Relationship between Fecal Content of Fatty Acids and Cyclooxygenase mRNA Expression and Fatty Acid Composition in Duodenal Biopsies, Serum Lipoproteins, and Dietary Fat in Colectomized Familial Adenomatous Polyposis Patients

Almendingen, Kari; Høstmark, Arne T.; Larsen, Laila N.; Fausa, O; Bratlie, Jorunn; Aabakken, Lars

doi:10.1155/2010/862569

Cited by 2 publications

(3 citation statements)

References 28 publications

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“…1 and 2). 1 Antibodies against ␣-gustducin (sc-395) (35,51), GLP-1 (sc-7782) (35), and GIP (sc-23554) (24,95) have been validated previously in the above-mentioned papers from our laboratory and/or from others.…”

Section: Methodsmentioning

confidence: 99%

“…The lumen of the colon lacks dietary sugars, but is filled with microbiota, nondigestible matter, and fermentation products, such as short-chain fatty acids (SCFAs), ammonia, phenols, amines, and bile acids (12,23,50,84). Medium-and long-chain fatty acids (LCFAs) are also detected in fecal content from patients with small bowel resection on a high-fat diet (36) and from colectomized patients (1). Interestingly, the SCFA receptor G protein-coupled receptor (GPR) 43 (6, 47) is coexpressed with GLP-1 in both human and rat colon L cells (37).…”

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confidence: 99%

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Gustducin couples fatty acid receptors to GLP-1 release in colon

Kokrashvili

Mosinger

et al. 2013

American Journal of Physiology-Endocrinology and Metabolism

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taste receptor subunits and ␣-gustducin found in enteroendocrine cells of the small intestine have been implicated in release of the incretin hormones glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) in response to glucose and noncaloric sweeteners. ␣-Gustducin has also been found in colon, although its function there is unclear. We examined expression of ␣-gustducin, GLP-1, and GIP throughout the intestine. The number of ␣-gustducin-expressing cells and those coexpressing ␣-gustducin together with GLP-1 and/or GIP increased from small intestine to colon. ␣-Gustducin also was coexpressed with fatty acid G protein-coupled receptor (GPR) 40, GPR41, GPR43, GPR119, GPR120, and bile acid G protein-coupled receptor TGR5 in enteroendocrine cells of the colon. In colon, GPR43 was coexpressed with GPR119 and GPR120, but not with TGR5. Treatment of colonic mucosa isolated from wild-type mice with acetate, butyrate, oleic acid, oleoylethanolamide, or lithocholic acid stimulated GLP-1 secretion. However, GLP-1 release in response to these fatty acids was impaired in colonic tissue from ␣-gustducin knockout mice.␣-gustducin; glucose-dependent insulinotropic polypeptide; glucagon-like peptide 1; fatty acid receptors; enteroendocrine cell THE INCRETIN HORMONES glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are estimated to account for ϳ50 -70% of total insulin release after oral glucose administration (13,30,59). The meal-related GLP-1 response in type 2 diabetes is decreased, which may contribute to the decreased incretin effect in this population (58,86).The sweet taste receptor subunits T1r2 and T1r3, and the G protein ␣-subunit ␣-gustducin, initially found in taste cells (48,54,55,60,91), have also been shown to be present in enteroendocrine and brush cells of the small intestine (3, 14, 29, 51). ␣-Gustducin and T1r receptors are also present in the small intestine's L-and K-type enteroendocrine cells, which release GLP-1 and GIP, respectively, in response to glucose in the gut lumen (35). In response to glucose gavage, ␣-gustducin null mice do not show the elevation of serum levels of GLP-1 found in gavaged wild-type mice (35). Furthermore, sweetenerstimulated GLP-1 release from L cell lines can be inhibited by small-interfering RNA against ␣-gustducin or pharmacological blocking of the T1r2ϩT1r3 sweet receptor (35, 51). In addition, other mechanisms independent of ␣-gustducin and T1rs, including sodium glucose cotransporter-1 (SGLT1) and ATPsensitive K ϩ channels (K ATP ), are known to regulate GLP-1 release from primary L cells (69).␣-Gustducin is also expressed with peptide YY (PYY) and GLP-1 in L cells of the human colon (74), although its functions in these cells are unknown. The lumen of the colon lacks dietary sugars, but is filled with microbiota, nondigestible matter, and fermentation products, such as short-chain fatty acids (SCFAs), ammonia, phenols, amines, and bile acids (12,23,50,84). Medium-and long-chain fatty acids (LCFAs) are a...

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

Gustducin couples fatty acid receptors to GLP-1 release in colon

Kokrashvili

Mosinger

et al. 2013

American Journal of Physiology-Endocrinology and Metabolism

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“…Concentrations of fecal LCFAs are related to various factors, such as dietary intake, gastrointestinal digestion and absorption of lipids, bile secretion, FA-binding proteins, FA transport protein, and small intestinal transit time, among others [30]. Some specific FAs have been linked to inflammatory activity [31][32][33], making the composition of fecal FAs a potential indicator for gastrointestinal health. In our study, we found increased fecal concentrations of 9 out of 12 targeted LCFAs in cats with CE; these increases might have resulted from maldigestion, malabsorption, inflammation, dysbiosis, and abnormal lipid metabolism.…”

Section: Discussionmentioning

confidence: 99%

Fecal Concentrations of Long-Chain Fatty Acids, Sterols, and Unconjugated Bile Acids in Cats with Chronic Enteropathy

Sung,

Pilla,

Marsilio

et al. 2023

Animals

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Chronic enteropathy (CE) in cats encompasses food-responsive enteropathy, chronic inflammatory enteropathy (or inflammatory bowel disease), and low-grade intestinal T-cell lymphoma. While alterations in the gut metabolome have been extensively studied in humans and dogs with gastrointestinal disorders, little is known about the specific metabolic profile of cats with CE. As lipids take part in energy storage, inflammation, and cellular structure, investigating the lipid profile in cats with CE is crucial. This study aimed to measure fecal concentrations of various fatty acids, sterols, and bile acids. Fecal samples from 56 cats with CE and 77 healthy control cats were analyzed using gas chromatography-mass spectrometry, targeting 12 fatty acids, 10 sterols, and 5 unconjugated bile acids. Fecal concentrations of nine targeted fatty acids and animal-derived sterols were significantly increased in cats with CE. However, fecal concentrations of plant-derived sterols were significantly decreased in cats with CE. Additionally, an increased percentage of primary bile acids was observed in a subset of cats with CE. These findings suggest the presence of lipid maldigestion, malabsorption, and inflammation in the gastrointestinal tract of cats with CE. Understanding the lipid alterations in cats with CE can provide insights into the disease mechanisms and potential future therapeutic strategies.

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Relationship between Fecal Content of Fatty Acids and Cyclooxygenase mRNA Expression and Fatty Acid Composition in Duodenal Biopsies, Serum Lipoproteins, and Dietary Fat in Colectomized Familial Adenomatous Polyposis Patients

Cited by 2 publications

References 28 publications

Gustducin couples fatty acid receptors to GLP-1 release in colon

Gustducin couples fatty acid receptors to GLP-1 release in colon

Fecal Concentrations of Long-Chain Fatty Acids, Sterols, and Unconjugated Bile Acids in Cats with Chronic Enteropathy

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