Deficiency of CB2 cannabinoid receptor in mice improves insulin sensitivity but increases food intake and obesity with age
Aims/hypothesis The endocannabinoid system has a key role in energy storage and metabolic disorders. The endocannabinoid receptor 2 (CB2R), which was first detected in immune cells, is present in the main peripheral organs responsible for metabolic control. During obesity, CB2R is involved in the de...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Agudo, J. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2010 |
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| Schlagwörter: |
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| Anmerkung: |
© Springer-Verlag 2010 |
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| Übergeordnetes Werk: |
Enthalten in: Diabetologia - Berlin : Springer, 1965, 53(2010), 12 vom: 11. Sept., Seite 2629-2640 |
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| Übergeordnetes Werk: |
volume:53 ; year:2010 ; number:12 ; day:11 ; month:09 ; pages:2629-2640 |
| Links: |
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| DOI / URN: |
10.1007/s00125-010-1894-6 |
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| Katalog-ID: |
SPR000981125 |
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| 100 | 1 | |a Agudo, J. |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Deficiency of CB2 cannabinoid receptor in mice improves insulin sensitivity but increases food intake and obesity with age |
| 264 | 1 | |c 2010 | |
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| 500 | |a © Springer-Verlag 2010 | ||
| 520 | |a Aims/hypothesis The endocannabinoid system has a key role in energy storage and metabolic disorders. The endocannabinoid receptor 2 (CB2R), which was first detected in immune cells, is present in the main peripheral organs responsible for metabolic control. During obesity, CB2R is involved in the development of adipose tissue inflammation and fatty liver. We examined the long-term effects of CB2R deficiency in glucose metabolism. Methods Mice deficient in CB2R (Cb2−/− [also known as Cnr2]) were studied at different ages (2–12 months). Two-month-old Cb2−/− and wild-type mice were treated with a selective CB2R antagonist or fed a high-fat diet. Results The lack of CB2R in Cb2−/− mice led to greater increases in food intake and body weight with age than in Cb2+/+ mice. However, 12-month-old obese Cb2−/− mice did not develop insulin resistance and showed enhanced insulin-stimulated glucose uptake in skeletal muscle. In agreement, adipose tissue hypertrophy was not associated with inflammation. Similarly, treatment of wild-type mice with CB2R antagonist resulted in improved insulin sensitivity. Moreover, when 2-month-old Cb2−/− mice were fed a high-fat diet, reduced body weight gain and normal insulin sensitivity were observed. Conclusions/interpretation These results indicate that the lack of CB2R-mediated responses protected mice from both age-related and diet-induced insulin resistance, suggesting that these receptors may be a potential therapeutic target in obesity and insulin resistance. | ||
| 650 | 4 | |a Endocannabinoids |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Food intake |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Glucose uptake |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Insulin resistance |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Obesity |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Martin, M. |4 aut | |
| 700 | 1 | |a Roca, C. |4 aut | |
| 700 | 1 | |a Molas, M. |4 aut | |
| 700 | 1 | |a Bura, A. S. |4 aut | |
| 700 | 1 | |a Zimmer, A. |4 aut | |
| 700 | 1 | |a Bosch, F. |4 aut | |
| 700 | 1 | |a Maldonado, R. |4 aut | |
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| 912 | |a GBV_ILN_2055 | ||
| 912 | |a GBV_ILN_2057 | ||
| 912 | |a GBV_ILN_2059 | ||
| 912 | |a GBV_ILN_2061 | ||
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| 912 | |a GBV_ILN_2065 | ||
| 912 | |a GBV_ILN_2068 | ||
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| 912 | |a GBV_ILN_2088 | ||
| 912 | |a GBV_ILN_2093 | ||
| 912 | |a GBV_ILN_2106 | ||
| 912 | |a GBV_ILN_2107 | ||
| 912 | |a GBV_ILN_2108 | ||
| 912 | |a GBV_ILN_2110 | ||
| 912 | |a GBV_ILN_2111 | ||
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| 912 | |a GBV_ILN_2113 | ||
| 912 | |a GBV_ILN_2116 | ||
