Eintrag weiter verarbeiten
Fructose consumption impairs serotonergic signaling in the murine enteric nervous system
Gespeichert in:
| Zeitschriftentitel: | Neurogastroenterology & Motility |
|---|---|
| Personen und Körperschaften: | , , , , |
| In: | Neurogastroenterology & Motility, 28, 2016, 9, S. 1438-1442 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
|
| Schlagwörter: |
| author_facet |
Lowette, K. Desmet, A.‐S. Farré, R.M. Tack, J. Vanden Berghe, P. Lowette, K. Desmet, A.‐S. Farré, R.M. Tack, J. Vanden Berghe, P. |
|---|---|
| author |
Lowette, K. Desmet, A.‐S. Farré, R.M. Tack, J. Vanden Berghe, P. |
| spellingShingle |
Lowette, K. Desmet, A.‐S. Farré, R.M. Tack, J. Vanden Berghe, P. Neurogastroenterology & Motility Fructose consumption impairs serotonergic signaling in the murine enteric nervous system Gastroenterology Endocrine and Autonomic Systems Physiology |
| author_sort |
lowette, k. |
| spelling |
Lowette, K. Desmet, A.‐S. Farré, R.M. Tack, J. Vanden Berghe, P. 1350-1925 1365-2982 Wiley Gastroenterology Endocrine and Autonomic Systems Physiology http://dx.doi.org/10.1111/nmo.12827 <jats:title>Abstract</jats:title><jats:p>The intake of free fructose has increased substantially since the development of high‐fructose corn syrup. This has not only been associated with metabolic disorders but recent evidence also indicates that chronic fructose consumption can affect neuronal and cognitive function. In this study we investigated the effects of fructose consumption on serotonergic signaling and neuronal activity in the mouse submucous plexus. Male mice were put on a control or fructose (23% solution) diet for 6 weeks or were assigned to a recovery group that received normal water (2 weeks) after 4 weeks of fructose. At the end of the diet, gene expressions and enteric neuronal activity, after depolarization with high K<jats:sup>+</jats:sup> and 5‐<jats:styled-content style="fixed-case">HT</jats:styled-content>, were measured using Ca<jats:sup>2+</jats:sup> imaging and <jats:styled-content style="fixed-case">RT</jats:styled-content>‐<jats:styled-content style="fixed-case">qPCR</jats:styled-content>, respectively. Even in the lack of gain weight and the absence of changes in duodenal permeability, the total number of 5‐<jats:styled-content style="fixed-case">HT</jats:styled-content>‐responding neurons and the depolarization and 5‐<jats:styled-content style="fixed-case">HT</jats:styled-content>‐evoked Ca<jats:sup>2+</jats:sup> amplitudes were significantly lower after fructose consumption. Expression of synaptobrevin Ca<jats:sub>V</jats:sub>2.1 and Ca<jats:sub>V</jats:sub>2.2 <jats:styled-content style="fixed-case">mRNA</jats:styled-content> did not differ after fructose intake; however, Ca<jats:sub>V</jats:sub>2.1 <jats:styled-content style="fixed-case">mRNA</jats:styled-content> levels were significantly higher in the recovery animals. <jats:styled-content style="fixed-case">SERT mRNA</jats:styled-content> concentration, isolated from submucosal plexus containing mucosal epithelium, was significantly decreased after fructose consumption. Chronic fructose consumption impairs serotonergic signaling in the mouse submucous plexus, prior to weight gain and detectable intestinal permeability problems.</jats:p> Fructose consumption impairs serotonergic signaling in the murine enteric nervous system Neurogastroenterology & Motility |
| doi_str_mv |
10.1111/nmo.12827 |
| facet_avail |
Online |
| finc_class_facet |
Medizin Biologie |
| format |
ElectronicArticle |
| fullrecord |
blob:ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTExMS9ubW8uMTI4Mjc |
| id |
ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTExMS9ubW8uMTI4Mjc |
| institution |
DE-14 DE-105 DE-Ch1 DE-L229 DE-D275 DE-Bn3 DE-Brt1 DE-D161 DE-Zi4 DE-Gla1 DE-15 DE-Pl11 DE-Rs1 |
| imprint |
Wiley, 2016 |
| imprint_str_mv |
Wiley, 2016 |
| issn |
1350-1925 1365-2982 |
| issn_str_mv |
1350-1925 1365-2982 |
| language |
English |
| mega_collection |
Wiley (CrossRef) |
| match_str |
lowette2016fructoseconsumptionimpairsserotonergicsignalinginthemurineentericnervoussystem |
