CCK Response Deficiency in Synphilin-1 Transgenic Mice.
Previously, we have identified a novel role for the cytoplasmic protein, synphilin-1(SP1), in the controls of food intake and body weight in both mice and Drosophila. Ubiquitous overexpression of human SP1 in brain neurons in transgenic mice results in hyperphagia expressed as an increase in meal si...
| Main Authors: | , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2015-01-01
|
| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC4646498?pdf=render |
| _version_ | 1818848221997301760 |
|---|---|
| author | Wanli W Smith Megan Smith Dejun Yang Pique P Choi Alexander Moghadam Tianxia Li Timothy H Moran |
| author_facet | Wanli W Smith Megan Smith Dejun Yang Pique P Choi Alexander Moghadam Tianxia Li Timothy H Moran |
| author_sort | Wanli W Smith |
| collection | DOAJ |
| description | Previously, we have identified a novel role for the cytoplasmic protein, synphilin-1(SP1), in the controls of food intake and body weight in both mice and Drosophila. Ubiquitous overexpression of human SP1 in brain neurons in transgenic mice results in hyperphagia expressed as an increase in meal size. However, the mechanisms underlying this action of SP1 remain to be determined. Here we investigate a potential role for altered gut feedback signaling in the effects of SP1 on food intake. We examined responses to peripheral administration of cholecytokinin (CCK), amylin, and the glucagon like peptide-1 (GLP-1) receptor agonist, exendin-4. Intraperitoneal administration of CCK at doses ranging from 1-10 nmol/kg significantly reduced glucose intake in wild type (WT) mice, but failed to affect intake in SP1 transgenic mice. Moreover, there was a significant attenuation of CCK-induced c-Fos expression in the dorsal vagal complex in SP1 transgenic mice. In contrast, WT and SP1 transgenic mice were similarly responsive to both amylin and exendin-4 treatment. These studies demonstrate that SP1 results in a CCK response deficiency that may contribute to the increased meal size and overall hyperphagia in synphillin-1 transgenic mice. |
| first_indexed | 2024-12-19T06:13:54Z |
| format | Article |
| id | doaj.art-e0a794c000c8405891b26d6adfba0778 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-19T06:13:54Z |
| publishDate | 2015-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-e0a794c000c8405891b26d6adfba07782022-12-21T20:32:56ZengPublic Library of Science (PLoS)PLoS ONE1932-62032015-01-011011e014231410.1371/journal.pone.0142314CCK Response Deficiency in Synphilin-1 Transgenic Mice.Wanli W SmithMegan SmithDejun YangPique P ChoiAlexander MoghadamTianxia LiTimothy H MoranPreviously, we have identified a novel role for the cytoplasmic protein, synphilin-1(SP1), in the controls of food intake and body weight in both mice and Drosophila. Ubiquitous overexpression of human SP1 in brain neurons in transgenic mice results in hyperphagia expressed as an increase in meal size. However, the mechanisms underlying this action of SP1 remain to be determined. Here we investigate a potential role for altered gut feedback signaling in the effects of SP1 on food intake. We examined responses to peripheral administration of cholecytokinin (CCK), amylin, and the glucagon like peptide-1 (GLP-1) receptor agonist, exendin-4. Intraperitoneal administration of CCK at doses ranging from 1-10 nmol/kg significantly reduced glucose intake in wild type (WT) mice, but failed to affect intake in SP1 transgenic mice. Moreover, there was a significant attenuation of CCK-induced c-Fos expression in the dorsal vagal complex in SP1 transgenic mice. In contrast, WT and SP1 transgenic mice were similarly responsive to both amylin and exendin-4 treatment. These studies demonstrate that SP1 results in a CCK response deficiency that may contribute to the increased meal size and overall hyperphagia in synphillin-1 transgenic mice.http://europepmc.org/articles/PMC4646498?pdf=render |
| spellingShingle | Wanli W Smith Megan Smith Dejun Yang Pique P Choi Alexander Moghadam Tianxia Li Timothy H Moran CCK Response Deficiency in Synphilin-1 Transgenic Mice. PLoS ONE |
| title | CCK Response Deficiency in Synphilin-1 Transgenic Mice. |
| title_full | CCK Response Deficiency in Synphilin-1 Transgenic Mice. |
| title_fullStr | CCK Response Deficiency in Synphilin-1 Transgenic Mice. |
| title_full_unstemmed | CCK Response Deficiency in Synphilin-1 Transgenic Mice. |
| title_short | CCK Response Deficiency in Synphilin-1 Transgenic Mice. |
| title_sort | cck response deficiency in synphilin 1 transgenic mice |
| url | http://europepmc.org/articles/PMC4646498?pdf=render |
| work_keys_str_mv | AT wanliwsmith cckresponsedeficiencyinsynphilin1transgenicmice AT megansmith cckresponsedeficiencyinsynphilin1transgenicmice AT dejunyang cckresponsedeficiencyinsynphilin1transgenicmice AT piquepchoi cckresponsedeficiencyinsynphilin1transgenicmice AT alexandermoghadam cckresponsedeficiencyinsynphilin1transgenicmice AT tianxiali cckresponsedeficiencyinsynphilin1transgenicmice AT timothyhmoran cckresponsedeficiencyinsynphilin1transgenicmice |