Ghrelin counteracts insulin-induced activation of vagal afferent neurons via growth hormone secretagogue receptor
Vagal afferent nerves sense meal-related gastrointestinal and pancreatic hormones and convey their information to the brain, thereby regulating brain functions including feeding. We have recently demonstrated that postprandial insulin directly acts on the vagal afferent neurons. Plasma concentration...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Iwasaki, Yusaku [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2015transfer abstract |
|---|
| Umfang: |
6 |
|---|
| Übergeordnetes Werk: |
Enthalten in: Medicaid acceptance among pediatric dermatologists - Fogel, Alexander L. ELSEVIER, 2015, [New York, NY] |
|---|---|
| Übergeordnetes Werk: |
volume:52 ; year:2015 ; pages:55-60 ; extent:6 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.npep.2015.06.003 |
|---|
| Katalog-ID: |
ELV028676769 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | ELV028676769 | ||
| 003 | DE-627 | ||
| 005 | 20230625162121.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 180603s2015 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.npep.2015.06.003 |2 doi | |
| 028 | 5 | 2 | |a GBVA2015003000030.pica |
| 035 | |a (DE-627)ELV028676769 | ||
| 035 | |a (ELSEVIER)S0143-4179(15)00060-8 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 082 | 0 | |a 610 | |
| 082 | 0 | 4 | |a 610 |q DE-600 |
| 082 | 0 | 4 | |a 610 |q VZ |
| 082 | 0 | 4 | |a 333.7 |a 610 |q VZ |
| 084 | |a 43.12 |2 bkl | ||
| 084 | |a 43.13 |2 bkl | ||
| 084 | |a 44.13 |2 bkl | ||
| 100 | 1 | |a Iwasaki, Yusaku |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Ghrelin counteracts insulin-induced activation of vagal afferent neurons via growth hormone secretagogue receptor |
| 264 | 1 | |c 2015transfer abstract | |
| 300 | |a 6 | ||
| 336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
| 337 | |a nicht spezifiziert |b z |2 rdamedia | ||
| 338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
| 520 | |a Vagal afferent nerves sense meal-related gastrointestinal and pancreatic hormones and convey their information to the brain, thereby regulating brain functions including feeding. We have recently demonstrated that postprandial insulin directly acts on the vagal afferent neurons. Plasma concentrations of orexigenic ghrelin and anorexigenic insulin show reciprocal dynamics before and after meals. The present study examined interactive effects of ghrelin and insulin on vagal afferent nerves. Cytosolic Ca2+ concentration ([Ca2+]i) in isolated nodose ganglion (NG) neurons was measured to monitor their activity. Insulin at 10−7 M increased [Ca2+]i in NG neurons, and the insulin-induced [Ca2+]i increase was inhibited by treatment with ghrelin at 10−8 M. This inhibitory effect of ghrelin was attenuated by [D-Lys3]-GHRP-6, an antagonist of growth hormone-secretagogue receptor (GHSR). Des-acyl ghrelin had little effect on insulin-induced [Ca2+]i increases in NG neurons. Ghrelin did not affect [Ca2+]i increases in response to cholecystokinin (CCK), a hormone that inhibits feeding via vagal afferent neurons, indicating that ghrelin selectively counteracts the insulin action. These results demonstrate that ghrelin via GHSR suppresses insulin-induced activation of NG neurons. The action of ghrelin to counteract insulin effects on NG might serve to efficiently inform the brain of the systemic change between fasting-associated ghrelin-dominant and fed-associated insulin-dominant states for the homeostatic central regulation of feeding and metabolism. | ||
| 520 | |a Vagal afferent nerves sense meal-related gastrointestinal and pancreatic hormones and convey their information to the brain, thereby regulating brain functions including feeding. We have recently demonstrated that postprandial insulin directly acts on the vagal afferent neurons. Plasma concentrations of orexigenic ghrelin and anorexigenic insulin show reciprocal dynamics before and after meals. The present study examined interactive effects of ghrelin and insulin on vagal afferent nerves. Cytosolic Ca2+ concentration ([Ca2+]i) in isolated nodose ganglion (NG) neurons was measured to monitor their activity. Insulin at 10−7 M increased [Ca2+]i in NG neurons, and the insulin-induced [Ca2+]i increase was inhibited by treatment with ghrelin at 10−8 M. This inhibitory effect of ghrelin was attenuated by [D-Lys3]-GHRP-6, an antagonist of growth hormone-secretagogue receptor (GHSR). Des-acyl ghrelin had little effect on insulin-induced [Ca2+]i increases in NG neurons. Ghrelin did not affect [Ca2+]i increases in response to cholecystokinin (CCK), a hormone that inhibits feeding via vagal afferent neurons, indicating that ghrelin selectively counteracts the insulin action. These results demonstrate that ghrelin via GHSR suppresses insulin-induced activation of NG neurons. The action of ghrelin to counteract insulin effects on NG might serve to efficiently inform the brain of the systemic change between fasting-associated ghrelin-dominant and fed-associated insulin-dominant states for the homeostatic central regulation of feeding and metabolism. | ||
| 700 | 1 | |a Dezaki, Katsuya |4 oth | |
| 700 | 1 | |a Kumari, Parmila |4 oth | |
| 700 | 1 | |a Kakei, Masafumi |4 oth | |
| 700 | 1 | |a Yada, Toshihiko |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier |a Fogel, Alexander L. ELSEVIER |t Medicaid acceptance among pediatric dermatologists |d 2015 |g [New York, NY] |w (DE-627)ELV01831726X |
| 773 | 1 | 8 | |g volume:52 |g year:2015 |g pages:55-60 |g extent:6 |
| 856 | 4 | 0 | |u https://doi.org/10.1016/j.npep.2015.06.003 |3 Volltext |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a GBV_ELV | ||
| 912 | |a SYSFLAG_U | ||
| 912 | |a SSG-OLC-PHA | ||
| 912 | |a SSG-OPC-GGO | ||
| 912 | |a GBV_ILN_24 | ||
| 912 | |a GBV_ILN_26 | ||
| 912 | |a GBV_ILN_40 | ||
| 912 | |a GBV_ILN_70 | ||
| 912 | |a GBV_ILN_132 | ||
| 912 | |a GBV_ILN_707 | ||
