Canine gut receptors mediating pancreatic responses to luminal L-amino acids

Jh, Meyer; Kelly, GA; Spingola, LJ; Rs, Jones

doi:10.1152/ajplegacy.1976.231.3.669

Cited by 68 publications

(33 citation statements)

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“…Fatty acids, dietary protein and peptides are potent stimulants [1]. Aromatic amino acids (phenylalanine and tryptophan) are also known to stimulate CCK and pancreatic secretion in humans and dogs [2–5]. The cellular mechanism by which these amino acids stimulate CCK secretion in enteroendocrine cells is still unclear.…”

supporting

confidence: 87%

Calcium‐sensing receptor mediates phenylalanine‐induced cholecystokinin secretion in enteroendocrine STC‐1 cells

et al. 2008

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Intraluminal l‐phenylalanine (Phe) stimulates cholecystokinin (CCK) secretion in vivo and in vitro. However, the cellular mechanism by which CCK‐producing enteroendocrine cells sense Phe is unknown. The calcium‐sensing receptor (CaR) can sense amino acids, and is expressed in the gastrointestinal tract. In the present study, we examined whether CaR functions as a receptor for Phe in CCK‐producing enteroendocrine cells. CCK secretion and intracellular Ca2+ concentration in response to Phe were measured in the murine CCK‐producing enteroendocrine cell line STC‐1 at various extracellular Ca2+ concentrations or after treatment with a CaR antagonist. At more than 20 mm, Phe induced dose‐dependent CCK secretion and intracellular Ca2+ mobilization in STC‐1 cells. In the presence of 3.0 mm extracellular Ca2+, 10 and 20 mm Phe induced significantly higher CCK secretion than under normal conditions (1.2 mm extracellular Ca2+). Intracellular Ca2+ mobilization, induced by 10 or 20 mm Phe, was also enhanced by increasing extracellular Ca2+ concentrations. In addition, intracellular Ca2+ mobilization induced by addition of extracellular Ca2+ was augmented by the presence of Phe. These results closely match the known CaR properties. Treatment with a specific CaR antagonist (NPS2143) completely inhibited Phe‐induced CCK secretion and the latter phase of intracellular Ca2+ mobilization. CaR mRNA expression was demonstrated by RT‐PCR in STC‐1 cells, as well as in other mouse tissues including the kidney, thyroid, stomach and intestine. In conclusion, CaR functions as a receptor for Phe, stimulating CCK secretion in enteroendocrine STC‐1 cells.

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confidence: 87%

Calcium‐sensing receptor mediates phenylalanine‐induced cholecystokinin secretion in enteroendocrine STC‐1 cells

et al. 2008

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“…However, duodenal infusion ofthe CCK secretagogues phenylalanine and tryptophan, in doses that would cause considerable release of CCK in dogs (Konturek, Radecki, Thor & Dembinski, 1973;Meyer, Kelly, Spingola & Jones, 1976) was only about 10 min longer than the control ileal (about 12 m) transit time yet with ileal fat infusion small intestinal transit time was some 30 min longer than the ileal transit time under the same conditions. It is possible therefore that in the pig fats do cause an 'ileal brake' but that this is masked by a stronger response causing accelerated transit.…”

Section: Discussionmentioning

confidence: 85%

The influence of intestinal infusion of fats on small intestinal motility and digesta transit in pigs.

