Centrally administered neuropeptide Y inhibits antro-pyloric motility and delays gastric emptying via Y2 receptors in conscious rats

2001 ◽  
Vol 120 (5) ◽  
pp. A289-A289
Author(s):  
T ISHIGUCHI ◽  
H ITOH ◽  
T TAKAHASHI
1991 ◽  
Vol 81 (2) ◽  
pp. 281-285 ◽  
Author(s):  
R. Fraser ◽  
J. Fuller ◽  
M. Horowitz ◽  
J. Dent

1. Hyperglycaemia alters gastric motility and delays gastric emptying. By contrast, there is little information regarding the effect of sub-normal blood glucose concentrations on gastric and, in particular, pyloric motility, although limited data suggest that hypoglycaemia is associated with accelerated gastric emptying despite an apparently increased basal pyloric pressure. 2. To determine the effects of hypoglycaemia on pyloric motility, we compared the effects of an intravenous injection of insulin (0.15 units/kg) with those of a placebo injection of saline in eight healthy human volunteers during phase I of the interdigestive migrating motor complex. 3. All subjects developed profound hypoglycaemia (mean blood glucose concentration 1.6 mmol/l compared with 4.0 mmol/l in the control group). 4. There was no significant difference in the number of antral (9 versus 7, P = 0.34), pyloric (3 versus 0, P = 0.31) or duodenal (21 versus 13, P = 0.42) pressure waves or in the basal pyloric pressure (0.3 mmHg versus 0.1 mmHg, P = 0.37) in the 45 min after insulin injection (hypoglycaemia) when compared with the 45 min after saline injection (euglycaemia). In both the euglycaemic and hypoglycaemic studies there was a time-dependent increase in the numbers of antral and duodenal waves consistent with the expected changes in the interdigestive migrating motor complex. 5. These results indicate that insulin-induced hypoglycaemia has no significant effect on pyloric motility during phase I of the interdigestive migrating motor complex.


2002 ◽  
Vol 95 (1-2) ◽  
pp. 112-120 ◽  
Author(s):  
Tadashi Ishiguchi ◽  
Hitoshi Tada ◽  
Kazuhiko Nakagawa ◽  
Takehira Yamamura ◽  
Toku Takahashi

2014 ◽  
Vol 306 (12) ◽  
pp. G1099-G1107 ◽  
Author(s):  
Maya Muramatsu ◽  
Tohru Hira ◽  
Arimi Mitsunaga ◽  
Eri Sato ◽  
Shingo Nakajima ◽  
...  

The calcium-sensing receptor (CaSR) is expressed in various tissues, including the gastrointestinal tract. To investigate the role of gut CaSR on glycemic control, we examined whether single oral administration of CaSR agonist peptides affected the glycemic response in rats. Glucose tolerance tests were performed under oral or duodenal administration of various CaSR agonist peptides (γGlu-Cys, protamine, and poly-d-lysine hydrobromide) in conscious rats. Involvement of CaSR was determined by using a CaSR antagonist. Signaling pathways underlying CaSR agonist-modified glycemia were investigated using gut hormone receptor antagonists. The gastric emptying rate after the administration of CaSR agonist peptides was measured by the phenol red recovery method. Oral and duodenal administration of CaSR agonist peptides attenuated glycemic responses under the oral glucose tolerance test, but the administration of casein did not. The promotive effect on glucose tolerance was weakened by luminal pretreatment with a CaSR antagonist. Treatment with a 5-HT3 receptor antagonist partially diminished the glucose-lowering effect of peptides. Furthermore, the gastric emptying rate was decreased by duodenal administration of CaSR agonist peptides. These results demonstrate that activation of the gut CaSR by peptide agonists promotes glucose tolerance in conscious rats. 5-HT3 receptor and the delayed gastric emptying rate appear to be involved in the glucose-lowering effect of CaSR agonist peptides. Thus, activation of gut CaSR by dietary peptides reduces glycemic responses so that gut CaSR may be a potential target for the improvement of postprandial glycemia.


2008 ◽  
Vol 146 (1-3) ◽  
pp. 112-116 ◽  
Author(s):  
Hajime Ariga ◽  
Yukiomi Nakade ◽  
Kiyoshi Tsukamoto ◽  
Kenji Imai ◽  
Cindy Chen ◽  
...  

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