| publishDateSort |
2016 |
| publisher |
Wiley |
| recordtype |
ai |
| record_format |
ai |
| series |
Neurogastroenterology & Motility |
| source_id |
49 |
| title |
Fructose consumption impairs serotonergic signaling in the murine enteric nervous system |
| title_unstemmed |
Fructose consumption impairs serotonergic signaling in the murine enteric nervous system |
| title_full |
Fructose consumption impairs serotonergic signaling in the murine enteric nervous system |
| title_fullStr |
Fructose consumption impairs serotonergic signaling in the murine enteric nervous system |
| title_full_unstemmed |
Fructose consumption impairs serotonergic signaling in the murine enteric nervous system |
| title_short |
Fructose consumption impairs serotonergic signaling in the murine enteric nervous system |
| title_sort |
fructose consumption impairs serotonergic signaling in the murine enteric nervous system |
| topic |
Gastroenterology Endocrine and Autonomic Systems Physiology |
| url |
http://dx.doi.org/10.1111/nmo.12827 |
| publishDate |
2016 |
| physical |
1438-1442 |
| description |
<jats:title>Abstract</jats:title><jats:p>The intake of free fructose has increased substantially since the development of high‐fructose corn syrup. This has not only been associated with metabolic disorders but recent evidence also indicates that chronic fructose consumption can affect neuronal and cognitive function. In this study we investigated the effects of fructose consumption on serotonergic signaling and neuronal activity in the mouse submucous plexus. Male mice were put on a control or fructose (23% solution) diet for 6 weeks or were assigned to a recovery group that received normal water (2 weeks) after 4 weeks of fructose. At the end of the diet, gene expressions and enteric neuronal activity, after depolarization with high K<jats:sup>+</jats:sup> and 5‐<jats:styled-content style="fixed-case">HT</jats:styled-content>, were measured using Ca<jats:sup>2+</jats:sup> imaging and <jats:styled-content style="fixed-case">RT</jats:styled-content>‐<jats:styled-content style="fixed-case">qPCR</jats:styled-content>, respectively. Even in the lack of gain weight and the absence of changes in duodenal permeability, the total number of 5‐<jats:styled-content style="fixed-case">HT</jats:styled-content>‐responding neurons and the depolarization and 5‐<jats:styled-content style="fixed-case">HT</jats:styled-content>‐evoked Ca<jats:sup>2+</jats:sup> amplitudes were significantly lower after fructose consumption. Expression of synaptobrevin Ca<jats:sub>V</jats:sub>2.1 and Ca<jats:sub>V</jats:sub>2.2 <jats:styled-content style="fixed-case">mRNA</jats:styled-content> did not differ after fructose intake; however, Ca<jats:sub>V</jats:sub>2.1 <jats:styled-content style="fixed-case">mRNA</jats:styled-content> levels were significantly higher in the recovery animals. <jats:styled-content style="fixed-case">SERT mRNA</jats:styled-content> concentration, isolated from submucosal plexus containing mucosal epithelium, was significantly decreased after fructose consumption. Chronic fructose consumption impairs serotonergic signaling in the mouse submucous plexus, prior to weight gain and detectable intestinal permeability problems.</jats:p> |
| container_issue |
9 |
| container_start_page |
1438 |
| container_title |
Neurogastroenterology & Motility |
| container_volume |
28 |
| format_de105 |
Article, E-Article |
| format_de14 |
Article, E-Article |
| format_de15 |
Article, E-Article |
| format_de520 |
Article, E-Article |
| format_de540 |
Article, E-Article |
| format_dech1 |
Article, E-Article |
| format_ded117 |
Article, E-Article |
| format_degla1 |
E-Article |
| format_del152 |
Buch |
| format_del189 |
Article, E-Article |
| format_dezi4 |
Article |
| format_dezwi2 |
Article, E-Article |
| format_finc |
Article, E-Article |
| format_nrw |
Article, E-Article |
| _version_ |
1792334559627444224 |
| geogr_code |
not assigned |
| last_indexed |
2024-03-01T14:30:35.238Z |
| geogr_code_person |
not assigned |
| openURL |