Gregory¹,

Rayner²,

Wenham³

1986

The Journal of Physiology

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SUMMARY1. The influence of duodenal and ileal infusion of nutrients on small intestinal transit of digesta, measured by the passage of phenol red marker, was studied in twelve pigs fitted with duodenal and ileal catheters, and a terminal ileal cannula.2. Changes in gastrointestinal motility were observed by electromyography and by use of an X-ray image intensifier in four of the pigs fitted additionally with nichrome wire electrodes in the gut wall and in seven pigs fitted only with a gastric catheter.3. Small intestinal transit time was unaffected by intestinal catheterization per se, or by duodenal or ileal infusion of glucose or peptone. It was reduced by duodenal infusion of fat or of some of the products of fat digestion including oleic acid and a monoglyceride containing unsaturated fatty acids (monoglyceride LS) but was not affected by infusion of glycerol, stearic acid or a monoglyceride containing saturated fatty acids (monoglyceride P).4. Ileal transit time was greatly reduced by ileal infusion of soya bean oil mixed with bile salts and lipase and by monoglyceride LS but not by soya bean oil alone. Total small intestinal transit time was reduced to a lesser degree by ileal infusion of soya bean oil mixed with bile salts and lipase and by monoglyceride LS and was unaffected by soya bean oil alone.5. The level of irregular spiking activity of the small intestine was greatly reduced by both duodenal and ileal infusion of fat, but rapidly propagated spike bursts were initiated from the point of infusion (identified radjologically as peristaltic rushes) many of which travelled right through to the ileo-caecal junction.6. It is concluded that intestinal infusion of fat accelerates small intestinal transit in pigs by induction of peristaltic rushes; that since the ileal transit times were more severely reduced than total small intestinal transit times by ileal infusion of fat the response is probably only seen over those areas of intestine in direct contact with the fat; and that the effect depends upon the presence of fat digestion products, i.e. the fatty acid and the monoglyceride, although probably only those containing unsaturated fatty acids.

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“…These include the regulation of gastric emptying (14), pancreatic exocrine secretion (27), and appetite (28). Gastric emptying of glucose solutions, in the range of concentrations evaluated in the current study, has been shown to be tightly regulated in both animals (14) and humans (15,29) so that in a given animal or human the rate at which glucose enters the small intestine is constant at ∼1-3 kcal/min independent of the glucose concentration (15).…”

Section: Discussionmentioning

confidence: 93%

Effects of Intraduodenal Glucose Concentration on Blood Pressure and Heart Rate in Healthy Older Subjects

et al. 2006

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The aims of this study were to determine whether the hypotensive and heart rate responses to small intestinal glucose infusion are dependent on the glucose concentration. Eight healthy subjects, aged 65-78 years, were studied on 3 separate days in random order. Each subject received intraduodenal infusions of 50 g of glucose in either 300 mL (16.7%), 600 mL (8.3%), or 1200 mL (4.1%) of saline (0.9%) at a rate of 3 kcal/min for 60 minutes (t = 0-60 minutes), followed by saline (0.9%) for a further 60 minutes (t = 60-120 minutes). During the infusions, blood pressure (systolic and diastolic) and heart rate were measured every 3 minutes, and blood glucose concentrations every 15 minutes. Systolic and diastolic blood pressure fell (P < .0001), and heart rate and blood glucose increased (P = .0001 for both) over time, during all 3 infusions. Between t = -2-120 minutes, there was no difference in systolic blood pressure (P = .20), diastolic blood pressure (P = .61), or heart rate (P = .09) over the study days. There was also no significant difference in the glycemic response to the infusions. We conclude that in healthy older subjects, glucose concentration does not affect the blood pressure or heart rate responses to intraduodenal glucose and that, therefore, the magnitude of the postprandial fall in blood pressure induced by oral glucose is likely to depend primarily on the small intestinal glucose load.

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Canine gut receptors mediating pancreatic responses to luminal L-amino acids

Cited by 68 publications

References 0 publications

Calcium‐sensing receptor mediates phenylalanine‐induced cholecystokinin secretion in enteroendocrine STC‐1 cells

Calcium‐sensing receptor mediates phenylalanine‐induced cholecystokinin secretion in enteroendocrine STC‐1 cells

The influence of intestinal infusion of fats on small intestinal motility and digesta transit in pigs.

Effects of Intraduodenal Glucose Concentration on Blood Pressure and Heart Rate in Healthy Older Subjects

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