Vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats

Aims/hypothesis High plasma copeptin, a marker of vasopressin (VP) secretion, has been shown to be associated with the metabolic syndrome and development of type 2 diabetes in humans. The present study was designed to determine the long-term influence of plasma VP concentration in a rodent model pro...
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Autor*in:	Taveau, Christopher [verfasserIn] Chollet, Catherine Waeckel, Ludovic Desposito, Dorinne Bichet, Daniel G. Arthus, Marie-Françoise Magnan, Christophe Philippe, Erwann Paradis, Valerie Foufelle, Fabienne Hainault, Isabelle Enhorning, Sofia Velho, Gilberto Roussel, Ronan Bankir, Lise Melander, Olle Bouby, Nadine

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2015

Schlagwörter:	Glucose metabolism Hydration Lipid metabolism Liver Vasopressin

Anmerkung:	© Springer-Verlag Berlin Heidelberg 2015

Übergeordnetes Werk:	Enthalten in: Diabetologia - Berlin : Springer, 1965, 58(2015), 5 vom: 27. Jan., Seite 1081-1090
Übergeordnetes Werk:	volume:58 ; year:2015 ; number:5 ; day:27 ; month:01 ; pages:1081-1090

Links:	Volltext

DOI / URN:	10.1007/s00125-015-3496-9

Katalog-ID:	SPR001002538

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100	1		\|a Taveau, Christopher \|e verfasserin \|4 aut
245	1	0	\|a Vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats
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520			\|a Aims/hypothesis High plasma copeptin, a marker of vasopressin (VP) secretion, has been shown to be associated with the metabolic syndrome and development of type 2 diabetes in humans. The present study was designed to determine the long-term influence of plasma VP concentration in a rodent model prone to metabolic dysfunction. Methods Obese Zucker rats and their lean counterparts were submitted for 4 weeks to one of three protocols inducing different levels of VP. Circulating VP was either reduced by increasing the daily water intake (low-VP), or increased by a chronic i.p. infusion of VP (high-VP). The control rats had normal VP levels that depended on their own regulation of water intake and VP secretion. Results Compared with controls with normal VP, lean rats with high-VP had a higher fasting glycaemia after 4 weeks. In obese rats, high-VP promoted hyperinsulinaemia, glucose intolerance, assessed by glucose and insulin tolerance tests, and an impaired response to a pyruvate challenge. Conversely, treatment with a selective arginine vasopressin receptor 1A (V1aR) antagonist reduced glucose intolerance. Low-VP obese rats had unchanged glucose tolerance but exhibited a drastic decrease in liver steatosis compared with control obese rats, associated with low hepatic triacylglycerol and cholesterol content, and reduced expression of hepatic lipogenic genes. These effects were independent of changes in body adiposity, and plasma sodium and osmolality did not differ among groups. Conclusion/interpretation These findings show a causal relationship between the VP–hydration axis and the metabolic risk. Therapeutic perspectives include diet recommendations regarding hydration, but also potential pharmacological interventions targeting the VP V1aR.