| 912 | |a GBV_ILN_2004 | ||
| 936 | b | k | |a 43.12 |j Umweltchemie |q VZ |
| 936 | b | k | |a 43.13 |j Umwelttoxikologie |q VZ |
| 936 | b | k | |a 44.13 |j Medizinische Ökologie |q VZ |
| 951 | |a AR | ||
| 952 | |d 52 |j 2015 |h 55-60 |g 6 | ||
| 953 | |2 045F |a 610 | ||
| author_variant |
y i yi |
|---|---|
| matchkey_str |
iwasakiyusakudezakikatsuyakumariparmilak:2015----:heicutrcsnuiidcdciainfaaafrnnuosigoth |
| hierarchy_sort_str |
2015transfer abstract |
| bklnumber |
43.12 43.13 44.13 |
| publishDate |
2015 |
| allfields |
10.1016/j.npep.2015.06.003 doi GBVA2015003000030.pica (DE-627)ELV028676769 (ELSEVIER)S0143-4179(15)00060-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Iwasaki, Yusaku verfasserin aut Ghrelin counteracts insulin-induced activation of vagal afferent neurons via growth hormone secretagogue receptor 2015transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Vagal afferent nerves sense meal-related gastrointestinal and pancreatic hormones and convey their information to the brain, thereby regulating brain functions including feeding. We have recently demonstrated that postprandial insulin directly acts on the vagal afferent neurons. Plasma concentrations of orexigenic ghrelin and anorexigenic insulin show reciprocal dynamics before and after meals. The present study examined interactive effects of ghrelin and insulin on vagal afferent nerves. Cytosolic Ca2+ concentration ([Ca2+]i) in isolated nodose ganglion (NG) neurons was measured to monitor their activity. Insulin at 10−7 M increased [Ca2+]i in NG neurons, and the insulin-induced [Ca2+]i increase was inhibited by treatment with ghrelin at 10−8 M. This inhibitory effect of ghrelin was attenuated by [D-Lys3]-GHRP-6, an antagonist of growth hormone-secretagogue receptor (GHSR). Des-acyl ghrelin had little effect on insulin-induced [Ca2+]i increases in NG neurons. Ghrelin did not affect [Ca2+]i increases in response to cholecystokinin (CCK), a hormone that inhibits feeding via vagal afferent neurons, indicating that ghrelin selectively counteracts the insulin action. These results demonstrate that ghrelin via GHSR suppresses insulin-induced activation of NG neurons. The action of ghrelin to counteract insulin effects on NG might serve to efficiently inform the brain of the systemic change between fasting-associated ghrelin-dominant and fed-associated insulin-dominant states for the homeostatic central regulation of feeding and metabolism. Vagal afferent nerves sense meal-related gastrointestinal and pancreatic hormones and convey their information to the brain, thereby regulating brain functions including feeding. We have recently demonstrated that postprandial insulin directly acts on the vagal afferent neurons. Plasma concentrations of orexigenic ghrelin and anorexigenic insulin show reciprocal dynamics before and after meals. The present study examined interactive effects of ghrelin and insulin on vagal afferent nerves. Cytosolic Ca2+ concentration ([Ca2+]i) in isolated nodose ganglion (NG) neurons was measured to monitor their activity. Insulin at 10−7 M increased [Ca2+]i in NG neurons, and the insulin-induced [Ca2+]i increase was inhibited by treatment with ghrelin at 10−8 M. This inhibitory effect of ghrelin was attenuated by [D-Lys3]-GHRP-6, an antagonist of growth hormone-secretagogue receptor (GHSR). Des-acyl ghrelin had little effect on insulin-induced [Ca2+]i increases in NG neurons. Ghrelin did not affect [Ca2+]i increases in response to cholecystokinin (CCK), a hormone that inhibits feeding via vagal afferent neurons, indicating that ghrelin selectively counteracts the insulin action. These results demonstrate that ghrelin via GHSR suppresses insulin-induced activation of NG neurons. The action of ghrelin to counteract insulin effects on NG might serve to efficiently inform the brain of the systemic change between fasting-associated ghrelin-dominant and fed-associated insulin-dominant states for the homeostatic central regulation of feeding and metabolism. Dezaki, Katsuya oth Kumari, Parmila oth Kakei, Masafumi oth Yada, Toshihiko oth Enthalten in Elsevier Fogel, Alexander L. ELSEVIER Medicaid acceptance among pediatric dermatologists 2015 [New York, NY] (DE-627)ELV01831726X volume:52 year:2015 pages:55-60 extent:6 https://doi.org/10.1016/j.npep.2015.06.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO GBV_ILN_24 GBV_ILN_26 GBV_ILN_40 GBV_ILN_70 GBV_ILN_132 GBV_ILN_707 GBV_ILN_2004 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 52 2015 55-60 6 045F 610 |
| spelling |
10.1016/j.npep.2015.06.003 doi GBVA2015003000030.pica (DE-627)ELV028676769 (ELSEVIER)S0143-4179(15)00060-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Iwasaki, Yusaku verfasserin aut Ghrelin counteracts insulin-induced activation of vagal afferent neurons via growth hormone secretagogue receptor 2015transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Vagal afferent nerves sense meal-related gastrointestinal and pancreatic hormones and convey their information to the brain, thereby regulating brain functions including feeding. We have recently demonstrated that postprandial insulin directly acts on the vagal afferent neurons. Plasma concentrations of orexigenic ghrelin and anorexigenic insulin show reciprocal dynamics before and after meals. The present study examined interactive effects of ghrelin and insulin on vagal afferent nerves. Cytosolic Ca2+ concentration ([Ca2+]i) in isolated nodose ganglion (NG) neurons was measured to monitor their activity. Insulin at 10−7 M increased [Ca2+]i in NG neurons, and the insulin-induced [Ca2+]i increase was inhibited by treatment with ghrelin at 10−8 M. This inhibitory effect of ghrelin was attenuated by [D-Lys3]-GHRP-6, an antagonist of growth hormone-secretagogue receptor (GHSR). Des-acyl ghrelin had little effect on insulin-induced [Ca2+]i increases in NG neurons. Ghrelin did not affect [Ca2+]i increases in response to