scholarly journals Individual Subtypes of Enteroendocrine Cells in the Mouse Small Intestine Exhibit Unique Patterns of Inositol 1,4,5-trisphosphate Receptor Expression

2004 ◽  
Vol 52 (1) ◽  
pp. 53-63 ◽  
Author(s):  
Songyan Wang ◽  
Jianfeng Liu ◽  
Lin Li ◽  
Burton M. Wice
2019 ◽  
Vol 105 (1) ◽  
pp. 266-275 ◽  
Author(s):  
Sara Lind Jepsen ◽  
Esben Thyssen Vestergaard ◽  
Pierre Larraufie ◽  
Fiona Mary Gribble ◽  
Frank Reimann ◽  
...  

Abstract Context The gastrointestinal hormone ghrelin stimulates growth hormone secretion and appetite, but recent studies indicate that ghrelin also stimulates the secretion of the appetite-inhibiting and insulinotropic hormone glucagon-like peptide-1 (GLP-1). Objective To investigate the putative effect of ghrelin on GLP-1 secretion in vivo and in vitro. Subjects and Methods A randomized placebo-controlled crossover study was performed in eight hypopituitary subjects. Ghrelin or saline was infused intravenously (1 pmol/min × kg) after collection of baseline sample (0 min), and blood was subsequently collected at time 30, 60, 90, and 120 minutes. Mouse small intestine was perfused (n = 6) and GLP-1 output from perfused mouse small intestine was investigated in response to vascular ghrelin administration in the presence and absence of a simultaneous luminal glucose stimulus. Ghrelin receptor expression was quantified in human (n = 11) and mouse L-cells (n = 3) by RNA sequencing and RT-qPCR, respectively. Results Ghrelin did not affect GLP-1 secretion in humans (area under the curve [AUC; 0–120 min]: ghrelin infusion = 1.37 ± 0.05 min × nmol vs. saline infusion = 1.40 ± 0.06 min × nmol [P = 0.63]), but induced peripheral insulin resistance. Likewise, ghrelin did not stimulate GLP-1 secretion from the perfused mouse small intestine model (mean outputs during baseline/ghrelin infusion = 19.3 ± 1.6/25.5 ± 2.0 fmol/min, n = 6, P = 0.16), whereas glucose-dependent insulinotropic polypeptide administration, used as a positive control, doubled GLP-1 secretion (P < 0.001). Intraluminal glucose increased GLP-1 secretion by 4-fold (P < 0.001), which was not potentiated by ghrelin. Finally, gene expression of the ghrelin receptor was undetectable in mouse L-cells and marginal in human L-cells. Conclusions Ghrelin does not interact directly with the L-cell and does not directly affect GLP-1 secretion.


1997 ◽  
Vol 44 (2) ◽  
pp. 347-354 ◽  
Author(s):  
Gregory Smutzer ◽  
John E Zimmerman ◽  
Chang-Gyu Hahn ◽  
Delta D Ruscheinsky ◽  
Amaris Rodrı́guez ◽  
...  

2007 ◽  
Vol 292 (5) ◽  
pp. G1420-G1428 ◽  
Author(s):  
Kate Sutherland ◽  
Richard L. Young ◽  
Nicole J. Cooper ◽  
Michael Horowitz ◽  
L. Ashley Blackshaw

Nutrient-evoked gastrointestinal reflexes are likely initiated by specialized epithelial cells located in the small intestine that detect luminal stimuli and release mediators that activate vagal endings. The G-protein α-gustducin, a key signal molecule in lingual taste detection, has been identified in mouse small intestine, where it may also subserve nutrient detection; however, the phenotype of α-gustducin cells is unknown. Immunohistochemistry was performed throughout the mouse small intestine for α-gustducin, enteroendocrine cell markers 5-HT and glucagon-like peptide-1 (GLP-1), and brush cell markers neuronal nitric oxide synthase and Ulex europaeus agglutinin-1 (UEA-1) lectin binding, singly, and in combination. α-Gustducin was expressed in solitary epithelial cells of the mid to upper villus, which were distributed in a regional manner with most occurring within the midjejunum. Here, 27% of α-gustducin cells colabeled for 5-HT and 15% for GLP-1; 57% of α-gustducin cells colabeled UEA-1, with no triple labeling. α-Gustducin cells that colabeled for 5-HT or GLP-1 were of distinct morphology and exhibited a different α-gustducin immunolabeling pattern to those colabeled with UEA-1. Neuronal nitric oxide synthase was absent from intestinal epithelium despite strong labeling in the myenteric plexus. We conclude that subsets of enteroendocrine cells in the midjejunum and brush cells (more generally distributed) are equipped to utilize α-gustducin signaling in mice. Intestinal taste modalities may be signaled by these enteroendocrine cells via the release of 5-HT, GLP-1, or coexpressed mediators or by brush cells via a nonnitrergic mediator in distinct regions of the intestine.


Sign in / Sign up

Export Citation Format

Share Document