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700	1		\|a Chollet, Catherine \|4 aut
700	1		\|a Waeckel, Ludovic \|4 aut
700	1		\|a Desposito, Dorinne \|4 aut
700	1		\|a Bichet, Daniel G. \|4 aut
700	1		\|a Arthus, Marie-Françoise \|4 aut
700	1		\|a Magnan, Christophe \|4 aut
700	1		\|a Philippe, Erwann \|4 aut
700	1		\|a Paradis, Valerie \|4 aut
700	1		\|a Foufelle, Fabienne \|4 aut
700	1		\|a Hainault, Isabelle \|4 aut
700	1		\|a Enhorning, Sofia \|4 aut
700	1		\|a Velho, Gilberto \|4 aut
700	1		\|a Roussel, Ronan \|4 aut
700	1		\|a Bankir, Lise \|4 aut
700	1		\|a Melander, Olle \|4 aut
700	1		\|a Bouby, Nadine \|4 aut
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912			\|a GBV_ILN_2061
912			\|a GBV_ILN_2064
912			\|a GBV_ILN_2065
912			\|a GBV_ILN_2068
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912			\|a GBV_ILN_4334
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Indexfelder

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hierarchy_sort_str	2015
publishDate	2015
allfields	10.1007/s00125-015-3496-9 doi (DE-627)SPR001002538 (SPR)s00125-015-3496-9-e DE-627 ger DE-627 rakwb eng Taveau, Christopher verfasserin aut Vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag Berlin Heidelberg 2015 Aims/hypothesis High plasma copeptin, a marker of vasopressin (VP) secretion, has been shown to be associated with the metabolic syndrome and development of type 2 diabetes in humans. The present study was designed to determine the long-term influence of plasma VP concentration in a rodent model prone to metabolic dysfunction. Methods Obese Zucker rats and their lean counterparts were submitted for 4 weeks to one of three protocols inducing different levels of VP. Circulating VP was either reduced by increasing the daily water intake (low-VP), or increased by a chronic i.p. infusion of VP (high-VP). The control rats had normal VP levels that depended on their own regulation of water intake and VP secretion. Results Compared with controls with normal VP, lean rats with high-VP had a higher fasting glycaemia after 4 weeks. In obese rats, high-VP promoted hyperinsulinaemia, glucose intolerance, assessed by glucose and insulin tolerance tests, and an impaired response to a pyruvate challenge. Conversely, treatment with a selective arginine vasopressin receptor 1A (V1aR) antagonist reduced glucose intolerance. Low-VP obese rats had unchanged glucose tolerance but exhibited a drastic decrease in liver steatosis compared with control obese rats, associated with low hepatic triacylglycerol and cholesterol content, and reduced expression of hepatic lipogenic genes. These effects were independent of changes in body adiposity, and plasma sodium and osmolality did not differ among groups. Conclusion/interpretation These findings show a causal relationship between the VP–hydration axis and the metabolic risk. Therapeutic perspectives include diet recommendations regarding hydration, but also potential pharmacological interventions targeting the VP V1aR. Glucose metabolism (dpeaa)DE-He213 Hydration (dpeaa)DE-He213 Lipid metabolism (dpeaa)DE-He213 Liver (dpeaa)DE-He213 Vasopressin (dpeaa)DE-He213 Chollet, Catherine aut Waeckel, Ludovic aut Desposito, Dorinne aut Bichet, Daniel G. aut Arthus, Marie-Françoise aut Magnan, Christophe aut Philippe, Erwann aut Paradis, Valerie aut Foufelle, Fabienne aut Hainault, Isabelle aut Enhorning, Sofia aut Velho, Gilberto aut Roussel, Ronan aut Bankir, Lise aut Melander, Olle aut Bouby, Nadine aut Enthalten in Diabetologia Berlin : Springer, 1965 58(2015), 5 vom: 27. Jan., Seite 1081-1090 (DE-627)253722209 (DE-600)1458993-X 1432-0428 nnns volume:58 year:2015 number:5 day:27 month:01 pages:1081-1090 https://dx.doi.org/10.1007/s00125-015-3496-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 58 2015 5 27 01 1081-1090
