scholarly journals Ileal short-chain fatty acids inhibit gastric motility by a humoral pathway

2000 ◽  
Vol 279 (5) ◽  
pp. G925-G930 ◽  
Author(s):  
G. Cuche ◽  
J. C. Cuber ◽  
C. H. Malbert
Keyword(s):  
Gastric Motility ◽  
Short Chain Fatty Acid ◽  
Peptide Yy ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
Maximal Amplitude ◽  
Inhibiting Factor ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

The aim of this study was to evaluate the nervous and humoral pathways involved in short-chain fatty acid (SCFA)-induced ileal brake in conscious pigs. The role of extrinsic ileal innervation was evaluated after SCFA infusion in innervated and denervated Babkin's ileal loops, and gastric motility was measured with strain gauges. Peptide YY (PYY) and glucagon-like peptide-1 (GLP-1) concentrations were evaluated in both situations. The possible involvement of absorbed SCFA was tested by using intravenous infusion of acetate. Ileal SCFA infusion in the intact terminal ileum decreased the amplitude of distal and terminal antral contractions (33 ± 1.2 vs. 49 ± 1.2% of the maximal amplitude recorded before infusion) and increased their frequency (1.5 ± 0.11 vs. 1.3 ± 0.10/min). Similar effects were observed during SCFA infusion in ileal innervated and denervated loops (amplitude, 35 ± 1.0 and 34 ± 0.8 vs. 47 ± 1.3 and 43 ± 1.2%; frequency, 1.4 ± 0.07 and 1.6 ± 0.06 vs. 1.1 ± 0.14 and 1.0 ± 0.12/min). Intravenous acetate did not modify the amplitude and frequency of antral contractions. PYY but not GLP-1 concentrations were increased during SCFA infusion in innervated and denervated loops. In conclusion, ileal SCFA inhibit distal gastric motility by a humoral pathway involving the release of an inhibiting factor, which is likely PYY.

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 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.

scholarly journals The effects of yam gruel on lowering fasted blood glucose in T2DM rats

2020 ◽  
Vol 15 (1) ◽  
pp. 763-773
Author(s):  
Xinjun Lin ◽  
Zongting Luo ◽  
Shuqin Pang ◽  
Carol Chunfeng Wang ◽  
Li Ge ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Gut Microbiota ◽  
Peptide Yy ◽  
Short Chain Fatty Acids ◽  
Scientific Basis ◽  
Probiotic Bacteria ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
G Protein Coupled

AbstractThere is increasing evidence of the linkage between type 2 diabetes mellitus (T2DM) and gut microbiota. Based on our previous studies, we investigated the hypoglycemic mechanisms of yam gruel to provide a scientific basis for its popularization and application. Wistar rats were randomly divided into control and T2DM model groups. Rats in the model group were stimulated by a high-sugar/high-fat diet combined with an intraperitoneal injection of streptozotocin to induce T2DM. The T2DM rats were further subdivided randomly into three groups: (1) DM, (2) DM + yam gruel, and (3) DM + metformin. After 4 weeks of intervention, the changes in gut microbiota, short-chain fatty acids (SCFAs) (acetic acid, propionic acid, and butyric acid), the expression of G protein-coupled receptor 43 (GPR43), glucagon-like peptide-1 (GLP-1), peptide YY (PYY), and fasted blood glucose (FBG) levels were observed. Yam gruel intervention elevated the abundance of probiotic bacteria and increased the expression of SCFAs, GPR43 receptor, GLP-1, and PYY. It also reduced FBG levels. We conclude that yam gruel can lower FBG by promoting the growth of probiotic bacteria, increasing the content of SCFAs, and enhancing the expression of GPR43 receptor to increase the content of GLP-1 and PYY in serum.

scholarly journals Short-Chain Fatty Acid Propionate Alleviates Akt2 Knockout-Induced Myocardial Contractile Dysfunction

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Linlin Li ◽  
Yinan Hua ◽  
Jun Ren
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Membrane Potential ◽  
Mitochondrial Membrane ◽  
Short Chain Fatty Acid ◽  
Contractile Function ◽  
Short Chain Fatty Acids ◽  
Chain Fatty Acid ◽  
Short Chain

Background and Aims. Dysregulation of Akt has been implicated in diseases such as cancer and diabetes, although little is known about the role of Akt deficiency on cardiomyocyte contractile function. This study was designed to examine the effect of Akt2 knockout-induced cardiomyocyte contractile response and the effect of dietary supplementation of short-chain fatty acid propionate on Akt2 knockout-induced cardiac dysfunction, if any.Methods and Results. Adult male wild-type (WT) and Akt2 knockout mice were treated with propionate (0.3 g/kg, p.o.) or vehicle for 7 days. Oral glucose tolerance test (OGTT) was performed. Cardiomyocyte contractile function and mitochondrial membrane potential were assessed. Expression of insulin-signaling molecules Akt, PTEN, GSK3β, and eNOS receptors for short-chain fatty acids GPR41, and GPR43 as well as protein phosphatase PP2AA, PP2AB, PP2C were evaluated using Western blot analysis. Our results revealed that Akt2 knockout led to overt glucose intolerance, compromised cardiomyocyte contractile function (reduced peak shortening and maximal velocity of shortening/relengthening as well as prolonged relengthening), loss of mitochondrial membrane potential, decreased GPR41 and elevated GPR43 expression, all of which, with the exception of glucose intolerance and elevated GPR43 level, were significantly attenuated by propionate. Neither Akt2 knockout nor propionate affected the expression of protein phosphatases, eNOS, pan, and phosphorylated PTEN and GSK3β.Conclusions. Taken together, these data depicted that Akt2 knockout may elicit cardiomyocyte contractile and mitochondrial defects and a beneficial role of propionate or short-chain fatty acids against Akt2 deficiency-induced cardiac anomalies.

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