Pyrazolone derivative C29 protects against HFD-induced obesity in mice via activation of AMPK in adipose tissue
Beige adipocytes have been considered as a potential strategy in anti-obesity therapy because of its thermogenic capacity. AMP-activated protein kinase (AMPK) plays important roles in regulating adipose tissue function. C29 is a novel pyrazolone derivative with AMPK activity. In the current study, w...
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Published in | Acta pharmacologica Sinica Vol. 42; no. 6; pp. 964 - 974 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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01.06.2021
Springer Singapore |
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Abstract | Beige adipocytes have been considered as a potential strategy in anti-obesity therapy because of its thermogenic capacity. AMP-activated protein kinase (AMPK) plays important roles in regulating adipose tissue function. C29 is a novel pyrazolone derivative with AMPK activity. In the current study, we investigated the role of C29 in the regulation of thermogenesis using differentiated adipocytes and diet-induced obese mice, and explored the mechanisms that might be involved in energy expenditure via adipocyte AMPK activation. We showed that treatment with C29 (2.5-10 μM) concentration-dependently increased thermogenesis in differentiated preadipocytes separated from inguinal white adipose tissue (iWAT), evidenced by increased expression levels of thermogenesis markers such as Ucp1, Pgc-1α, Dio2, Prdm16, Cox7a1, Cox8b, Elovl3, and Cidea, fatty acid oxidation (FAO) genes including Cpt1a, Lcad and Pparα, as well as beige-selective genes such as Cd137, Tmem26, Slc27a1, and Tbx1. In high-fat diet (HFD)-fed mice, oral administration of C29 (30 mg·kg
·day
) for 9 weeks alleviated HFD-induced obesity, promoted energy expenditure and modulated iWAT browning. However, these effects were not observed in adipose-specific AMPKα1/α2 knockout (AKO) mice following C29 administration. Together, this study demonstrates that C29 regulates energy balance via adipocyte AMPK. Our findings show that the discovery of AMPK activators that specifically target adipose tissue may have therapeutic potential for treating obesity-related metabolic diseases. |
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AbstractList | Beige adipocytes have been considered as a potential strategy in anti-obesity therapy because of its thermogenic capacity. AMP-activated protein kinase (AMPK) plays important roles in regulating adipose tissue function. C29 is a novel pyrazolone derivative with AMPK activity. In the current study, we investigated the role of C29 in the regulation of thermogenesis using differentiated adipocytes and diet-induced obese mice, and explored the mechanisms that might be involved in energy expenditure via adipocyte AMPK activation. We showed that treatment with C29 (2.5-10 μM) concentration-dependently increased thermogenesis in differentiated preadipocytes separated from inguinal white adipose tissue (iWAT), evidenced by increased expression levels of thermogenesis markers such as Ucp1, Pgc-1α, Dio2, Prdm16, Cox7a1, Cox8b, Elovl3, and Cidea, fatty acid oxidation (FAO) genes including Cpt1a, Lcad and Pparα, as well as beige-selective genes such as Cd137, Tmem26, Slc27a1, and Tbx1. In high-fat diet (HFD)-fed mice, oral administration of C29 (30 mg·kg-1·day-1) for 9 weeks alleviated HFD-induced obesity, promoted energy expenditure and modulated iWAT browning. However, these effects were not observed in adipose-specific AMPKα1/α2 knockout (AKO) mice following C29 administration. Together, this study demonstrates that C29 regulates energy balance via adipocyte AMPK. Our findings show that the discovery of AMPK activators that specifically target adipose tissue may have therapeutic potential for treating obesity-related metabolic diseases. Beige adipocytes have been considered as a potential strategy in anti-obesity therapy because of its thermogenic capacity. AMP-activated protein kinase (AMPK) plays important roles in regulating adipose tissue function. C29 is a novel pyrazolone derivative with AMPK activity. In the current study, we investigated the role of C29 in the regulation of thermogenesis using differentiated adipocytes and diet-induced obese mice, and explored the mechanisms that might be involved in energy expenditure via adipocyte AMPK activation. We showed that treatment with C29 (2.5-10 μM) concentration-dependently increased thermogenesis in differentiated preadipocytes separated from inguinal white adipose tissue (iWAT), evidenced by increased expression levels of thermogenesis markers such as Ucp1, Pgc-1α, Dio2, Prdm16, Cox7a1, Cox8b, Elovl3, and Cidea, fatty acid oxidation (FAO) genes including Cpt1a, Lcad and Pparα, as well as beige-selective genes such as Cd137, Tmem26, Slc27a1, and Tbx1. In high-fat diet (HFD)-fed mice, oral administration of C29 (30 mg·kg ·day ) for 9 weeks alleviated HFD-induced obesity, promoted energy expenditure and modulated iWAT browning. However, these effects were not observed in adipose-specific AMPKα1/α2 knockout (AKO) mice following C29 administration. Together, this study demonstrates that C29 regulates energy balance via adipocyte AMPK. Our findings show that the discovery of AMPK activators that specifically target adipose tissue may have therapeutic potential for treating obesity-related metabolic diseases. Beige adipocytes have been considered as a potential strategy in anti-obesity therapy because of its thermogenic capacity. AMP-activated protein kinase (AMPK) plays important roles in regulating adipose tissue function. C29 is a novel pyrazolone derivative with AMPK activity. In the current study, we investigated the role of C29 in the regulation of thermogenesis using differentiated adipocytes and diet-induced obese mice, and explored the mechanisms that might be involved in energy expenditure via adipocyte AMPK