spelling	10.1007/s00125-015-3496-9 doi (DE-627)SPR001002538 (SPR)s00125-015-3496-9-e DE-627 ger DE-627 rakwb eng Taveau, Christopher verfasserin aut Vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag Berlin Heidelberg 2015 Aims/hypothesis High plasma copeptin, a marker of vasopressin (VP) secretion, has been shown to be associated with the metabolic syndrome and development of type 2 diabetes in humans. The present study was designed to determine the long-term influence of plasma VP concentration in a rodent model prone to metabolic dysfunction. Methods Obese Zucker rats and their lean counterparts were submitted for 4 weeks to one of three protocols inducing different levels of VP. Circulating VP was either reduced by increasing the daily water intake (low-VP), or increased by a chronic i.p. infusion of VP (high-VP). The control rats had normal VP levels that depended on their own regulation of water intake and VP secretion. Results Compared with controls with normal VP, lean rats with high-VP had a higher fasting glycaemia after 4 weeks. In obese rats, high-VP promoted hyperinsulinaemia, glucose intolerance, assessed by glucose and insulin tolerance tests, and an impaired response to a pyruvate challenge. Conversely, treatment with a selective arginine vasopressin receptor 1A (V1aR) antagonist reduced glucose intolerance. Low-VP obese rats had unchanged glucose tolerance but exhibited a drastic decrease in liver steatosis compared with control obese rats, associated with low hepatic triacylglycerol and cholesterol content, and reduced expression of hepatic lipogenic genes. These effects were independent of changes in body adiposity, and plasma sodium and osmolality did not differ among groups. Conclusion/interpretation These findings show a causal relationship between the VP–hydration axis and the metabolic risk. Therapeutic perspectives include diet recommendations regarding hydration, but also potential pharmacological interventions targeting the VP V1aR. Glucose metabolism (dpeaa)DE-He213 Hydration (dpeaa)DE-He213 Lipid metabolism (dpeaa)DE-He213 Liver (dpeaa)DE-He213 Vasopressin (dpeaa)DE-He213 Chollet, Catherine aut Waeckel, Ludovic aut Desposito, Dorinne aut Bichet, Daniel G. aut Arthus, Marie-Françoise aut Magnan, Christophe aut Philippe, Erwann aut Paradis, Valerie aut Foufelle, Fabienne aut Hainault, Isabelle aut Enhorning, Sofia aut Velho, Gilberto aut Roussel, Ronan aut Bankir, Lise aut Melander, Olle aut Bouby, Nadine aut Enthalten in Diabetologia Berlin : Springer, 1965 58(2015), 5 vom: 27. Jan., Seite 1081-1090 (DE-627)253722209 (DE-600)1458993-X 1432-0428 nnns volume:58 year:2015 number:5 day:27 month:01 pages:1081-1090 https://dx.doi.org/10.1007/s00125-015-3496-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 58 2015 5 27 01 1081-1090
allfields_unstemmed	10.1007/s00125-015-3496-9 doi (DE-627)SPR001002538 (SPR)s00125-015-3496-9-e DE-627 ger DE-627 rakwb eng Taveau, Christopher verfasserin aut Vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag Berlin Heidelberg 2015 Aims/hypothesis High plasma copeptin, a marker of vasopressin (VP) secretion, has been shown to be associated with the metabolic syndrome and development of type 2 diabetes in humans. The present study was designed to determine the long-term influence of plasma VP concentration in a rodent model prone to metabolic dysfunction. Methods Obese Zucker rats and their lean counterparts were submitted for 4 weeks to one of three protocols inducing different levels of VP. Circulating VP was either reduced by increasing the daily water intake (low-VP), or increased by a chronic i.p. infusion of VP (high-VP). The control rats had normal VP levels that depended on their own regulation of water intake and VP secretion. Results Compared with controls with normal VP, lean rats with high-VP had a higher fasting glycaemia after 4 weeks. In obese rats, high-VP promoted hyperinsulinaemia, glucose intolerance, assessed by glucose and insulin tolerance tests, and an impaired response to a pyruvate challenge. Conversely, treatment with a selective arginine vasopressin receptor 1A (V1aR) antagonist reduced glucose intolerance. Low-VP obese rats had unchanged glucose tolerance but exhibited a drastic decrease in liver steatosis compared with control obese rats, associated with low hepatic