url_ver=Z39.88-2004&ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fvufind.svn.sourceforge.net%3Agenerator&rft.title=Fructose+consumption+impairs+serotonergic+signaling+in+the+murine+enteric+nervous+system&rft.date=2016-09-01&genre=article&issn=1365-2982&volume=28&issue=9&spage=1438&epage=1442&pages=1438-1442&jtitle=Neurogastroenterology+%26+Motility&atitle=Fructose+consumption+impairs+serotonergic+signaling+in+the+murine+enteric+nervous+system&aulast=Vanden+Berghe&aufirst=P.&rft_id=info%3Adoi%2F10.1111%2Fnmo.12827&rft.language%5B0%5D=eng |
| SOLR | |
| _version_ | 1792334559627444224 |
| author | Lowette, K., Desmet, A.‐S., Farré, R.M., Tack, J., Vanden Berghe, P. |
| author_facet | Lowette, K., Desmet, A.‐S., Farré, R.M., Tack, J., Vanden Berghe, P., Lowette, K., Desmet, A.‐S., Farré, R.M., Tack, J., Vanden Berghe, P. |
| author_sort | lowette, k. |
| container_issue | 9 |
| container_start_page | 1438 |
| container_title | Neurogastroenterology & Motility |
| container_volume | 28 |
| description | <jats:title>Abstract</jats:title><jats:p>The intake of free fructose has increased substantially since the development of high‐fructose corn syrup. This has not only been associated with metabolic disorders but recent evidence also indicates that chronic fructose consumption can affect neuronal and cognitive function. In this study we investigated the effects of fructose consumption on serotonergic signaling and neuronal activity in the mouse submucous plexus. Male mice were put on a control or fructose (23% solution) diet for 6 weeks or were assigned to a recovery group that received normal water (2 weeks) after 4 weeks of fructose. At the end of the diet, gene expressions and enteric neuronal activity, after depolarization with high K<jats:sup>+</jats:sup> and 5‐<jats:styled-content style="fixed-case">HT</jats:styled-content>, were measured using Ca<jats:sup>2+</jats:sup> imaging and <jats:styled-content style="fixed-case">RT</jats:styled-content>‐<jats:styled-content style="fixed-case">qPCR</jats:styled-content>, respectively. Even in the lack of gain weight and the absence of changes in duodenal permeability, the total number of 5‐<jats:styled-content style="fixed-case">HT</jats:styled-content>‐responding neurons and the depolarization and 5‐<jats:styled-content style="fixed-case">HT</jats:styled-content>‐evoked Ca<jats:sup>2+</jats:sup> amplitudes were significantly lower after fructose consumption. Expression of synaptobrevin Ca<jats:sub>V</jats:sub>2.1 and Ca<jats:sub>V</jats:sub>2.2 <jats:styled-content style="fixed-case">mRNA</jats:styled-content> did not differ after fructose intake; however, Ca<jats:sub>V</jats:sub>2.1 <jats:styled-content style="fixed-case">mRNA</jats:styled-content> levels were significantly higher in the recovery animals. <jats:styled-content style="fixed-case">SERT mRNA</jats:styled-content> concentration, isolated from submucosal plexus containing mucosal epithelium, was significantly decreased after fructose consumption. Chronic fructose consumption impairs serotonergic signaling in the mouse submucous plexus, prior to weight gain and detectable intestinal permeability problems.</jats:p> |
| doi_str_mv | 10.1111/nmo.12827 |
| facet_avail | Online |
| finc_class_facet | Medizin, Biologie |
| format | ElectronicArticle |
| format_de105 | Article, E-Article |
| format_de14 | Article, E-Article |
| format_de15 | Article, E-Article |
| format_de520 | Article, E-Article |
| format_de540 | Article, E-Article |
| format_dech1 | Article, E-Article |
| format_ded117 | Article, E-Article |
| format_degla1 | E-Article |
| format_del152 | Buch |
| format_del189 | Article, E-Article |
| format_dezi4 | Article |
| format_dezwi2 | Article, E-Article |
| format_finc | Article, E-Article |
| format_nrw | Article, E-Article |
| geogr_code | not assigned |
| geogr_code_person | not assigned |
| id | ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTExMS9ubW8uMTI4Mjc |
| imprint | Wiley, 2016 |
| imprint_str_mv | Wiley, 2016 |
| institution | DE-14, DE-105, DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-D161, DE-Zi4, DE-Gla1, DE-15, DE-Pl11, DE-Rs1 |
