FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4286008506> ?p ?o ?g. }

• W4286008506 endingPage "E306" @default.
• W4286008506 startingPage "E290" @default.
• W4286008506 abstract "Free fatty acid receptor 3 (FFA3) is a recently-deorphanized G-protein-coupled receptor. Its ligands are short-chain fatty acids (SCFAs), which are key nutrients derived from the gut microbiome fermentation process that play diverse roles in the regulation of metabolic homeostasis and glycemic control. FFA3 is highly expressed within the intestine, where its role and its effects on physiology and metabolism are unclear. Previous in vivo studies involving this receptor have relied on global knockout mouse models, making it difficult to isolate intestine-specific roles of FFA3. To overcome this challenge, we generated an intestine-specific knockout mouse model for FFA3, Villin-Cre-FFA3 (Vil-FFA3). Model validation and general metabolic assessment of male mice fed a standard chow diet revealed no major congenital defects. Because dietary changes are known to alter gut microbial composition, and thereby SCFA production, an obesogenic challenge was performed on male Vil-FFA3 mice and their littermate controls to probe for a phenotype on a high-fat, high-sugar Western diet (WD) compared with a low-fat control diet (CD). Vil-FFA3 mice versus FFA3fl/fl controls on WD, but not CD, were protected from the development of diet-induced obesity and exhibited significantly less fat mass as well as smaller adipose depositions and adipocytes. Although overall glycemic control was unchanged in the WD-fed Vil-FFA3 group, fasted glucose levels trended lower. Intestinal inflammation was significantly reduced in the WD-fed Vil-FFA3 mice, supporting protection from obesogenic effects. Furthermore, we observed lower levels of gastric inhibitory protein (GIP) in the WD-fed Vil-FFA3 mice, which may contribute to phenotypic changes. Our findings suggest a novel role of intestinal FFA3 in promoting the metabolic consequences of a WD, including the development of obesity and inflammation. Moreover, these data support an intestine-specific role of FFA3 in whole body metabolic homeostasis and in the development of adiposity.NEW & NOTEWORTHY Here, we generated a novel intestine-specific knockout mouse model for FFA3 (Vil-FFA3) and performed a comprehensive metabolic characterization of mice in response to an obesogenic challenge. We found that Vil-FFA3 mice fed with a Western diet were largely protected from obesity, exhibiting significantly lower levels of fat mass, lower intestinal inflammation, and altered expression of intestinal incretin hormones. Results support an important role of intestinal FFA3 in contributing to metabolism and in the development of diet-induced obesity." @default.
• W4286008506 created "2022-07-21" @default.
• W4286008506 creator A5007339313 @default.
• W4286008506 creator A5020254328 @default.
• W4286008506 creator A5032940889 @default.
• W4286008506 creator A5036472346 @default.
• W4286008506 creator A5053322598 @default.
• W4286008506 creator A5057812053 @default.
• W4286008506 creator A5071376661 @default.
• W4286008506 creator A5076070266 @default.
• W4286008506 creator A5080665608 @default.
• W4286008506 creator A5083106775 @default.
• W4286008506 date "2022-09-01" @default.
• W4286008506 modified "2023-09-28" @default.
• W4286008506 title "Intestinal FFA3 mediates obesogenic effects in mice on a Western diet" @default.
• W4286008506 cites W1930796554 @default.
• W4286008506 cites W2001938165 @default.
• W4286008506 cites W2002811300 @default.
• W4286008506 cites W2004507897 @default.
• W4286008506 cites W2004549986 @default.
• W4286008506 cites W2033829415 @default.
• W4286008506 cites W2035421462 @default.
• W4286008506 cites W2037921130 @default.
• W4286008506 cites W2046315492 @default.
• W4286008506 cites W2057154465 @default.
• W4286008506 cites W2062967108 @default.
• W4286008506 cites W2067689880 @default.
• W4286008506 cites W2069247721 @default.
• W4286008506 cites W2073332363 @default.
• W4286008506 cites W2085708523 @default.
• W4286008506 cites W2090981739 @default.
• W4286008506 cites W2097788076 @default.
• W4286008506 cites W2102392334 @default.
• W4286008506 cites W2116085563 @default.
• W4286008506 cites W2116318925 @default.
• W4286008506 cites W2124001121 @default.
• W4286008506 cites W2128654255 @default.
• W4286008506 cites W2131592975 @default.
• W4286008506 cites W2132198562 @default.
• W4286008506 cites W2133856765 @default.
• W4286008506 cites W2142336938 @default.
• W4286008506 cites W2145622931 @default.
• W4286008506 cites W2149573313 @default.
• W4286008506 cites W2157201312 @default.
• W4286008506 cites W2163092495 @default.
• W4286008506 cites W2166171121 @default.
• W4286008506 cites W2166562121 @default.
• W4286008506 cites W2168842536 @default.
• W4286008506 cites W2174790239 @default.
• W4286008506 cites W2203058642 @default.
• W4286008506 cites W2262043001 @default.
• W4286008506 cites W2310854600 @default.
• W4286008506 cites W2400773242 @default.
• W4286008506 cites W2405624971 @default.
• W4286008506 cites W2612161536 @default.
• W4286008506 cites W2752435500 @default.
• W4286008506 cites W2774595101 @default.
• W4286008506 cites W2800284674 @default.
• W4286008506 cites W2800861529 @default.
• W4286008506 cites W2888795824 @default.
• W4286008506 cites W2889696246 @default.
• W4286008506 cites W2895975223 @default.
• W4286008506 cites W2913914265 @default.
• W4286008506 cites W2921966151 @default.
• W4286008506 cites W2940243545 @default.
• W4286008506 cites W2941039646 @default.
• W4286008506 cites W2944549000 @default.
• W4286008506 cites W2970854520 @default.
• W4286008506 cites W2992883720 @default.
• W4286008506 cites W3006914536 @default.
• W4286008506 cites W3025458562 @default.
• W4286008506 cites W3040512164 @default.
• W4286008506 cites W3081331242 @default.
• W4286008506 cites W3083241614 @default.
• W4286008506 cites W3123690892 @default.
• W4286008506 cites W3139312899 @default.
• W4286008506 cites W3162144801 @default.
• W4286008506 cites W3162308028 @default.
• W4286008506 cites W3174702068 @default.
• W4286008506 cites W3202033667 @default.
• W4286008506 cites W3206302034 @default.
• W4286008506 doi "https://doi.org/10.1152/ajpendo.00016.2022" @default.
• W4286008506 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35858247" @default.
• W4286008506 hasPublicationYear "2022" @default.
• W4286008506 type Work @default.
• W4286008506 citedByCount "1" @default.
• W4286008506 countsByYear W42860085062023 @default.
• W4286008506 crossrefType "journal-article" @default.
• W4286008506 hasAuthorship W4286008506A5007339313 @default.
• W4286008506 hasAuthorship W4286008506A5020254328 @default.
• W4286008506 hasAuthorship W4286008506A5032940889 @default.
• W4286008506 hasAuthorship W4286008506A5036472346 @default.
• W4286008506 hasAuthorship W4286008506A5053322598 @default.
• W4286008506 hasAuthorship W4286008506A5057812053 @default.
• W4286008506 hasAuthorship W4286008506A5071376661 @default.
• W4286008506 hasAuthorship W4286008506A5076070266 @default.
• W4286008506 hasAuthorship W4286008506A5080665608 @default.
• W4286008506 hasAuthorship W4286008506A5083106775 @default.

• next