Reduced food intake and body weight in mice deficient for the G protein-coupled receptor GPR82.
G protein-coupled receptors (GPCR) are involved in the regulation of numerous physiological functions. Therefore, GPCR variants may have conferred important selective advantages during periods of human evolution. Indeed, several genomic loci with signatures of recent selection in humans contain GPCR...
Guardado en:
| Autores principales: | , , , , , , , , , , , , , , , , , , |
|---|---|
| Formato: | article |
| Lenguaje: | EN |
| Publicado: |
Public Library of Science (PLoS)
2011
|
| Materias: | |
| Acceso en línea: | https://doaj.org/article/e5ae27ba1230404bbea5b73fe1fbfc0a |
| Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
| id |
oai:doaj.org-article:e5ae27ba1230404bbea5b73fe1fbfc0a |
|---|---|
| record_format |
dspace |
| spelling |
oai:doaj.org-article:e5ae27ba1230404bbea5b73fe1fbfc0a2021-11-18T07:31:22ZReduced food intake and body weight in mice deficient for the G protein-coupled receptor GPR82.1932-620310.1371/journal.pone.0029400https://doaj.org/article/e5ae27ba1230404bbea5b73fe1fbfc0a2011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22216272/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203G protein-coupled receptors (GPCR) are involved in the regulation of numerous physiological functions. Therefore, GPCR variants may have conferred important selective advantages during periods of human evolution. Indeed, several genomic loci with signatures of recent selection in humans contain GPCR genes among them the X-chromosomally located gene for GPR82. This gene encodes a so-called orphan GPCR with unknown function. To address the functional relevance of GPR82 gene-deficient mice were characterized. GPR82-deficient mice were viable, reproduced normally, and showed no gross anatomical abnormalities. However, GPR82-deficient mice have a reduced body weight and body fat content associated with a lower food intake. Moreover, GPR82-deficient mice showed decreased serum triacylglyceride levels, increased insulin sensitivity and glucose tolerance, most pronounced under Western diet. Because there were no differences in respiratory and metabolic rates between wild-type and GPR82-deficient mice our data suggest that GPR82 function influences food intake and, therefore, energy and body weight balance. GPR82 may represent a thrifty gene most probably representing an advantage during human expansion into new environments.Kathrin M Y EngelKristin SchröckDaniel TeupserLesca Miriam HoldtAnke TönjesMatthias KernKerstin DietrichPeter KovacsUte KrügelHolger A ScheidtJürgen SchillerDaniel HusterGudrun A BrockmannMartin AugustinJoachim ThieryMatthias BlüherMichael StumvollTorsten SchönebergAngela SchulzPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 12, p e29400 (2011) |
| institution |
DOAJ |
| collection |
DOAJ |
| language |
EN |
| topic |
Medicine R Science Q |
| spellingShingle |
Medicine R Science Q Kathrin M Y Engel Kristin Schröck Daniel Teupser Lesca Miriam Holdt Anke Tönjes Matthias Kern Kerstin Dietrich Peter Kovacs Ute Krügel Holger A Scheidt Jürgen Schiller Daniel Huster Gudrun A Brockmann Martin Augustin Joachim Thiery Matthias Blüher Michael Stumvoll Torsten Schöneberg Angela Schulz Reduced food intake and body weight in mice deficient for the G protein-coupled receptor GPR82. |
| description |
G protein-coupled receptors (GPCR) are involved in the regulation of numerous physiological functions. Therefore, GPCR variants may have conferred important selective advantages during periods of human evolution. Indeed, several genomic loci with signatures of recent selection in humans contain GPCR genes among them the X-chromosomally located gene for GPR82. This gene encodes a so-called orphan GPCR with unknown function. To address the functional relevance of GPR82 gene-deficient mice were characterized. GPR82-deficient mice were viable, reproduced normally, and showed no gross anatomical abnormalities. However, GPR82-deficient mice have a reduced body weight and body fat content associated with a lower food intake. Moreover, GPR82-deficient mice showed decreased serum triacylglyceride levels, increased insulin sensitivity and glucose tolerance, most pronounced under Western diet. Because there were no differences in respiratory and metabolic rates between wild-type and GPR82-deficient mice our data suggest that GPR82 function influences food intake and, therefore, energy and body weight balance. GPR82 may represent a thrifty gene most probably representing an advantage during human expansion into new environments. |