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| 912 | |a GBV_ILN_2119 | ||
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10.1007/s00125-010-1894-6 doi (DE-627)SPR000981125 (SPR)s00125-010-1894-6-e DE-627 ger DE-627 rakwb eng Agudo, J. verfasserin aut Deficiency of CB2 cannabinoid receptor in mice improves insulin sensitivity but increases food intake and obesity with age 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2010 Aims/hypothesis The endocannabinoid system has a key role in energy storage and metabolic disorders. The endocannabinoid receptor 2 (CB2R), which was first detected in immune cells, is present in the main peripheral organs responsible for metabolic control. During obesity, CB2R is involved in the development of adipose tissue inflammation and fatty liver. We examined the long-term effects of CB2R deficiency in glucose metabolism. Methods Mice deficient in CB2R (Cb2−/− [also known as Cnr2]) were studied at different ages (2–12 months). Two-month-old Cb2−/− and wild-type mice were treated with a selective CB2R antagonist or fed a high-fat diet. Results The lack of CB2R in Cb2−/− mice led to greater increases in food intake and body weight with age than in Cb2+/+ mice. However, 12-month-old obese Cb2−/− mice did not develop insulin resistance and showed enhanced insulin-stimulated glucose uptake in skeletal muscle. In agreement, adipose tissue hypertrophy was not associated with inflammation. Similarly, treatment of wild-type mice with CB2R antagonist resulted in improved insulin sensitivity. Moreover, when 2-month-old Cb2−/− mice were fed a high-fat diet, reduced body weight gain and normal insulin sensitivity were observed. Conclusions/interpretation These results indicate that the lack of CB2R-mediated responses protected mice from both age-related and diet-induced insulin resistance, suggesting that these receptors may be a potential therapeutic target in obesity and insulin resistance. Endocannabinoids (dpeaa)DE-He213 Food intake (dpeaa)DE-He213 Glucose uptake (dpeaa)DE-He213 Insulin resistance (dpeaa)DE-He213 Obesity (dpeaa)DE-He213 Martin, M. aut Roca, C. aut Molas, M. aut Bura, A. S. aut Zimmer, A. aut Bosch, F. aut Maldonado, R. aut Enthalten in Diabetologia Berlin : Springer, 1965 53(2010), 12 vom: 11. Sept., Seite 2629-2640 (DE-627)253722209 (DE-600)1458993-X 1432-0428 nnns volume:53 year:2010 number:12 day:11 month:09 pages:2629-2640 https://dx.doi.org/10.1007/s00125-010-1894-6 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 53 2010 12 11 09 2629-2640 |
| spelling |
10.1007/s00125-010-1894-6 doi (DE-627)SPR000981125 (SPR)s00125-010-1894-6-e DE-627 ger DE-627 rakwb eng Agudo, J. verfasserin aut Deficiency of CB2 cannabinoid receptor in mice improves insulin sensitivity but increases food intake and obesity with age 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2010 Aims/hypothesis The endocannabinoid system has a key role in energy storage and metabolic disorders. The endocannabinoid receptor 2 (CB2R), which was first detected in immune cells, is present in the main peripheral organs responsible for metabolic control. During obesity, CB2R is involved in the development of adipose tissue inflammation and fatty liver. We examined the long-term effects of CB2R deficiency in glucose metabolism. Methods Mice deficient in CB2R (Cb2−/− [also known as Cnr2]) were studied at different ages (2–12 months). Two-month-old Cb2−/− and wild-type mice were treated with a selective CB2R antagonist or fed a high-fat diet. Results The lack of CB2R in Cb2−/− mice led to greater increases in food intake and body weight with age than in Cb2+/+ mice. However, 12-month-old obese Cb2−/− mice did not develop insulin resistance and showed enhanced insulin-stimulated glucose uptake in skeletal muscle. In agreement, adipose tissue hypertrophy was not associated with inflammation. Similarly, treatment of wild-type mice with CB2R antagonist resulted in improved insulin sensitivity. Moreover, when 2-month-old Cb2−/− mice were fed a high-fat diet, reduced body weight gain and normal insulin sensitivity were observed. Conclusions/interpretation These results indicate that the lack of CB2R-mediated responses protected mice from both age-related and diet-induced insulin resistance, suggesting that these receptors may be a potential therapeutic target in obesity and insulin resistance. Endocannabinoids (dpeaa)DE-He213 Food intake (dpeaa)DE-He213 Glucose uptake (dpeaa)DE-He213 Insulin resistance (dpeaa)DE-He213 Obesity (dpeaa)DE-He213 Martin, M. aut Roca, C. aut Molas, M. aut Bura, A. S. aut Zimmer, A. aut Bosch, F. aut Maldonado, R. aut Enthalten in Diabetologia Berlin : Springer, 1965 53(2010), 12 vom: 11. Sept., Seite 2629-2640 (DE-627)253722209 (DE-600)1458993-X 1432-0428 nnns volume:53 year:2010 number:12 day:11 month:09 pages:2629-2640 https://dx.doi.org/10.1007/s00125-010-1894-6 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 53 2010 12 11 09 2629-2640 |
