scholarly journals Short-Chain Fatty Acids Stimulate Glucagon-Like Peptide-1 Secretion via the G-Protein-Coupled Receptor FFAR2

Diabetes ◽  
2011 ◽  
Vol 61 (2) ◽  
pp. 364-371 ◽  
Author(s):  
G. Tolhurst ◽  
H. Heffron ◽  
Y. S. Lam ◽  
H. E. Parker ◽  
A. M. Habib ◽  
...  
Keyword(s):  
Fatty Acids ◽  
G Protein ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
G Protein Coupled Receptor ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
G Protein Coupled ◽  
Chain Fatty Acids

scholarly journals G-protein-coupled receptor for short-chain fatty acids suppresses colon cancer

2010 ◽  
Vol 128 (4) ◽  
pp. 847-856 ◽  
Author(s):  
Yong Tang ◽  
Yakun Chen ◽  
Hongmei Jiang ◽  
Gregory T. Robbins ◽  
Daotai Nie
Keyword(s):  
Fatty Acids ◽  
Colon Cancer ◽  
G Protein ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
G Protein Coupled Receptor ◽  
G Protein Coupled ◽  
Chain Fatty Acids

scholarly journals The olfactory G protein-coupled receptor (Olfr-78/OR51E2) modulates the intestinal response to colitis

2020 ◽  
Vol 318 (3) ◽  
pp. C502-C513
Author(s):  
Kumar Kotlo ◽  
Arivarasu N. Anbazhagan ◽  
Shubha Priyamvada ◽  
Dulari Jayawardena ◽  
Anoop Kumar ◽  
...  
Keyword(s):  
Fatty Acids ◽  
G Protein ◽  
Olfactory Receptor ◽  
Intestinal Inflammation ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
G Protein Coupled Receptor ◽  
Trinitrobenzenesulfonic Acid ◽  
G Protein Coupled ◽  
Chain Fatty Acids

Olfactory receptor-78 (Olfr-78) is a recently identified G protein-coupled receptor activated by short-chain fatty acids acetate and propionate. A suggested role for this receptor exists in the prostate where it may influence chronic inflammatory response leading to intraepithelial neoplasia. Olfr-78 has also been shown to be expressed in mouse colon. Short-chain fatty acids and their receptors are well known to modulate inflammation in the gut. Considering this possibility, we first explored if colitis regulated Olfr-78 expression in the gut, where we observed a significant reduction in the expression of Olfr-78 transcript in mouse models of dextran sodium sulfate (DSS)- and 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis. To more directly test this, mice deficient in Olfr-78 were administered with DSS in water for 7 days and were found to have increased expression of IL-1β and inflammatory signs in colon compared with control mice. Next, we explored the expression of its human counterpart olfactory receptor family 51, subfamily E, member 2 (OR51E2) in human intestinal samples and observed that it was in fact also expressed in human colon samples. RNA sequence analysis revealed significant changes in the genes involved in infection, immunity, inflammation, and colorectal cancer between wild-type and Olfr-78 knockout mice. Collectively, our findings show that Olfr-78 is highly expressed in colon and downregulated in DSS- and TNBS-induced colitis, and DSS-treated Olfr-78 null mice had increased colonic expression of cytokine RNA levels, suggesting a potential role for this receptor in intestinal inflammation. Future investigations are needed to understand how Olfr-78/OR51E2 in both mouse and human intestine modulates gastrointestinal pathophysiology.

scholarly journals Short-chain fatty acids stimulate leptin production in adipocytes through the G protein-coupled receptor GPR41

2004 ◽  
Vol 101 (4) ◽  
pp. 1045-1050 ◽  
Author(s):  
Y. Xiong ◽  
N. Miyamoto ◽  
K. Shibata ◽  
M. A. Valasek ◽  
T. Motoike ◽  
...  
Keyword(s):  
Fatty Acids ◽  
G Protein ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
G Protein Coupled Receptor ◽  
G Protein Coupled ◽  
Chain Fatty Acids

scholarly journals The impact of short-chain fatty acids on GLP-1 and PYY secretion from the isolated perfused rat colon

2018 ◽  
Vol 315 (1) ◽  
pp. G53-G65 ◽  
Author(s):  
Charlotte Bayer Christiansen ◽  
Maria Buur Nordskov Gabe ◽  
Berit Svendsen ◽  
Lars Ove Dragsted ◽  
Mette Marie Rosenkilde ◽  
...  
Keyword(s):  
Energy Source ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
Rat Colon ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Free Fatty Acid Receptors ◽  
Chain Fatty Acids

The colonic epithelium harbors a large number of endocrine cells, but little is known about the endocrine functions of the colon. However, the high density of glucagon like peptide-1 (GLP-1)- and peptide-YY (PYY)-secreting L cells is of great interest because of the potential antidiabetic and antiobesity effects of GLP-1 and PYY. Short-chain fatty acids (SCFAs) produced by local bacterial fermentation are suggested to activate the colonic free fatty acid receptors FFAR2 (GPR43) and FFAR3 (GPR41), stimulating the colonic L cells. We used the isolated perfused rat colon as a model of colonic endocrine secretion and studied the effects of the predominant SCFAs formed: acetate, propionate, and butyrate. We show that luminal and especially vascular infusion of acetate and butyrate significantly increases colonic GLP-1 secretion, and to a minor extent also PYY secretion, but only after enhancement of intracellular cAMP. Propionate neither affected GLP-1 nor PYY secretion whether administered luminally or vascularly. A FFAR2- and FFAR3–specific agonist [( S)-2-(4-chlorophenyl)-3,3-dimethyl- N-(5-phenylthiazol-2-yl)butamide (CFMB)/ AR420626 ] had no effect on colonic GLP-1 output, and a FFAR3 antagonist ( AR399519 ) did not decrease the SCFA-induced GLP-1 response. However, the voltage-gated Ca2+-channel blocker nifedipine, the KATP-channel opener diazoxide, and the ATP synthesis inhibitor 2,4-dinitrophenol completely abolished the responses. FFAR2 receptor studies confirmed low-potent partial agonism of acetate, propionate, and butyrate, compared with CFMB, which is a full agonist with ~750-fold higher potency than the SCFAs. In conclusion, SCFAs may increase colonic GLP-1/PYY secretion, but FFAR2/FFAR3 do not seem to be involved. Rather, SCFAs are metabolized and appear to function as a colonocyte energy source.NEW & NOTEWORTHY By the use of in situ isolated perfused rat colon we show that short-chain fatty acids (SCFAs) primarily are used as a colonocyte energy source in the rat, subsequently triggering glucagon like peptide-1 (GLP-1) secretion independent of the free fatty acid receptors FFAR2 and FFAR3. Opposite many previous studies on SCFAs and FFAR2/FFAR3 and GLP-1 secretion, this experimental model allows investigation of the physiological interactions between luminal nutrients and secretion from cells whose function depend critically on their blood supply as well as nerve and paracrine interactions.

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