triacylglycerol and cholesterol content, and reduced expression of hepatic lipogenic genes. These effects were independent of changes in body adiposity, and plasma sodium and osmolality did not differ among groups. Conclusion/interpretation These findings show a causal relationship between the VP–hydration axis and the metabolic risk. Therapeutic perspectives include diet recommendations regarding hydration, but also potential pharmacological interventions targeting the VP V1aR. Glucose metabolism (dpeaa)DE-He213 Hydration (dpeaa)DE-He213 Lipid metabolism (dpeaa)DE-He213 Liver (dpeaa)DE-He213 Vasopressin (dpeaa)DE-He213 Chollet, Catherine aut Waeckel, Ludovic aut Desposito, Dorinne aut Bichet, Daniel G. aut Arthus, Marie-Françoise aut Magnan, Christophe aut Philippe, Erwann aut Paradis, Valerie aut Foufelle, Fabienne aut Hainault, Isabelle aut Enhorning, Sofia aut Velho, Gilberto aut Roussel, Ronan aut Bankir, Lise aut Melander, Olle aut Bouby, Nadine aut Enthalten in Diabetologia Berlin : Springer, 1965 58(2015), 5 vom: 27. Jan., Seite 1081-1090 (DE-627)253722209 (DE-600)1458993-X 1432-0428 nnns volume:58 year:2015 number:5 day:27 month:01 pages:1081-1090 https://dx.doi.org/10.1007/s00125-015-3496-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 58 2015 5 27 01 1081-1090
allfieldsGer	10.1007/s00125-015-3496-9 doi (DE-627)SPR001002538 (SPR)s00125-015-3496-9-e DE-627 ger DE-627 rakwb eng Taveau, Christopher verfasserin aut Vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag Berlin Heidelberg 2015 Aims/hypothesis High plasma copeptin, a marker of vasopressin (VP) secretion, has been shown to be associated with the metabolic syndrome and development of type 2 diabetes in humans. The present study was designed to determine the long-term influence of plasma VP concentration in a rodent model prone to metabolic dysfunction. Methods Obese Zucker rats and their lean counterparts were submitted for 4 weeks to one of three protocols inducing different levels of VP. Circulating VP was either reduced by increasing the daily water intake (low-VP), or increased by a chronic i.p. infusion of VP (high-VP). The control rats had normal VP levels that depended on their own regulation of water intake and VP secretion. Results Compared with controls with normal VP, lean rats with high-VP had a higher fasting glycaemia after 4 weeks. In obese rats, high-VP promoted hyperinsulinaemia, glucose intolerance, assessed by glucose and insulin tolerance tests, and an impaired response to a pyruvate challenge. Conversely, treatment with a selective arginine vasopressin receptor 1A (V1aR) antagonist reduced glucose intolerance. Low-VP obese rats had unchanged glucose tolerance but exhibited a drastic decrease in liver steatosis compared with control obese rats, associated with low hepatic triacylglycerol and cholesterol content, and reduced expression of hepatic lipogenic genes. These effects were independent of changes in body adiposity, and plasma sodium and osmolality did not differ among groups. Conclusion/interpretation These findings show a causal relationship between the VP–hydration axis and the metabolic risk. Therapeutic perspectives include diet recommendations regarding hydration, but also potential pharmacological interventions targeting the VP V1aR. Glucose metabolism (dpeaa)DE-He213 Hydration (dpeaa)DE-He213 Lipid metabolism (dpeaa)DE-He213 Liver (dpeaa)DE-He213 Vasopressin (dpeaa)DE-He213 Chollet, Catherine aut Waeckel, Ludovic aut Desposito, Dorinne aut Bichet, Daniel G. aut Arthus, Marie-Françoise aut Magnan, Christophe aut Philippe, Erwann aut Paradis, Valerie aut Foufelle, Fabienne aut Hainault, Isabelle aut Enhorning, Sofia aut Velho, Gilberto aut Roussel, Ronan aut Bankir, Lise aut Melander, Olle aut Bouby, Nadine aut Enthalten in Diabetologia Berlin : Springer, 1965 58(2015), 5 vom: 27. Jan., Seite 1081-1090 (DE-627)253722209 (DE-600)1458993-X 1432-0428 nnns volume:58 year:2015 number:5 day:27 month:01 pages:1081-1090 https://dx.doi.org/10.1007/s00125-015-3496-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 58 2015 5 27 01 1081-1090