cholecystokinin (CCK), a hormone that inhibits feeding via vagal afferent neurons, indicating that ghrelin selectively counteracts the insulin action. These results demonstrate that ghrelin via GHSR suppresses insulin-induced activation of NG neurons. The action of ghrelin to counteract insulin effects on NG might serve to efficiently inform the brain of the systemic change between fasting-associated ghrelin-dominant and fed-associated insulin-dominant states for the homeostatic central regulation of feeding and metabolism. Vagal afferent nerves sense meal-related gastrointestinal and pancreatic hormones and convey their information to the brain, thereby regulating brain functions including feeding. We have recently demonstrated that postprandial insulin directly acts on the vagal afferent neurons. Plasma concentrations of orexigenic ghrelin and anorexigenic insulin show reciprocal dynamics before and after meals. The present study examined interactive effects of ghrelin and insulin on vagal afferent nerves. Cytosolic Ca2+ concentration ([Ca2+]i) in isolated nodose ganglion (NG) neurons was measured to monitor their activity. Insulin at 10−7 M increased [Ca2+]i in NG neurons, and the insulin-induced [Ca2+]i increase was inhibited by treatment with ghrelin at 10−8 M. This inhibitory effect of ghrelin was attenuated by [D-Lys3]-GHRP-6, an antagonist of growth hormone-secretagogue receptor (GHSR). Des-acyl ghrelin had little effect on insulin-induced [Ca2+]i increases in NG neurons. Ghrelin did not affect [Ca2+]i increases in response to cholecystokinin (CCK), a hormone that inhibits feeding via vagal afferent neurons, indicating that ghrelin selectively counteracts the insulin action. These results demonstrate that ghrelin via GHSR suppresses insulin-induced activation of NG neurons. The action of ghrelin to counteract insulin effects on NG might serve to efficiently inform the brain of the systemic change between fasting-associated ghrelin-dominant and fed-associated insulin-dominant states for the homeostatic central regulation of feeding and metabolism. Dezaki, Katsuya oth Kumari, Parmila oth Kakei, Masafumi oth Yada, Toshihiko oth Enthalten in Elsevier Fogel, Alexander L. ELSEVIER Medicaid acceptance among pediatric dermatologists 2015 [New York, NY] (DE-627)ELV01831726X volume:52 year:2015 pages:55-60 extent:6 https://doi.org/10.1016/j.npep.2015.06.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO GBV_ILN_24 GBV_ILN_26 GBV_ILN_40 GBV_ILN_70 GBV_ILN_132 GBV_ILN_707 GBV_ILN_2004 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 52 2015 55-60 6 045F 610 |
| allfields_unstemmed |
10.1016/j.npep.2015.06.003 doi GBVA2015003000030.pica (DE-627)ELV028676769 (ELSEVIER)S0143-4179(15)00060-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Iwasaki, Yusaku verfasserin aut Ghrelin counteracts insulin-induced activation of vagal afferent neurons via growth hormone secretagogue receptor 2015transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Vagal afferent nerves sense meal-related gastrointestinal and pancreatic hormones and convey their information to the brain, thereby regulating brain functions including feeding. We have recently demonstrated that postprandial insulin directly acts on the vagal afferent neurons. Plasma concentrations of orexigenic ghrelin and anorexigenic insulin show reciprocal dynamics before and after meals. The present study examined interactive effects of ghrelin and insulin on vagal afferent nerves. Cytosolic Ca2+ concentration ([Ca2+]i) in isolated nodose ganglion (NG) neurons was measured to monitor their activity. Insulin at 10−7 M increased [Ca2+]i in NG neurons, and the insulin-induced [Ca2+]i increase was inhibited by treatment with ghrelin at 10−8 M. This inhibitory effect of ghrelin was attenuated by [D-Lys3]-GHRP-6, an antagonist of growth hormone-secretagogue receptor (GHSR). Des-acyl ghrelin had little effect on insulin-induced [Ca2+]i increases in NG neurons. Ghrelin did not affect [Ca2+]i increases in response to cholecystokinin (CCK), a hormone that inhibits feeding via vagal afferent neurons, indicating that ghrelin selectively counteracts the insulin action. These results demonstrate that ghrelin via GHSR suppresses insulin-induced activation of NG neurons. The action of ghrelin to counteract insulin effects on NG might serve to efficiently inform the brain of the systemic change between fasting-associated ghrelin-dominant and fed-associated insulin-dominant states for the homeostatic central regulation of feeding and metabolism. Vagal afferent nerves sense meal-related gastrointestinal and pancreatic hormones and convey their information to the brain, thereby regulating brain functions including feeding. We have recently demonstrated that postprandial insulin directly acts on the vagal afferent neurons. Plasma concentrations of orexigenic ghrelin and anorexigenic insulin show reciprocal dynamics before and after meals. The present study examined interactive effects of ghrelin and insulin on vagal afferent nerves. Cytosolic Ca2+ concentration ([Ca2+]i) in isolated nodose ganglion (NG) neurons was measured to monitor their activity. Insulin at 10−7 M increased [Ca2+]i in NG neurons, and the insulin-induced [Ca2+]i increase was inhibited by treatment with ghrelin at 10−8 M. This inhibitory effect of ghrelin was attenuated by [D-Lys3]-GHRP-6, an antagonist of growth hormone-secretagogue receptor (GHSR). Des-acyl ghrelin had little effect on insulin-induced [Ca2+]i increases in NG neurons. Ghrelin did not affect [Ca2+]i increases in response to cholecystokinin (CCK), a hormone that inhibits feeding via vagal afferent neurons, indicating that ghrelin selectively counteracts the insulin action. These results demonstrate that ghrelin via GHSR suppresses insulin-induced activation of NG neurons. The action of ghrelin to counteract insulin effects on NG might serve to efficiently inform the brain of the systemic change between fasting-associated ghrelin-dominant and fed-associated insulin-dominant states for the homeostatic central regulation of feeding and metabolism. Dezaki, Katsuya oth Kumari, Parmila oth Kakei, Masafumi oth Yada, Toshihiko oth Enthalten in Elsevier Fogel, Alexander L. ELSEVIER Medicaid acceptance among pediatric dermatologists 2015 [New York, NY] (DE-627)ELV01831726X volume:52 year:2015 pages:55-60 extent:6 https://doi.org/10.1016/j.npep.2015.06.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO GBV_ILN_24 GBV_ILN_26 GBV_ILN_40 GBV_ILN_70 GBV_ILN_132 GBV_ILN_707 GBV_ILN_2004 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 52 2015 55-60 6 045F 610 |