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10.1007/s00125-010-1894-6 doi (DE-627)SPR000981125 (SPR)s00125-010-1894-6-e DE-627 ger DE-627 rakwb eng Agudo, J. verfasserin aut Deficiency of CB2 cannabinoid receptor in mice improves insulin sensitivity but increases food intake and obesity with age 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2010 Aims/hypothesis The endocannabinoid system has a key role in energy storage and metabolic disorders. The endocannabinoid receptor 2 (CB2R), which was first detected in immune cells, is present in the main peripheral organs responsible for metabolic control. During obesity, CB2R is involved in the development of adipose tissue inflammation and fatty liver. We examined the long-term effects of CB2R deficiency in glucose metabolism. Methods Mice deficient in CB2R (Cb2−/− [also known as Cnr2]) were studied at different ages (2–12 months). Two-month-old Cb2−/− and wild-type mice were treated with a selective CB2R antagonist or fed a high-fat diet. Results The lack of CB2R in Cb2−/− mice led to greater increases in food intake and body weight with age than in Cb2+/+ mice. However, 12-month-old obese Cb2−/− mice did not develop insulin resistance and showed enhanced insulin-stimulated glucose uptake in skeletal muscle. In agreement, adipose tissue hypertrophy was not associated with inflammation. Similarly, treatment of wild-type mice with CB2R antagonist resulted in improved insulin sensitivity. Moreover, when 2-month-old Cb2−/− mice were fed a high-fat diet, reduced body weight gain and normal insulin sensitivity were observed. Conclusions/interpretation These results indicate that the lack of CB2R-mediated responses protected mice from both age-related and diet-induced insulin resistance, suggesting that these receptors may be a potential therapeutic target in obesity and insulin resistance. Endocannabinoids (dpeaa)DE-He213 Food intake (dpeaa)DE-He213 Glucose uptake (dpeaa)DE-He213 Insulin resistance (dpeaa)DE-He213 Obesity (dpeaa)DE-He213 Martin, M. aut Roca, C. aut Molas, M. aut Bura, A. S. aut Zimmer, A. aut Bosch, F. aut Maldonado, R. aut Enthalten in Diabetologia Berlin : Springer, 1965 53(2010), 12 vom: 11. Sept., Seite 2629-2640 (DE-627)253722209 (DE-600)1458993-X 1432-0428 nnns volume:53 year:2010 number:12 day:11 month:09 pages:2629-2640 https://dx.doi.org/10.1007/s00125-010-1894-6 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 53 2010 12 11 09 2629-2640 |
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10.1007/s00125-010-1894-6 doi (DE-627)SPR000981125 (SPR)s00125-010-1894-6-e DE-627 ger DE-627 rakwb eng Agudo, J. verfasserin aut Deficiency of CB2 cannabinoid receptor in mice improves insulin sensitivity but increases food intake and obesity with age 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2010 Aims/hypothesis The endocannabinoid system has a key role in energy storage and metabolic disorders. The endocannabinoid receptor 2 (CB2R), which was first detected in immune cells, is present in the main peripheral organs responsible for metabolic control. During obesity, CB2R is involved in the development of adipose tissue inflammation and fatty liver. We examined the long-term effects of CB2R deficiency in glucose metabolism. Methods Mice deficient in CB2R (Cb2−/− [also known as Cnr2]) were studied at different ages (2–12 months). Two-month-old Cb2−/− and wild-type mice were treated with a selective CB2R antagonist or fed a high-fat diet. Results The lack of CB2R in Cb2−/− mice led to greater increases in food intake and body weight with age than in Cb2+/+ mice. However, 12-month-old obese Cb2−/− mice did not develop insulin resistance and showed enhanced insulin-stimulated glucose uptake in skeletal muscle. In agreement, adipose tissue hypertrophy was not associated with inflammation. Similarly, treatment