAs). Previous in vitro work has shown SCFA receptors and transporters play a role in mediating GLP‐2 production. Therefore, the aim of this study was to examine SLC5A8, MCT‐1, GPR43, and T2R38 abundance in vivo following SCFA production. Piglets were randomized to a control formula, formula supplemented with 7.5 g/L soy polysaccharides (SPS), or formula supplemented with 7.5 g/L fructooligosaccharides (FOS) for 14 days. Expression of GPR43 and T2R38 was not significantly different between the treatment groups. Colonic, but not ileal, MCT‐1 abundance was significantly elevated with SPS (1.35 vs. 2.67 MCT‐1/18S; p = 0.0163); expression in the FOS treated animals was intermediate, but not significantly different from either the control or SPS groups. The abundance of SLC5A8 was significantly elevated in the ileum, but not the colon, with FOS fermentation (0.388 vs. 0.880 SLC5A8/18S; p = 0.0578), while SPS was not significantly different than the control animals. Together, these results indicate that SCFAs increase transporter mRNA abundance, particularly in the intestinal segment in which the fiber was fermented, and thus may have implications for the types of fermentable substrates best suited for stimulating GLP‐2. Grant Funding Source : NIH T32 DK59802