Selective FFA2 agonism appears to act via intestinal PYY to reduce transit and food intake, but does not improve glucose tolerance in mouse models. Running title: Selective FFA2 agonism acts via PYY not GLP-1

نویسندگان

  • Sarah Forbes
  • Stuart Stafford
  • Gareth Coope
  • Helen Heffron
  • Katia Real
  • Rob Newman
  • Richard Davenport
  • Matt Barnes
  • Johannes Grosse
  • Helen Cox
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Selective FFA2 Agonism Appears to Act via Intestinal PYY to Reduce Transit and Food Intake but Does Not Improve Glucose Tolerance in Mouse Models.

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Peptide YY (PYY) is released following food intake and regulates intestinal function and glucose homeostasis, but the mechanisms underpinning these processes are unclear. Enteroendocrine L cells contain PYY and express the acylethanolamine receptor, Gpr119. Here, we show that Gpr119 activation inhibited epithelial electrolyte secretion in human and mouse colon in a glucose-sensitive manner. End...

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PYY transgenic mice are protected against diet-induced and genetic obesity.

The gut-derived hormone, peptide YY (PYY) reduces food intake and enhances satiety in both humans and animals. Obese individuals also have a deficiency in circulating peptide YY, although whether this is a cause or a consequence of obesity is unclear. Our aims were to determine whether peptide YY (PYY) over-expression may have therapeutic effects for the treatment of obesity by altering energy ...

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Pharmacological properties of acid N-thiazolylamide FFA2 agonists

FFA2 is a receptor for short-chain fatty acids. Propionate (C3) and 4-chloro-α-(1-methylethyl)-N-2-thiazolyl-benzeneacetamide (4-CMTB), the prototypical synthetic FFA2 agonist, evoke calcium mobilization in neutrophils and inhibit lipolysis in adipocytes via this G-protein-coupled receptor. 4-CMTB contains an N-thiazolylamide motif but no acid group, and 4-CMTB and C3 bind to different sites on...

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تاریخ انتشار 2015