of wild-type mice with CB2R antagonist resulted in improved insulin sensitivity. Moreover, when 2-month-old Cb2−/− mice were fed a high-fat diet, reduced body weight gain and normal insulin sensitivity were observed. Conclusions/interpretation These results indicate that the lack of CB2R-mediated responses protected mice from both age-related and diet-induced insulin resistance, suggesting that these receptors may be a potential therapeutic target in obesity and insulin resistance. Endocannabinoids (dpeaa)DE-He213 Food intake (dpeaa)DE-He213 Glucose uptake (dpeaa)DE-He213 Insulin resistance (dpeaa)DE-He213 Obesity (dpeaa)DE-He213 Martin, M. aut Roca, C. aut Molas, M. aut Bura, A. S. aut Zimmer, A. aut Bosch, F. aut Maldonado, R. aut Enthalten in Diabetologia Berlin : Springer, 1965 53(2010), 12 vom: 11. Sept., Seite 2629-2640 (DE-627)253722209 (DE-600)1458993-X 1432-0428 nnns volume:53 year:2010 number:12 day:11 month:09 pages:2629-2640 https://dx.doi.org/10.1007/s00125-010-1894-6 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 53 2010 12 11 09 2629-2640 |
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10.1007/s00125-010-1894-6 doi (DE-627)SPR000981125 (SPR)s00125-010-1894-6-e DE-627 ger DE-627 rakwb eng Agudo, J. verfasserin aut Deficiency of CB2 cannabinoid receptor in mice improves insulin sensitivity but increases food intake and obesity with age 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2010 Aims/hypothesis The endocannabinoid system has a key role in energy storage and metabolic disorders. The endocannabinoid receptor 2 (CB2R), which was first detected in immune cells, is present in the main peripheral organs responsible for metabolic control. During obesity, CB2R is involved in the development of adipose tissue inflammation and fatty liver. We examined the long-term effects of CB2R deficiency in glucose metabolism. Methods Mice deficient in CB2R (Cb2−/− [also known as Cnr2]) were studied at different ages (2–12 months). Two-month-old Cb2−/− and wild-type mice were treated with a selective CB2R antagonist or fed a high-fat diet. Results The lack of CB2R in Cb2−/− mice led to greater increases in food intake and body weight with age than in Cb2+/+ mice. However, 12-month-old obese Cb2−/− mice did not develop insulin resistance and showed enhanced insulin-stimulated glucose uptake in skeletal muscle. In agreement, adipose tissue hypertrophy was not associated with inflammation. Similarly, treatment of wild-type mice with CB2R antagonist resulted in improved insulin sensitivity. Moreover, when 2-month-old Cb2−/− mice were fed a high-fat diet, reduced body weight gain and normal insulin sensitivity were observed. Conclusions/interpretation These results indicate that the lack of CB2R-mediated responses protected mice from both age-related and diet-induced insulin resistance, suggesting that these receptors may be a potential therapeutic target in obesity and insulin resistance. Endocannabinoids (dpeaa)DE-He213 Food intake (dpeaa)DE-He213 Glucose uptake (dpeaa)DE-He213 Insulin resistance (dpeaa)DE-He213 Obesity (dpeaa)DE-He213 Martin, M. aut Roca, C. aut Molas, M. aut Bura, A. S. aut Zimmer, A. aut Bosch, F. aut Maldonado, R. aut Enthalten in Diabetologia Berlin : Springer, 1965 53(2010), 12 vom: 11. Sept., Seite 2629-2640 (DE-627)253722209 (DE-600)1458993-X 1432-0428 nnns volume:53 year:2010 number:12 day:11 month:09 pages:2629-2640 https://dx.doi.org/10.1007/s00125-010-1894-6 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 53 2010 12 11 09 2629-2640 |
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Agudo, J. @@aut@@ Martin, M. @@aut@@ Roca, C. @@aut@@ Molas, M. @@aut@@ Bura, A. S. @@aut@@ Zimmer, A. @@aut@@ Bosch, F. @@aut@@ Maldonado, R. @@aut@@ |