| issn | 1350-1925, 1365-2982 |
| issn_str_mv | 1350-1925, 1365-2982 |
| language | English |
| last_indexed | 2024-03-01T14:30:35.238Z |
| match_str | lowette2016fructoseconsumptionimpairsserotonergicsignalinginthemurineentericnervoussystem |
| mega_collection | Wiley (CrossRef) |
| physical | 1438-1442 |
| publishDate | 2016 |
| publishDateSort | 2016 |
| publisher | Wiley |
| record_format | ai |
| recordtype | ai |
| series | Neurogastroenterology & Motility |
| source_id | 49 |
| spelling | Lowette, K. Desmet, A.‐S. Farré, R.M. Tack, J. Vanden Berghe, P. 1350-1925 1365-2982 Wiley Gastroenterology Endocrine and Autonomic Systems Physiology http://dx.doi.org/10.1111/nmo.12827 <jats:title>Abstract</jats:title><jats:p>The intake of free fructose has increased substantially since the development of high‐fructose corn syrup. This has not only been associated with metabolic disorders but recent evidence also indicates that chronic fructose consumption can affect neuronal and cognitive function. In this study we investigated the effects of fructose consumption on serotonergic signaling and neuronal activity in the mouse submucous plexus. Male mice were put on a control or fructose (23% solution) diet for 6 weeks or were assigned to a recovery group that received normal water (2 weeks) after 4 weeks of fructose. At the end of the diet, gene expressions and enteric neuronal activity, after depolarization with high K<jats:sup>+</jats:sup> and 5‐<jats:styled-content style="fixed-case">HT</jats:styled-content>, were measured using Ca<jats:sup>2+</jats:sup> imaging and <jats:styled-content style="fixed-case">RT</jats:styled-content>‐<jats:styled-content style="fixed-case">qPCR</jats:styled-content>, respectively. Even in the lack of gain weight and the absence of changes in duodenal permeability, the total number of 5‐<jats:styled-content style="fixed-case">HT</jats:styled-content>‐responding neurons and the depolarization and 5‐<jats:styled-content style="fixed-case">HT</jats:styled-content>‐evoked Ca<jats:sup>2+</jats:sup> amplitudes were significantly lower after fructose consumption. Expression of synaptobrevin Ca<jats:sub>V</jats:sub>2.1 and Ca<jats:sub>V</jats:sub>2.2 <jats:styled-content style="fixed-case">mRNA</jats:styled-content> did not differ after fructose intake; however, Ca<jats:sub>V</jats:sub>2.1 <jats:styled-content style="fixed-case">mRNA</jats:styled-content> levels were significantly higher in the recovery animals. <jats:styled-content style="fixed-case">SERT mRNA</jats:styled-content> concentration, isolated from submucosal plexus containing mucosal epithelium, was significantly decreased after fructose consumption. Chronic fructose consumption impairs serotonergic signaling in the mouse submucous plexus, prior to weight gain and detectable intestinal permeability problems.</jats:p> Fructose consumption impairs serotonergic signaling in the murine enteric nervous system Neurogastroenterology & Motility |
| spellingShingle | Lowette, K., Desmet, A.‐S., Farré, R.M., Tack, J., Vanden Berghe, P., Neurogastroenterology & Motility, Fructose consumption impairs serotonergic signaling in the murine enteric nervous system, Gastroenterology, Endocrine and Autonomic Systems, Physiology |
| title | Fructose consumption impairs serotonergic signaling in the murine enteric nervous system |
| title_full | Fructose consumption impairs serotonergic signaling in the murine enteric nervous system |
| title_fullStr | Fructose consumption impairs serotonergic signaling in the murine enteric nervous system |
| title_full_unstemmed | Fructose consumption impairs serotonergic signaling in the murine enteric nervous system |
| title_short | Fructose consumption impairs serotonergic signaling in the murine enteric nervous system |
| title_sort | fructose consumption impairs serotonergic signaling in the murine enteric nervous system |
| title_unstemmed | Fructose consumption impairs serotonergic signaling in the murine enteric nervous system |
| topic | Gastroenterology, Endocrine and Autonomic Systems, Physiology |
| url | http://dx.doi.org/10.1111/nmo.12827 |