| allfieldsGer |
10.1016/j.npep.2015.06.003 doi GBVA2015003000030.pica (DE-627)ELV028676769 (ELSEVIER)S0143-4179(15)00060-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Iwasaki, Yusaku verfasserin aut Ghrelin counteracts insulin-induced activation of vagal afferent neurons via growth hormone secretagogue receptor 2015transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Vagal afferent nerves sense meal-related gastrointestinal and pancreatic hormones and convey their information to the brain, thereby regulating brain functions including feeding. We have recently demonstrated that postprandial insulin directly acts on the vagal afferent neurons. Plasma concentrations of orexigenic ghrelin and anorexigenic insulin show reciprocal dynamics before and after meals. The present study examined interactive effects of ghrelin and insulin on vagal afferent nerves. Cytosolic Ca2+ concentration ([Ca2+]i) in isolated nodose ganglion (NG) neurons was measured to monitor their activity. Insulin at 10−7 M increased [Ca2+]i in NG neurons, and the insulin-induced [Ca2+]i increase was inhibited by treatment with ghrelin at 10−8 M. This inhibitory effect of ghrelin was attenuated by [D-Lys3]-GHRP-6, an antagonist of growth hormone-secretagogue receptor (GHSR). Des-acyl ghrelin had little effect on insulin-induced [Ca2+]i increases in NG neurons. Ghrelin did not affect [Ca2+]i increases in response to cholecystokinin (CCK), a hormone that inhibits feeding via vagal afferent neurons, indicating that ghrelin selectively counteracts the insulin action. These results demonstrate that ghrelin via GHSR suppresses insulin-induced activation of NG neurons. The action of ghrelin to counteract insulin effects on NG might serve to efficiently inform the brain of the systemic change between fasting-associated ghrelin-dominant and fed-associated insulin-dominant states for the homeostatic central regulation of feeding and metabolism. Vagal afferent nerves sense meal-related gastrointestinal and pancreatic hormones and convey their information to the brain, thereby regulating brain functions including feeding. We have recently demonstrated that postprandial insulin directly acts on the vagal afferent neurons. Plasma concentrations of orexigenic ghrelin and anorexigenic insulin show reciprocal dynamics before and after meals. The present study examined interactive effects of ghrelin and insulin on vagal afferent nerves. Cytosolic Ca2+ concentration ([Ca2+]i) in isolated nodose ganglion (NG) neurons was measured to monitor their activity. Insulin at 10−7 M increased [Ca2+]i in NG neurons, and the insulin-induced [Ca2+]i increase was inhibited by treatment with ghrelin at 10−8 M. This inhibitory effect of ghrelin was attenuated by [D-Lys3]-GHRP-6, an antagonist of growth hormone-secretagogue receptor (GHSR). Des-acyl ghrelin had little effect on insulin-induced [Ca2+]i increases in NG neurons. Ghrelin did not affect [Ca2+]i increases in response to cholecystokinin (CCK), a hormone that inhibits feeding via vagal afferent neurons, indicating that ghrelin selectively counteracts the insulin action. These results demonstrate that ghrelin via GHSR suppresses insulin-induced activation of NG neurons. The action of ghrelin to counteract insulin effects on NG might serve to efficiently inform the brain of the systemic change between fasting-associated ghrelin-dominant and fed-associated insulin-dominant states for the homeostatic central regulation of feeding and metabolism. Dezaki, Katsuya oth Kumari, Parmila oth Kakei, Masafumi oth Yada, Toshihiko oth Enthalten in Elsevier Fogel, Alexander L. ELSEVIER Medicaid acceptance among pediatric dermatologists 2015 [New York, NY] (DE-627)ELV01831726X volume:52 year:2015 pages:55-60 extent:6 https://doi.org/10.1016/j.npep.2015.06.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO GBV_ILN_24 GBV_ILN_26 GBV_ILN_40 GBV_ILN_70 GBV_ILN_132 GBV_ILN_707 GBV_ILN_2004 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 52 2015 55-60 6 045F 610 |
| allfieldsSound |
10.1016/j.npep.2015.06.003 doi GBVA2015003000030.pica (DE-627)ELV028676769 (ELSEVIER)S0143-4179(15)00060-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Iwasaki, Yusaku verfasserin aut Ghrelin counteracts insulin-induced activation of vagal afferent neurons via growth hormone secretagogue receptor 2015transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Vagal afferent nerves sense meal-related gastrointestinal and pancreatic hormones and convey their information to the brain, thereby regulating brain functions including feeding. We have recently demonstrated that postprandial insulin directly acts on the vagal afferent neurons. Plasma concentrations of orexigenic ghrelin and anorexigenic insulin show reciprocal dynamics before and after meals. The present study examined interactive effects of ghrelin and insulin on vagal afferent nerves. Cytosolic Ca2+ concentration ([Ca2+]i) in isolated nodose ganglion (NG) neurons was measured to monitor their activity. Insulin at 10−7 M increased [Ca2+]i in NG neurons, and the insulin-induced [Ca2+]i increase was inhibited by treatment with ghrelin at 10−8 M. This inhibitory effect of ghrelin was attenuated by [D-Lys3]-GHRP-6, an antagonist of growth hormone-secretagogue receptor (GHSR). Des-acyl