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The endocannabinoid receptor 2 (CB2R), which was first detected in immune cells, is present in the main peripheral organs responsible for metabolic control. During obesity, CB2R is involved in the development of adipose tissue inflammation and fatty liver. We examined the long-term effects of CB2R deficiency in glucose metabolism. Methods Mice deficient in CB2R (Cb2−/− [also known as Cnr2]) were studied at different ages (2–12 months). Two-month-old Cb2−/− and wild-type mice were treated with a selective CB2R antagonist or fed a high-fat diet. Results The lack of CB2R in Cb2−/− mice led to greater increases in food intake and body weight with age than in Cb2+/+ mice. However, 12-month-old obese Cb2−/− mice did not develop insulin resistance and showed enhanced insulin-stimulated glucose uptake in skeletal muscle. In agreement, adipose tissue hypertrophy was not associated with inflammation. Similarly, treatment of wild-type mice with CB2R antagonist resulted in improved insulin sensitivity. Moreover, when 2-month-old Cb2−/− mice were fed a high-fat diet, reduced body weight gain and normal insulin sensitivity were observed. Conclusions/interpretation These results indicate that the lack of CB2R-mediated responses protected mice from both age-related and diet-induced insulin resistance, suggesting that these receptors may be a potential therapeutic target in obesity and insulin resistance.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Endocannabinoids</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Food intake</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Glucose uptake</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Insulin resistance</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Obesity</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Martin, M.</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Roca, C.</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Molas, M.</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bura, A. 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Agudo, J. |
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Agudo, J. misc Endocannabinoids misc Food intake misc Glucose uptake misc Insulin resistance misc Obesity Deficiency of CB2 cannabinoid receptor in mice improves insulin sensitivity but increases food intake and obesity with age |
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Deficiency of CB2 cannabinoid receptor in mice improves insulin sensitivity but increases food intake and obesity with age Endocannabinoids (dpeaa)DE-He213 Food intake (dpeaa)DE-He213 Glucose uptake (dpeaa)DE-He213 Insulin resistance (dpeaa)DE-He213 Obesity (dpeaa)DE-He213 |
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misc Endocannabinoids misc Food intake misc Glucose uptake misc Insulin resistance misc Obesity |
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misc Endocannabinoids misc Food intake misc Glucose uptake misc Insulin resistance misc Obesity |
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Deficiency of CB2 cannabinoid receptor in mice improves insulin sensitivity but increases food intake and obesity with age |
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Deficiency of CB2 cannabinoid receptor in mice improves insulin sensitivity but increases food intake and obesity with age |
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Agudo, J. |
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Diabetologia |
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Agudo, J. Martin, M. Roca, C. Molas, M. Bura, A. S. Zimmer, A. Bosch, F. Maldonado, R. |
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Agudo, J. |
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10.1007/s00125-010-1894-6 |
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deficiency of cb2 cannabinoid receptor in mice improves insulin sensitivity but increases food intake and obesity with age |
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Deficiency of CB2 cannabinoid receptor in mice improves insulin sensitivity but increases food intake and obesity with age |
| abstract |
Aims/hypothesis The endocannabinoid system has a key role in energy storage and metabolic disorders. The endocannabinoid receptor 2 (CB2R), which was first detected in immune cells, is present in the main peripheral organs responsible for metabolic control. During obesity, CB2R is involved in the development of adipose tissue inflammation and fatty liver. We examined the long-term effects of CB2R deficiency in glucose metabolism. Methods Mice deficient in CB2R (Cb2−/− [also known as Cnr2]) were studied at different ages (2–12 months). Two-month-old Cb2−/− and wild-type mice were treated with a selective CB2R antagonist or fed a high-fat diet. Results The lack of CB2R in Cb2−/− mice led to greater increases in food intake and body weight with age than in Cb2+/+ mice. However, 12-month-old obese Cb2−/− mice did not develop insulin resistance and showed