allfieldsSound	10.1007/s00125-015-3496-9 doi (DE-627)SPR001002538 (SPR)s00125-015-3496-9-e DE-627 ger DE-627 rakwb eng Taveau, Christopher verfasserin aut Vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag Berlin Heidelberg 2015 Aims/hypothesis High plasma copeptin, a marker of vasopressin (VP) secretion, has been shown to be associated with the metabolic syndrome and development of type 2 diabetes in humans. The present study was designed to determine the long-term influence of plasma VP concentration in a rodent model prone to metabolic dysfunction. Methods Obese Zucker rats and their lean counterparts were submitted for 4 weeks to one of three protocols inducing different levels of VP. Circulating VP was either reduced by increasing the daily water intake (low-VP), or increased by a chronic i.p. infusion of VP (high-VP). The control rats had normal VP levels that depended on their own regulation of water intake and VP secretion. Results Compared with controls with normal VP, lean rats with high-VP had a higher fasting glycaemia after 4 weeks. In obese rats, high-VP promoted hyperinsulinaemia, glucose intolerance, assessed by glucose and insulin tolerance tests, and an impaired response to a pyruvate challenge. Conversely, treatment with a selective arginine vasopressin receptor 1A (V1aR) antagonist reduced glucose intolerance. Low-VP obese rats had unchanged glucose tolerance but exhibited a drastic decrease in liver steatosis compared with control obese rats, associated with low hepatic triacylglycerol and cholesterol content, and reduced expression of hepatic lipogenic genes. These effects were independent of changes in body adiposity, and plasma sodium and osmolality did not differ among groups. Conclusion/interpretation These findings show a causal relationship between the VP–hydration axis and the metabolic risk. Therapeutic perspectives include diet recommendations regarding hydration, but also potential pharmacological interventions targeting the VP V1aR. Glucose metabolism (dpeaa)DE-He213 Hydration (dpeaa)DE-He213 Lipid metabolism (dpeaa)DE-He213 Liver (dpeaa)DE-He213 Vasopressin (dpeaa)DE-He213 Chollet, Catherine aut Waeckel, Ludovic aut Desposito, Dorinne aut Bichet, Daniel G. aut Arthus, Marie-Françoise aut Magnan, Christophe aut Philippe, Erwann aut Paradis, Valerie aut Foufelle, Fabienne aut Hainault, Isabelle aut Enhorning, Sofia aut Velho, Gilberto aut Roussel, Ronan aut Bankir, Lise aut Melander, Olle aut Bouby, Nadine aut Enthalten in Diabetologia Berlin : Springer, 1965 58(2015), 5 vom: 27. Jan., Seite 1081-1090 (DE-627)253722209 (DE-600)1458993-X 1432-0428 nnns volume:58 year:2015 number:5 day:27 month:01 pages:1081-1090 https://dx.doi.org/10.1007/s00125-015-3496-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 58 2015 5 27 01 1081-1090
language	English
source	Enthalten in Diabetologia 58(2015), 5 vom: 27. Jan., Seite 1081-1090 volume:58 year:2015 number:5 day:27 month:01 pages:1081-1090
sourceStr	Enthalten in Diabetologia 58(2015), 5 vom: 27. Jan., Seite 1081-1090 volume:58 year:2015 number:5 day:27 month:01 pages:1081-1090
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Glucose metabolism Hydration Lipid metabolism Liver Vasopressin
isfreeaccess_bool	false
container_title	Diabetologia
authorswithroles_txt_mv	Taveau, Christopher @@aut@@ Chollet, Catherine @@aut@@ Waeckel, Ludovic @@aut@@ Desposito, Dorinne @@aut@@ Bichet, Daniel G. @@aut@@ Arthus, Marie-Françoise @@aut@@ Magnan, Christophe @@aut@@ Philippe, Erwann @@aut@@ Paradis, Valerie @@aut@@ Foufelle, Fabienne @@aut@@ Hainault, Isabelle @@aut@@ Enhorning, Sofia @@aut@@ Velho, Gilberto @@aut@@ Roussel, Ronan @@aut@@ Bankir, Lise @@aut@@ Melander, Olle @@aut@@ Bouby, Nadine @@aut@@
publishDateDaySort_date	2015-01-27T00:00:00Z
hierarchy_top_id	253722209
id	SPR001002538
language_de	englisch
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author	Taveau, Christopher
spellingShingle	Taveau, Christopher misc Glucose metabolism misc Hydration misc Lipid metabolism misc Liver misc Vasopressin Vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats
