Central glucagon like peptide-1 delays solid gastric emptying via central CRF and peripheral sympathetic pathway in rats

2006 ◽  
Vol 1111 (1) ◽  
pp. 117-121 ◽  
Author(s):  
Yukiomi Nakade ◽  
Kiyoshi Tsukamoto ◽  
Theodore N. Pappas ◽  
Toku Takahashi
2010 ◽  
Vol 38 (5) ◽  
pp. 1261-1269 ◽  
Author(s):  
Adam M. Deane ◽  
Marianne J. Chapman ◽  
Robert J. L. Fraser ◽  
Matthew J. Summers ◽  
Antony V. Zaknic ◽  
...  

Diabetes Care ◽  
2013 ◽  
Vol 36 (7) ◽  
pp. 1913-1918 ◽  
Author(s):  
T. Wu ◽  
M. J. Bound ◽  
B. R. Zhao ◽  
S. D. Standfield ◽  
M. Bellon ◽  
...  

2020 ◽  
Vol 22 (12) ◽  
pp. 2504-2506 ◽  
Author(s):  
Michael Horowitz ◽  
Christopher K. Rayner ◽  
Chinmay S. Marathe ◽  
Tongzhi Wu ◽  
Karen L. Jones

2009 ◽  
Vol 297 (3) ◽  
pp. R632-R639 ◽  
Author(s):  
Tanya J. Little ◽  
Nili Gupta ◽  
R. Maynard Case ◽  
David G. Thompson ◽  
John T. McLaughlin

In cell line and animal models, sweet and bitter tastants induce secretion of signaling peptides (e.g., glucagon-like peptide-1 and cholecystokinin) and slow gastric emptying (GE). Whether human GE and appetite responses are regulated by the sweetness or bitterness per se of ingested food is, however, unknown. We aimed to determine whether intragastric infusion of “equisweet” ( Study A) or “equibitter” ( Study B) solutions slow GE to the same extent, and whether a glucose solution made sweeter by the addition of saccharin will slow GE more potently than glucose alone. Healthy nonobese subjects were studied in a single-blind, randomized fashion. Subjects received 500-ml intragastric infusions of predetermined equisweet solutions of glucose (560 mosmol/kgH2O), fructose (290 mosmol/kgH2O), aspartame (200 mg), and saccharin (50 mg); twice as sweet glucose + saccharin, water (volumetric control) ( Study A); or equibitter solutions of quinine (0.198 mM), naringin (1 mM), or water ( Study B). GE was evaluated using a [13C]acetate breath test, and hunger and fullness were scored using visual analog scales. In Study A, equisweet solutions did not empty similarly. Fructose, aspartame, and saccharin did not slow GE compared with water, but glucose did ( P < 0.05). There was no additional effect of the sweeter glucose + saccharin solution ( P > 0.05, compared with glucose alone). In Study B, neither bitter tastant slowed GE compared with water. None of the solutions modulated perceptions of hunger or fullness. We conclude that, in humans, the presence of sweetness and bitterness taste per se in ingested solutions does not appear to signal to influence GE or appetite perceptions.


2001 ◽  
Vol 281 (3) ◽  
pp. G752-G763 ◽  
Author(s):  
Feruze Y. Enç ◽  
Neşe I˙meryüz ◽  
Levent Akin ◽  
Turgut Turoğlu ◽  
Fuat Dede ◽  
...  

We investigated the effect of acarbose, an α-glucosidase and pancreatic α-amylase inhibitor, on gastric emptying of solid meals of varying nutrient composition and plasma responses of gut hormones. Gastric emptying was determined with scintigraphy in healthy subjects, and all studies were performed with and without 100 mg of acarbose, in random order, at least 1 wk apart. Acarbose did not alter the emptying of a carbohydrate-free meal, but it delayed emptying of a mixed meal and a carbohydrate-free meal given 2 h after sucrose ingestion. In meal groups with carbohydrates, acarbose attenuated responses of plasma insulin and glucose-dependent insulinotropic polypeptide (GIP) while augmenting responses of CCK, glucagon-like peptide-1 (GLP-1), and peptide YY (PYY). With mixed meal + acarbose, area under the curve (AUC) of gastric emptying was positively correlated with integrated plasma response of GLP-1 ( r = 0.68 , P < 0.02). With the carbohydrate-free meal after sucrose and acarbose ingestion, AUC of gastric emptying was negatively correlated with integrated plasma response of GIP, implying that prior alteration of carbohydrate absorption modifies gastric emptying of a meal. The results demonstrate that acarbose delays gastric emptying of solid meals and augments release of CCK, GLP-1, and PYY mainly by retarding/inhibiting carbohydrate absorption. Augmented GLP-1 release by acarbose appears to play a major role in the inhibition of gastric emptying of a mixed meal, whereas CCK and PYY may have contributory roles.


2001 ◽  
Vol 120 (5) ◽  
pp. A74
Author(s):  
Ayhan Bozkurt ◽  
Mustafa Deniz ◽  
Nese Imrryuz ◽  
Nefise B. Ulusoy ◽  
Berrak C. Yegen

1997 ◽  
Vol 273 (5) ◽  
pp. E981-E988 ◽  
Author(s):  
Michael A. Nauck ◽  
Ulrich Niedereichholz ◽  
Rainer Ettler ◽  
Jens Juul Holst ◽  
Cathrine Ørskov ◽  
...  

Glucagon-like peptide 1 (GLP-1) has been shown to inhibit gastric emptying of liquid meals in type 2 diabetic patients. It was the aim of the present study to compare the action of physiological and pharmacological doses of intravenous GLP-1-(7—36) amide and GLP-1-(7—37) on gastric emptying in normal volunteers. Nine healthy subjects participated (26 ± 3 yr; body mass index 22.9 ± 1.6 kg/m2; hemoglobin A1C 5.0 ± 0.2%) in five experiments on separate occasions after an overnight fast. A nasogastric tube was positioned for the determination of gastric volume by use of a dye-dilution technique (phenol red). GLP-1-(7—36) amide (0.4, 0.8, or 1.2 pmol ⋅ kg−1 ⋅ min−1), GLP-1-(7—37) (1.2 pmol ⋅ kg−1 ⋅ min−1), or placebo was infused intravenously from −30 to 240 min. A liquid meal (50 g sucrose, 8% amino acids, 440 ml, 327 kcal) was administered at 0 min. Glucose, insulin, and C-peptide were measured over 240 min. Gastric emptying was dose dependently slowed by GLP-1-(7—36) amide ( P < 0.0001). Effects of GLP-1-(7—37) at 1.2 pmol ⋅ kg−1 ⋅ min−1were virtually identical. GLP-1 dose dependently stimulated fasting insulin secretion (−30 to 0 min) and slightly reduced glucose concentrations. After the meal (0–240 min), integrated incremental glucose ( P < 0.0001) and insulin responses ( P = 0.01) were reduced (dose dependently) rather than enhanced. In conclusion, 1) GLP-1-(7—36) amide or -(7—37) inhibits gastric emptying also in normal subjects, 2) physiological doses (0.4 pmol ⋅ kg−1 ⋅ min−1) still have a significant effect, 3) despite the known insulinotropic actions of GLP-1-(7—36) amide and -(7—37), the net effect of administering GLP-1 with a meal is no change or a reduction in meal-related insulin responses. These findings suggest a primarily inhibitory function for GLP-1 (ileal brake mechanisms).


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