enhanced insulin-stimulated glucose uptake in skeletal muscle. In agreement, adipose tissue hypertrophy was not associated with inflammation. Similarly, treatment of wild-type mice with CB2R antagonist resulted in improved insulin sensitivity. Moreover, when 2-month-old Cb2−/− mice were fed a high-fat diet, reduced body weight gain and normal insulin sensitivity were observed. Conclusions/interpretation These results indicate that the lack of CB2R-mediated responses protected mice from both age-related and diet-induced insulin resistance, suggesting that these receptors may be a potential therapeutic target in obesity and insulin resistance. © Springer-Verlag 2010 |
| abstractGer |
Aims/hypothesis The endocannabinoid system has a key role in energy storage and metabolic disorders. The endocannabinoid receptor 2 (CB2R), which was first detected in immune cells, is present in the main peripheral organs responsible for metabolic control. During obesity, CB2R is involved in the development of adipose tissue inflammation and fatty liver. We examined the long-term effects of CB2R deficiency in glucose metabolism. Methods Mice deficient in CB2R (Cb2−/− [also known as Cnr2]) were studied at different ages (2–12 months). Two-month-old Cb2−/− and wild-type mice were treated with a selective CB2R antagonist or fed a high-fat diet. Results The lack of CB2R in Cb2−/− mice led to greater increases in food intake and body weight with age than in Cb2+/+ mice. However, 12-month-old obese Cb2−/− mice did not develop insulin resistance and showed enhanced insulin-stimulated glucose uptake in skeletal muscle. In agreement, adipose tissue hypertrophy was not associated with inflammation. Similarly, treatment of wild-type mice with CB2R antagonist resulted in improved insulin sensitivity. Moreover, when 2-month-old Cb2−/− mice were fed a high-fat diet, reduced body weight gain and normal insulin sensitivity were observed. Conclusions/interpretation These results indicate that the lack of CB2R-mediated responses protected mice from both age-related and diet-induced insulin resistance, suggesting that these receptors may be a potential therapeutic target in obesity and insulin resistance. © Springer-Verlag 2010 |
| abstract_unstemmed |
Aims/hypothesis The endocannabinoid system has a key role in energy storage and metabolic disorders. The endocannabinoid receptor 2 (CB2R), which was first detected in immune cells, is present in the main peripheral organs responsible for metabolic control. During obesity, CB2R is involved in the development of adipose tissue inflammation and fatty liver. We examined the long-term effects of CB2R deficiency in glucose metabolism. Methods Mice deficient in CB2R (Cb2−/− [also known as Cnr2]) were studied at different ages (2–12 months). Two-month-old Cb2−/− and wild-type mice were treated with a selective CB2R antagonist or fed a high-fat diet. Results The lack of CB2R in Cb2−/− mice led to greater increases in food intake and body weight with age than in Cb2+/+ mice. However, 12-month-old obese Cb2−/− mice did not develop insulin resistance and showed enhanced insulin-stimulated glucose uptake in skeletal muscle. In agreement, adipose tissue hypertrophy was not associated with inflammation. Similarly, treatment of wild-type mice with CB2R antagonist resulted in improved insulin sensitivity. Moreover, when 2-month-old Cb2−/− mice were fed a high-fat diet, reduced body weight gain and normal insulin sensitivity were observed. Conclusions/interpretation These results indicate that the lack of CB2R-mediated responses protected mice from both age-related and diet-induced insulin resistance, suggesting that these receptors may be a potential therapeutic target in obesity and insulin resistance. © Springer-Verlag 2010 |
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| title_short |
Deficiency of CB2 cannabinoid receptor in mice improves insulin sensitivity but increases food intake and obesity with age |
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Martin, M. Roca, C. Molas, M. Bura, A. S. Zimmer, A. Bosch, F. Maldonado, R. |
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Martin, M. Roca, C. Molas, M. Bura, A. S. Zimmer, A. Bosch, F. Maldonado, R. |
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10.1007/s00125-010-1894-6 |
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| score |
7.3987026 |