authorStr	Taveau, Christopher
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topic_title	Vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats Glucose metabolism (dpeaa)DE-He213 Hydration (dpeaa)DE-He213 Lipid metabolism (dpeaa)DE-He213 Liver (dpeaa)DE-He213 Vasopressin (dpeaa)DE-He213
topic	misc Glucose metabolism misc Hydration misc Lipid metabolism misc Liver misc Vasopressin
topic_unstemmed	misc Glucose metabolism misc Hydration misc Lipid metabolism misc Liver misc Vasopressin
topic_browse	misc Glucose metabolism misc Hydration misc Lipid metabolism misc Liver misc Vasopressin
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title	Vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats
ctrlnum	(DE-627)SPR001002538 (SPR)s00125-015-3496-9-e
title_full	Vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats
author_sort	Taveau, Christopher
journal	Diabetologia
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author_browse	Taveau, Christopher Chollet, Catherine Waeckel, Ludovic Desposito, Dorinne Bichet, Daniel G. Arthus, Marie-Françoise Magnan, Christophe Philippe, Erwann Paradis, Valerie Foufelle, Fabienne Hainault, Isabelle Enhorning, Sofia Velho, Gilberto Roussel, Ronan Bankir, Lise Melander, Olle Bouby, Nadine
container_volume	58
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author-letter	Taveau, Christopher
doi_str_mv	10.1007/s00125-015-3496-9
title_sort	vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats
title_auth	Vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats
abstract	Aims/hypothesis High plasma copeptin, a marker of vasopressin (VP) secretion, has been shown to be associated with the metabolic syndrome and development of type 2 diabetes in humans. The present study was designed to determine the long-term influence of plasma VP concentration in a rodent model prone to metabolic dysfunction. Methods Obese Zucker rats and their lean counterparts were submitted for 4 weeks to one of three protocols inducing different levels of VP. Circulating VP was either reduced by increasing the daily water intake (low-VP), or increased by a chronic i.p. infusion of VP (high-VP). The control rats had normal VP levels that depended on their own regulation of water intake and VP secretion. Results Compared with controls with normal VP, lean rats with high-VP had a higher fasting glycaemia after 4 weeks. In obese rats, high-VP promoted hyperinsulinaemia, glucose intolerance, assessed by glucose and insulin tolerance tests, and an impaired response to a pyruvate challenge. Conversely, treatment with a selective arginine vasopressin receptor 1A (V1aR) antagonist reduced glucose intolerance. Low-VP obese rats had unchanged glucose tolerance but exhibited a drastic decrease in liver steatosis compared with control obese rats, associated with low hepatic triacylglycerol and cholesterol content, and reduced expression of hepatic lipogenic genes. These effects were independent of changes in body adiposity, and plasma sodium and osmolality did not differ among groups. Conclusion/interpretation These findings show a causal relationship between the VP–hydration axis and the metabolic risk. Therapeutic perspectives include diet recommendations regarding hydration, but also potential pharmacological interventions targeting the VP V1aR. © Springer-Verlag Berlin Heidelberg 2015
abstractGer	Aims/hypothesis High plasma copeptin, a marker of vasopressin (VP) secretion, has been shown to be associated with the metabolic syndrome and development of type 2 diabetes in humans. The present study was designed to determine the long-term influence of plasma VP concentration in a rodent model prone to metabolic dysfunction. Methods Obese Zucker rats and their lean counterparts were submitted for 4 weeks to one of three protocols inducing different levels of VP. Circulating VP was either reduced by increasing the daily water intake (low-VP), or increased by a chronic i.p. infusion of VP (high-VP). The control rats had normal VP levels that depended on their own