ghrelin had little effect on insulin-induced [Ca2+]i increases in NG neurons. Ghrelin did not affect [Ca2+]i increases in response to cholecystokinin (CCK), a hormone that inhibits feeding via vagal afferent neurons, indicating that ghrelin selectively counteracts the insulin action. These results demonstrate that ghrelin via GHSR suppresses insulin-induced activation of NG neurons. The action of ghrelin to counteract insulin effects on NG might serve to efficiently inform the brain of the systemic change between fasting-associated ghrelin-dominant and fed-associated insulin-dominant states for the homeostatic central regulation of feeding and metabolism. Vagal afferent nerves sense meal-related gastrointestinal and pancreatic hormones and convey their information to the brain, thereby regulating brain functions including feeding. We have recently demonstrated that postprandial insulin directly acts on the vagal afferent neurons. Plasma concentrations of orexigenic ghrelin and anorexigenic insulin show reciprocal dynamics before and after meals. The present study examined interactive effects of ghrelin and insulin on vagal afferent nerves. Cytosolic Ca2+ concentration ([Ca2+]i) in isolated nodose ganglion (NG) neurons was measured to monitor their activity. Insulin at 10−7 M increased [Ca2+]i in NG neurons, and the insulin-induced [Ca2+]i increase was inhibited by treatment with ghrelin at 10−8 M. This inhibitory effect of ghrelin was attenuated by [D-Lys3]-GHRP-6, an antagonist of growth hormone-secretagogue receptor (GHSR). Des-acyl ghrelin had little effect on insulin-induced [Ca2+]i increases in NG neurons. Ghrelin did not affect [Ca2+]i increases in response to cholecystokinin (CCK), a hormone that inhibits feeding via vagal afferent neurons, indicating that ghrelin selectively counteracts the insulin action. These results demonstrate that ghrelin via GHSR suppresses insulin-induced activation of NG neurons. The action of ghrelin to counteract insulin effects on NG might serve to efficiently inform the brain of the systemic change between fasting-associated ghrelin-dominant and fed-associated insulin-dominant states for the homeostatic central regulation of feeding and metabolism. Dezaki, Katsuya oth Kumari, Parmila oth Kakei, Masafumi oth Yada, Toshihiko oth Enthalten in Elsevier Fogel, Alexander L. ELSEVIER Medicaid acceptance among pediatric dermatologists 2015 [New York, NY] (DE-627)ELV01831726X volume:52 year:2015 pages:55-60 extent:6 https://doi.org/10.1016/j.npep.2015.06.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO GBV_ILN_24 GBV_ILN_26 GBV_ILN_40 GBV_ILN_70 GBV_ILN_132 GBV_ILN_707 GBV_ILN_2004 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 52 2015 55-60 6 045F 610 |
| language |
English |
| source |
Enthalten in Medicaid acceptance among pediatric dermatologists [New York, NY] volume:52 year:2015 pages:55-60 extent:6 |
| sourceStr |
Enthalten in Medicaid acceptance among pediatric dermatologists [New York, NY] volume:52 year:2015 pages:55-60 extent:6 |
| format_phy_str_mv |
Article |
| bklname |
Umweltchemie Umwelttoxikologie Medizinische Ökologie |
| institution |
findex.gbv.de |
| dewey-raw |
610 |
| isfreeaccess_bool |
false |
| container_title |
Medicaid acceptance among pediatric dermatologists |
| authorswithroles_txt_mv |
Iwasaki, Yusaku @@aut@@ Dezaki, Katsuya @@oth@@ Kumari, Parmila @@oth@@ Kakei, Masafumi @@oth@@ Yada, Toshihiko @@oth@@ |
| publishDateDaySort_date |
2015-01-01T00:00:00Z |
| hierarchy_top_id |
ELV01831726X |
| dewey-sort |
3610 |
| id |
ELV028676769 |
| language_de |
englisch |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV028676769</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625162121.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2015 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.npep.2015.06.003</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2015003000030.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV028676769</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0143-4179(15)00060-8</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">333.7</subfield><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">43.12</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">43.13</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.13</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Iwasaki, Yusaku</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Ghrelin counteracts insulin-induced activation of vagal afferent neurons via growth hormone secretagogue receptor</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2015transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">6</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Vagal afferent nerves sense meal-related gastrointestinal and pancreatic hormones and convey their information to the brain, thereby regulating brain functions including feeding. We have recently demonstrated that postprandial insulin directly acts on the vagal afferent neurons. Plasma concentrations of orexigenic ghrelin and anorexigenic insulin show reciprocal dynamics before and after meals. The present study examined interactive effects of ghrelin and insulin on vagal afferent nerves. Cytosolic Ca2+ concentration ([Ca2+]i) in isolated nodose ganglion (NG) neurons was measured to monitor their activity. Insulin at 10−7 M increased [Ca2+]i in NG neurons, and the insulin-induced [Ca2+]i increase was inhibited by treatment with ghrelin at 10−8 M. This inhibitory effect of ghrelin was attenuated by [D-Lys3]-GHRP-6, an antagonist of growth hormone-secretagogue receptor (GHSR). Des-acyl ghrelin had little effect on insulin-induced [Ca2+]i increases in NG neurons. Ghrelin did not affect [Ca2+]i increases in response to cholecystokinin (CCK), a hormone that inhibits feeding via vagal afferent neurons, indicating that ghrelin selectively counteracts the insulin action. These results demonstrate that ghrelin via GHSR suppresses insulin-induced activation of NG neurons. The action of ghrelin to counteract insulin effects on NG might serve to efficiently inform the brain of the systemic change between fasting-associated ghrelin-dominant and fed-associated insulin-dominant states for the homeostatic central regulation of feeding and metabolism.