| format |
article |
| author |
Kathrin M Y Engel Kristin Schröck Daniel Teupser Lesca Miriam Holdt Anke Tönjes Matthias Kern Kerstin Dietrich Peter Kovacs Ute Krügel Holger A Scheidt Jürgen Schiller Daniel Huster Gudrun A Brockmann Martin Augustin Joachim Thiery Matthias Blüher Michael Stumvoll Torsten Schöneberg Angela Schulz |
| author_facet |
Kathrin M Y Engel Kristin Schröck Daniel Teupser Lesca Miriam Holdt Anke Tönjes Matthias Kern Kerstin Dietrich Peter Kovacs Ute Krügel Holger A Scheidt Jürgen Schiller Daniel Huster Gudrun A Brockmann Martin Augustin Joachim Thiery Matthias Blüher Michael Stumvoll Torsten Schöneberg Angela Schulz |
| author_sort |
Kathrin M Y Engel |
| title |
Reduced food intake and body weight in mice deficient for the G protein-coupled receptor GPR82. |
| title_short |
Reduced food intake and body weight in mice deficient for the G protein-coupled receptor GPR82. |
| title_full |
Reduced food intake and body weight in mice deficient for the G protein-coupled receptor GPR82. |
| title_fullStr |
Reduced food intake and body weight in mice deficient for the G protein-coupled receptor GPR82. |
| title_full_unstemmed |
Reduced food intake and body weight in mice deficient for the G protein-coupled receptor GPR82. |
| title_sort |
reduced food intake and body weight in mice deficient for the g protein-coupled receptor gpr82. |
| publisher |
Public Library of Science (PLoS) |
| publishDate |
2011 |
| url |
https://doaj.org/article/e5ae27ba1230404bbea5b73fe1fbfc0a |
| work_keys_str_mv |
AT kathrinmyengel reducedfoodintakeandbodyweightinmicedeficientforthegproteincoupledreceptorgpr82 AT kristinschrock reducedfoodintakeandbodyweightinmicedeficientforthegproteincoupledreceptorgpr82 AT danielteupser reducedfoodintakeandbodyweightinmicedeficientforthegproteincoupledreceptorgpr82 AT lescamiriamholdt reducedfoodintakeandbodyweightinmicedeficientforthegproteincoupledreceptorgpr82 AT anketonjes reducedfoodintakeandbodyweightinmicedeficientforthegproteincoupledreceptorgpr82 AT matthiaskern reducedfoodintakeandbodyweightinmicedeficientforthegproteincoupledreceptorgpr82 AT kerstindietrich reducedfoodintakeandbodyweightinmicedeficientforthegproteincoupledreceptorgpr82 AT peterkovacs reducedfoodintakeandbodyweightinmicedeficientforthegproteincoupledreceptorgpr82 AT utekrugel reducedfoodintakeandbodyweightinmicedeficientforthegproteincoupledreceptorgpr82 AT holgerascheidt reducedfoodintakeandbodyweightinmicedeficientforthegproteincoupledreceptorgpr82 AT jurgenschiller reducedfoodintakeandbodyweightinmicedeficientforthegproteincoupledreceptorgpr82 AT danielhuster reducedfoodintakeandbodyweightinmicedeficientforthegproteincoupledreceptorgpr82 AT gudrunabrockmann reducedfoodintakeandbodyweightinmicedeficientforthegproteincoupledreceptorgpr82 AT martinaugustin reducedfoodintakeandbodyweightinmicedeficientforthegproteincoupledreceptorgpr82 AT joachimthiery reducedfoodintakeandbodyweightinmicedeficientforthegproteincoupledreceptorgpr82 AT matthiasbluher reducedfoodintakeandbodyweightinmicedeficientforthegproteincoupledreceptorgpr82 AT michaelstumvoll reducedfoodintakeandbodyweightinmicedeficientforthegproteincoupledreceptorgpr82 AT torstenschoneberg reducedfoodintakeandbodyweightinmicedeficientforthegproteincoupledreceptorgpr82 AT angelaschulz reducedfoodintakeandbodyweightinmicedeficientforthegproteincoupledreceptorgpr82 |
| _version_ |
1718423382535438336 |