regulation of water intake and VP secretion. Results Compared with controls with normal VP, lean rats with high-VP had a higher fasting glycaemia after 4 weeks. In obese rats, high-VP promoted hyperinsulinaemia, glucose intolerance, assessed by glucose and insulin tolerance tests, and an impaired response to a pyruvate challenge. Conversely, treatment with a selective arginine vasopressin receptor 1A (V1aR) antagonist reduced glucose intolerance. Low-VP obese rats had unchanged glucose tolerance but exhibited a drastic decrease in liver steatosis compared with control obese rats, associated with low hepatic triacylglycerol and cholesterol content, and reduced expression of hepatic lipogenic genes. These effects were independent of changes in body adiposity, and plasma sodium and osmolality did not differ among groups. Conclusion/interpretation These findings show a causal relationship between the VP–hydration axis and the metabolic risk. Therapeutic perspectives include diet recommendations regarding hydration, but also potential pharmacological interventions targeting the VP V1aR. © Springer-Verlag Berlin Heidelberg 2015
abstract_unstemmed	Aims/hypothesis High plasma copeptin, a marker of vasopressin (VP) secretion, has been shown to be associated with the metabolic syndrome and development of type 2 diabetes in humans. The present study was designed to determine the long-term influence of plasma VP concentration in a rodent model prone to metabolic dysfunction. Methods Obese Zucker rats and their lean counterparts were submitted for 4 weeks to one of three protocols inducing different levels of VP. Circulating VP was either reduced by increasing the daily water intake (low-VP), or increased by a chronic i.p. infusion of VP (high-VP). The control rats had normal VP levels that depended on their own regulation of water intake and VP secretion. Results Compared with controls with normal VP, lean rats with high-VP had a higher fasting glycaemia after 4 weeks. In obese rats, high-VP promoted hyperinsulinaemia, glucose intolerance, assessed by glucose and insulin tolerance tests, and an impaired response to a pyruvate challenge. Conversely, treatment with a selective arginine vasopressin receptor 1A (V1aR) antagonist reduced glucose intolerance. Low-VP obese rats had unchanged glucose tolerance but exhibited a drastic decrease in liver steatosis compared with control obese rats, associated with low hepatic triacylglycerol and cholesterol content, and reduced expression of hepatic lipogenic genes. These effects were independent of changes in body adiposity, and plasma sodium and osmolality did not differ among groups. Conclusion/interpretation These findings show a causal relationship between the VP–hydration axis and the metabolic risk. Therapeutic perspectives include diet recommendations regarding hydration, but also potential pharmacological interventions targeting the VP V1aR. © Springer-Verlag Berlin Heidelberg 2015
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container_issue	5
title_short	Vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats
url	https://dx.doi.org/10.1007/s00125-015-3496-9
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author2	Chollet, Catherine Waeckel, Ludovic Desposito, Dorinne Bichet, Daniel G. Arthus, Marie-Françoise Magnan, Christophe Philippe, Erwann Paradis, Valerie Foufelle, Fabienne Hainault, Isabelle Enhorning, Sofia Velho, Gilberto Roussel, Ronan Bankir, Lise Melander, Olle Bouby, Nadine
author2Str	Chollet, Catherine Waeckel, Ludovic Desposito, Dorinne Bichet, Daniel G. Arthus, Marie-Françoise Magnan, Christophe Philippe, Erwann Paradis, Valerie Foufelle, Fabienne Hainault, Isabelle Enhorning, Sofia Velho, Gilberto Roussel, Ronan Bankir, Lise Melander, Olle Bouby, Nadine
ppnlink	253722209
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doi_str	10.1007/s00125-015-3496-9
up_date	2024-07-03T19:38:16.307Z
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Vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats

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