Helmholtz Gemeinschaft

Search
Browse
Statistics
Feeds

Glucagon-producing cells are increased in Mas-deficient mice

[thumbnail of 16221oa.pdf]
Preview
PDF - Requires a PDF viewer such as GSview, Xpdf or Adobe Acrobat Reader
956kB

Item Type:Article
Title:Glucagon-producing cells are increased in Mas-deficient mice
Creators Name:Felix Braga, J., Ravizzoni Dartora, D., Alenina, N., Bader, M. and Santos, R.A.S.
Abstract:It has been shown that Angiotensin-(1-7) [Ang-(1-7)] produces several effects related to glucose homeostasis. In this study, we aimed to investigate the effects of genetic deletion of Ang-(1-7), the GPCR Mas, on the glucagon -producing cells. C57BL6/N Mas-/- mice presented a significant and marked increase in pancreatic {alpha}-cells (number of cells: 146 +/- 21 vs. 67 +/- 8 in WT - p<0.001) and the percentage per islet (17.9±0.91 vs. 12.3 +/- 0.9% in WT - p<0.0001) with subsequent reduction of {beta}-cells percentage (82.1 +/- 0.91 vs. 87.7 +/- 0.9% in WT - p<0.0001). Accordingly, glucagon plasma levels were increased (516.7 +/- 36.35 vs 390.8 +/- 56.45 pg/mL in WT, p<0.05 ) and insulin plasma levels were decreased in C57BL6/N Mas-/- mice (0.25 +/- 0.01 vs 0.31 +/- 56.45 pg/mL in WT- p=0.02). In order to eliminate the possibility of a background-related phenotype we determined the number of glucagon-producing cells in FVB/N Mas-/- mice. In keeping with the observations in C57BL6/N Mas-/- mice, the number and percentage of pancreatic {alpha}-cells were also significantly increased in these mice (number of {alpha}-cells: 260 +/- 22 vs. 156 +/- 12 in WT, p<0.001; percentage per islet: 16 +/- 0.8 vs. 10 +/- 0.5% in WT, p<0.0001). These results suggest that Mas has a previously unexpected role on the pancreatic glucagon production.
Keywords:Metabolsim, Diabetes, Animals, Mice
Source:Endocrine Connections
ISSN:2049-3614
Publisher:BioScientifica
Volume:6
Number:1
Page Range:27-32
Date:January 2017
Official Publication:https://doi.org/10.1530/EC-16-0098
PubMed:View item in PubMed

Repository Staff Only: item control page

Downloads

Downloads per month over past year

Open Access
MDC Library