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Vagal afferent nerves sense meal-related gastrointestinal and pancreatic hormones and convey their information to the brain, thereby regulating brain functions including feeding. We have recently demonstrated that postprandial insulin directly acts on the vagal afferent neurons. Plasma concentrations of orexigenic ghrelin and anorexigenic insulin show reciprocal dynamics before and after meals. The present study examined interactive effects of ghrelin and insulin on vagal afferent nerves. Cytosolic Ca2+ concentration ([Ca2+]i) in isolated nodose ganglion (NG) neurons was measured to monitor their activity. Insulin at 10−7 M increased [Ca2+]i in NG neurons, and the insulin-induced [Ca2+]i increase was inhibited by treatment with ghrelin at 10−8 M. This inhibitory effect of ghrelin was attenuated by [D-Lys3]-GHRP-6, an antagonist of growth hormone-secretagogue receptor (GHSR). Des-acyl ghrelin had little effect on insulin-induced [Ca2+]i increases in NG neurons. Ghrelin did not affect [Ca2+]i increases in response to cholecystokinin (CCK), a hormone that inhibits feeding via vagal afferent neurons, indicating that ghrelin selectively counteracts the insulin action. These results demonstrate that ghrelin via GHSR suppresses insulin-induced activation of NG neurons. The action of ghrelin to counteract insulin effects on NG might serve to efficiently inform the brain of the systemic change between fasting-associated ghrelin-dominant and fed-associated insulin-dominant states for the homeostatic central regulation of feeding and metabolism.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Dezaki, Katsuya</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kumari, Parmila</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kakei, Masafumi</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yada, Toshihiko</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier</subfield><subfield code="a">Fogel, Alexander L. ELSEVIER</subfield><subfield code="t">Medicaid acceptance among pediatric dermatologists</subfield><subfield code="d">2015</subfield><subfield code="g">[New York, NY]</subfield><subfield code="w">(DE-627)ELV01831726X</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:52</subfield><subfield code="g">year:2015</subfield><subfield code="g">pages:55-60</subfield><subfield code="g">extent:6</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.npep.2015.06.003</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-GGO</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_24</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_26</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_70</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_132</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_707</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2004</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">43.12</subfield><subfield code="j">Umweltchemie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">43.13</subfield><subfield code="j">Umwelttoxikologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.13</subfield><subfield code="j">Medizinische Ökologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">52</subfield><subfield code="j">2015</subfield><subfield code="h">55-60</subfield><subfield code="g">6</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
| author |
Iwasaki, Yusaku |
| spellingShingle |
Iwasaki, Yusaku ddc 610 ddc 333.7 bkl 43.12 bkl 43.13 bkl 44.13 Ghrelin counteracts insulin-induced activation of vagal afferent neurons via growth hormone secretagogue receptor |
| authorStr |
Iwasaki, Yusaku |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)ELV01831726X |
| format |
electronic Article |
| dewey-ones |
610 - Medicine & health 333 - Economics of land & energy |
| delete_txt_mv |
keep |
| author_role |
aut |
| collection |
elsevier |
| remote_str |
true |
| illustrated |
Not Illustrated |
| topic_title |
610 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Ghrelin counteracts insulin-induced activation of vagal afferent neurons via growth hormone secretagogue receptor |
| topic |
ddc 610 ddc 333.7 bkl 43.12 bkl 43.13 bkl 44.13 |
| topic_unstemmed |
ddc 610 ddc 333.7 bkl 43.12 bkl 43.13 bkl 44.13 |
| topic_browse |
ddc 610 ddc 333.7 bkl 43.12 bkl 43.13 bkl 44.13 |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| author2_variant |
k d kd p k pk m k mk t y ty |
| hierarchy_parent_title |
Medicaid acceptance among pediatric dermatologists |
| hierarchy_parent_id |
ELV01831726X |
| dewey-tens |
610 - Medicine & health 330 - Economics |
| hierarchy_top_title |
Medicaid acceptance among pediatric dermatologists |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)ELV01831726X |
| title |
Ghrelin counteracts insulin-induced activation of vagal afferent neurons via growth hormone secretagogue receptor |
| ctrlnum |
(DE-627)ELV028676769 (ELSEVIER)S0143-4179(15)00060-8 |
| title_full |
Ghrelin counteracts insulin-induced activation of vagal afferent neurons via growth hormone secretagogue receptor |
| author_sort |
Iwasaki, Yusaku |
| journal |
Medicaid acceptance among pediatric dermatologists |
| journalStr |
Medicaid acceptance among pediatric dermatologists |
| lang_code |
eng |
| isOA_bool |
false |
| dewey-hundreds |
600 - Technology 300 - Social sciences |
| recordtype |
marc |
| publishDateSort |
2015 |
| contenttype_str_mv |
zzz |
| container_start_page |
55 |
| author_browse |
Iwasaki, Yusaku |
| container_volume |
52 |
| physical |
6 |
| class |
610 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl |
| format_se |
Elektronische Aufsätze |