activation. We showed that treatment with C29 (2.5–10 μM) concentration-dependently increased thermogenesis in differentiated preadipocytes separated from inguinal white adipose tissue (iWAT), evidenced by increased expression levels of thermogenesis markers such as Ucp1, Pgc-1α, Dio2, Prdm16, Cox7a1, Cox8b, Elovl3, and Cidea, fatty acid oxidation (FAO) genes including Cpt1a, Lcad and Pparα, as well as beige-selective genes such as Cd137, Tmem26, Slc27a1, and Tbx1. In high-fat diet (HFD)-fed mice, oral administration of C29 (30 mg·kg−1·day−1) for 9 weeks alleviated HFD-induced obesity, promoted energy expenditure and modulated iWAT browning. However, these effects were not observed in adipose-specific AMPKα1/α2 knockout (AKO) mice following C29 administration. Together, this study demonstrates that C29 regulates energy balance via adipocyte AMPK. Our findings show that the discovery of AMPK activators that specifically target adipose tissue may have therapeutic potential for treating obesity-related metabolic diseases. Beige adipocytes have been considered as a potential strategy in anti-obesity therapy because of its thermogenic capacity. AMP-activated protein kinase (AMPK) plays important roles in regulating adipose tissue function. C29 is a novel pyrazolone derivative with AMPK activity. In the current study, we investigated the role of C29 in the regulation of thermogenesis using differentiated adipocytes and diet-induced obese mice, and explored the mechanisms that might be involved in energy expenditure via adipocyte AMPK activation. We showed that treatment with C29 (2.5–10 μM) concentration-dependently increased thermogenesis in differentiated preadipocytes separated from inguinal white adipose tissue (iWAT), evidenced by increased expression levels of thermogenesis markers such as Ucp1 , Pgc-1α , Dio2 , Prdm16 , Cox7a1 , Cox8b , Elovl3, and Cidea , fatty acid oxidation (FAO) genes including Cpt1a , Lcad and Pparα , as well as beige-selective genes such as Cd137 , Tmem26 , Slc27a1, and Tbx1 . In high-fat diet (HFD)-fed mice, oral administration of C29 (30 mg·kg −1 ·day −1 ) for 9 weeks alleviated HFD-induced obesity, promoted energy expenditure and modulated iWAT browning. However, these effects were not observed in adipose-specific AMPKα1/α2 knockout (AKO) mice following C29 administration. Together, this study demonstrates that C29 regulates energy balance via adipocyte AMPK. Our findings show that the discovery of AMPK activators that specifically target adipose tissue may have therapeutic potential for treating obesity-related metabolic diseases. |
Author | Duan, Ya-Nan Li, Jia Nan, Fa-Jun Jiang, Hao-Wen Li, Jing-Ya Zhang, Mei Li, Bo-Han Shuai, Lin |
Author_xml | – sequence: 1 givenname: Bo-Han surname: Li fullname: Li, Bo-Han organization: University of Chinese Academy of Sciences, Beijing, 100049, China – sequence: 2 givenname: Mei surname: Zhang fullname: Zhang, Mei organization: State Key Laboratory of Drug Research, the National Drug Screening Center, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China – sequence: 3 givenname: Ya-Nan surname: Duan fullname: Duan, Ya-Nan organization: State Key Laboratory of Drug Research, the National Drug Screening Center, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China – sequence: 4 givenname: Lin surname: Shuai fullname: Shuai, Lin organization: State Key Laboratory of Drug Research, the National Drug Screening Center, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China – sequence: 5 givenname: Hao-Wen surname: Jiang fullname: Jiang, Hao-Wen organization: State Key Laboratory of Drug Research, the National Drug Screening Center, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China – sequence: 6 givenname: Jia surname: Li fullname: Li, Jia organization: University of Chinese Academy of Sciences, Beijing, 100049, China – sequence: 7 givenname: Fa-Jun surname: Nan fullname: Nan, Fa-Jun email: fjnan@simm.ac.cn organization: State Key Laboratory of Drug Research, the National Drug Screening Center, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China. fjnan@simm.ac.cn – sequence: 8 givenname: Jing-Ya surname: Li fullname: Li, Jing-Ya email: jyli@simm.ac.cn organization: State Key Laboratory of Drug Research, the National Drug Screening Center, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China. jyli@simm.ac.cn |
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CitedBy_id | crossref_primary_10_3390_biom14040483 crossref_primary_10_1007_s12011_023_03854_2 crossref_primary_10_3390_biom14060618 crossref_primary_10_1016_j_foodchem_2021_131755 crossref_primary_10_1039_D2FO01935C crossref_primary_10_3390_ph15040469 |
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Keywords | thermogenesis inguinal white adipose tissue pyrazolone derivative C29 AMP-activated protein kinase energy expenditure white adipose browning obesity |
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SubjectTerms | Adipocytes Adipocytes - drug effects Adipose tissue Adipose Tissue, Beige - enzymology Adipose Tissue, Beige - metabolism Adipose Tissue, White - drug effects Adipose Tissue, White - enzymology Adipose Tissue, White - metabolism AMP AMP-activated protein kinase AMP-Activated Protein Kinases - metabolism Animals Body Temperature - drug effects CD137 antigen Cell Differentiation - drug effects Diet, High-Fat Energy balance Energy expenditure Enzyme Activators - therapeutic use High fat diet Insulin Resistance - physiology Kinases Male Metabolic disorders Mice Mice, Inbred C57BL Obesity Obesity - drug therapy Obesity - enzymology Obesity - metabolism Oral administration Oxidation Preadipocytes Pyrazolones - therapeutic use Tbx1 protein Thermogenesis Thermogenesis - drug effects |
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Title | Pyrazolone derivative C29 protects against HFD-induced obesity in mice via activation of AMPK in adipose tissue |
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