| author-letter |
Iwasaki, Yusaku |
| doi_str_mv |
10.1016/j.npep.2015.06.003 |
| dewey-full |
610 333.7 |
| title_sort |
ghrelin counteracts insulin-induced activation of vagal afferent neurons via growth hormone secretagogue receptor |
| title_auth |
Ghrelin counteracts insulin-induced activation of vagal afferent neurons via growth hormone secretagogue receptor |
| abstract |
Vagal afferent nerves sense meal-related gastrointestinal and pancreatic hormones and convey their information to the brain, thereby regulating brain functions including feeding. We have recently demonstrated that postprandial insulin directly acts on the vagal afferent neurons. Plasma concentrations of orexigenic ghrelin and anorexigenic insulin show reciprocal dynamics before and after meals. The present study examined interactive effects of ghrelin and insulin on vagal afferent nerves. Cytosolic Ca2+ concentration ([Ca2+]i) in isolated nodose ganglion (NG) neurons was measured to monitor their activity. Insulin at 10−7 M increased [Ca2+]i in NG neurons, and the insulin-induced [Ca2+]i increase was inhibited by treatment with ghrelin at 10−8 M. This inhibitory effect of ghrelin was attenuated by [D-Lys3]-GHRP-6, an antagonist of growth hormone-secretagogue receptor (GHSR). Des-acyl ghrelin had little effect on insulin-induced [Ca2+]i increases in NG neurons. Ghrelin did not affect [Ca2+]i increases in response to cholecystokinin (CCK), a hormone that inhibits feeding via vagal afferent neurons, indicating that ghrelin selectively counteracts the insulin action. These results demonstrate that ghrelin via GHSR suppresses insulin-induced activation of NG neurons. The action of ghrelin to counteract insulin effects on NG might serve to efficiently inform the brain of the systemic change between fasting-associated ghrelin-dominant and fed-associated insulin-dominant states for the homeostatic central regulation of feeding and metabolism. |
| abstractGer |
Vagal afferent nerves sense meal-related gastrointestinal and pancreatic hormones and convey their information to the brain, thereby regulating brain functions including feeding. We have recently demonstrated that postprandial insulin directly acts on the vagal afferent neurons. Plasma concentrations of orexigenic ghrelin and anorexigenic insulin show reciprocal dynamics before and after meals. The present study examined interactive effects of ghrelin and insulin on vagal afferent nerves. Cytosolic Ca2+ concentration ([Ca2+]i) in isolated nodose ganglion (NG) neurons was measured to monitor their activity. Insulin at 10−7 M increased [Ca2+]i in NG neurons, and the insulin-induced [Ca2+]i increase was inhibited by treatment with ghrelin at 10−8 M. This inhibitory effect of ghrelin was attenuated by [D-Lys3]-GHRP-6, an antagonist of growth hormone-secretagogue receptor (GHSR). Des-acyl ghrelin had little effect on insulin-induced [Ca2+]i increases in NG neurons. Ghrelin did not affect [Ca2+]i increases in response to cholecystokinin (CCK), a hormone that inhibits feeding via vagal afferent neurons, indicating that ghrelin selectively counteracts the insulin action. These results demonstrate that ghrelin via GHSR suppresses insulin-induced activation of NG neurons. The action of ghrelin to counteract insulin effects on NG might serve to efficiently inform the brain of the systemic change between fasting-associated ghrelin-dominant and fed-associated insulin-dominant states for the homeostatic central regulation of feeding and metabolism. |
| abstract_unstemmed |
Vagal afferent nerves sense meal-related gastrointestinal and pancreatic hormones and convey their information to the brain, thereby regulating brain functions including feeding. We have recently demonstrated that postprandial insulin directly acts on the vagal afferent neurons. Plasma concentrations of orexigenic ghrelin and anorexigenic insulin show reciprocal dynamics before and after meals. The present study examined interactive effects of ghrelin and insulin on vagal afferent nerves. Cytosolic Ca2+ concentration ([Ca2+]i) in isolated nodose ganglion (NG) neurons was measured to monitor their activity. Insulin at 10−7 M increased [Ca2+]i in NG neurons, and the insulin-induced [Ca2+]i increase was inhibited by treatment with ghrelin at 10−8 M. This inhibitory effect of ghrelin was attenuated by [D-Lys3]-GHRP-6, an antagonist of growth hormone-secretagogue receptor (GHSR). Des-acyl ghrelin had little effect on insulin-induced [Ca2+]i increases in NG neurons. Ghrelin did not affect [Ca2+]i increases in response to cholecystokinin (CCK), a hormone that inhibits feeding via vagal afferent neurons, indicating that ghrelin selectively counteracts the insulin action. These results demonstrate that ghrelin via GHSR suppresses insulin-induced activation of NG neurons. The action of ghrelin to counteract insulin effects on NG might serve to efficiently inform the brain of the systemic change between fasting-associated ghrelin-dominant and fed-associated insulin-dominant states for the homeostatic central regulation of feeding and metabolism. |
| collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO GBV_ILN_24 GBV_ILN_26 GBV_ILN_40 GBV_ILN_70 GBV_ILN_132 GBV_ILN_707 GBV_ILN_2004 |
| title_short |
Ghrelin counteracts insulin-induced activation of vagal afferent neurons via growth hormone secretagogue receptor |
| url |
https://doi.org/10.1016/j.npep.2015.06.003 |
| remote_bool |
true |
| author2 |
Dezaki, Katsuya Kumari, Parmila Kakei, Masafumi Yada, Toshihiko |
| author2Str |
Dezaki, Katsuya Kumari, Parmila Kakei, Masafumi Yada, Toshihiko |
| ppnlink |
ELV01831726X |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth oth oth |
| doi_str |
10.1016/j.npep.2015.06.003 |
| up_date |
2024-07-06T19:26:37.018Z |
| _version_ |
1803858998218194944 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV028676769</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625162121.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2015 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.npep.2015.06.003</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2015003000030.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV028676769</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0143-4179(15)00060-8</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">333.7</subfield><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">43.12</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">43.13</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.13</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Iwasaki, Yusaku</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Ghrelin counteracts insulin-induced activation of vagal afferent neurons via growth hormone secretagogue receptor</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2015transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">6</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Vagal afferent nerves sense meal-related gastrointestinal and pancreatic hormones and convey their information to the brain, thereby regulating brain functions including feeding. We have recently demonstrated that postprandial insulin directly acts on the vagal afferent neurons. Plasma concentrations of orexigenic ghrelin and anorexigenic insulin show reciprocal dynamics before and after meals. The present study examined interactive effects of ghrelin and insulin on vagal afferent nerves. Cytosolic Ca2+ concentration ([Ca2+]i) in isolated nodose ganglion (NG) neurons was measured to monitor their activity. Insulin at 10−7 M increased [Ca2+]i in NG neurons, and the insulin-induced [Ca2+]i increase was inhibited by treatment with ghrelin at 10−8 M. This inhibitory effect of ghrelin was attenuated by [D-Lys3]-GHRP-6, an antagonist of growth hormone-secretagogue receptor (GHSR). Des-acyl ghrelin had little effect on insulin-induced [Ca2+]i increases in NG neurons. Ghrelin did not affect [Ca2+]i increases in response to cholecystokinin (CCK), a hormone that inhibits feeding via vagal afferent neurons, indicating that ghrelin selectively counteracts the insulin action. These results demonstrate that ghrelin via GHSR suppresses insulin-induced activation of NG neurons. The action of ghrelin to counteract insulin effects on NG might serve to efficiently inform the brain of the systemic change between fasting-associated ghrelin-dominant and fed-associated insulin-dominant states for the homeostatic central regulation of feeding and metabolism.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Vagal afferent nerves sense meal-related gastrointestinal and pancreatic hormones and convey their information to the brain, thereby regulating brain functions including feeding. We have recently demonstrated that postprandial insulin directly acts on the vagal afferent neurons. Plasma concentrations of orexigenic ghrelin and anorexigenic insulin show reciprocal dynamics before and after meals. The present study examined interactive effects of ghrelin and insulin on vagal afferent nerves. Cytosolic Ca2+ concentration ([Ca2+]i) in isolated nodose ganglion (NG) neurons was measured to monitor their activity. Insulin at 10−7 M increased [Ca2+]i in NG neurons, and the insulin-induced [Ca2+]i increase was inhibited by treatment with ghrelin at 10−8 M. This inhibitory effect of ghrelin was attenuated by [D-Lys3]-GHRP-6, an antagonist of growth hormone-secretagogue receptor (GHSR). Des-acyl ghrelin had little effect on insulin-induced [Ca2+]i increases in NG neurons. Ghrelin did not affect [Ca2+]i increases in response to cholecystokinin (CCK), a hormone that inhibits feeding via vagal afferent neurons, indicating that ghrelin selectively counteracts the insulin action. These results demonstrate that ghrelin via GHSR suppresses insulin-induced activation of NG neurons. The action of ghrelin to counteract insulin effects on NG might serve to efficiently inform the brain of the systemic change between fasting-associated ghrelin-dominant and fed-associated insulin-dominant states for the homeostatic central regulation of feeding and metabolism.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Dezaki, Katsuya</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kumari, Parmila</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kakei, Masafumi</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yada, Toshihiko</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier</subfield><subfield code="a">Fogel, Alexander L. ELSEVIER</subfield><subfield code="t">Medicaid acceptance among pediatric dermatologists</subfield><subfield code="d">2015</subfield><subfield code="g">[New York, NY]</subfield><subfield code="w">(DE-627)ELV01831726X</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:52</subfield><subfield code="g">year:2015</subfield><subfield code="g">pages:55-60</subfield><subfield code="g">extent:6</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.npep.2015.06.003</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-GGO</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_24</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_26</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_70</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_132</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_707</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2004</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">43.12</subfield><subfield code="j">Umweltchemie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">43.13</subfield><subfield code="j">Umwelttoxikologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.13</subfield><subfield code="j">Medizinische Ökologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">52</subfield><subfield code="j">2015</subfield><subfield code="h">55-60</subfield><subfield code="g">6</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
| score |
7.4013443 |