Revisiting PPARγ as a target for the treatment of metabolic disorders
As the prevalence of obesity has increased explosively over the last several decades, associated metabolic disorders, including type 2 diabetes, dyslipidemia, hypertension, and cardiovascular diseases, have been also increased. Thus, new strategies for preventing and treating them are needed. The nu...
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| Published in | BMB reports Vol. 47; no. 11; pp. 599 - 608 |
|---|---|
| Main Authors | , , |
| Format | Journal Article |
| Language | English |
| Published |
Korea (South)
Korean Society for Biochemistry and Molecular Biology
01.11.2014
생화학분자생물학회 |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1976-6696 1976-670X |
| DOI | 10.5483/BMBRep.2014.47.11.174 |
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| Abstract | As the prevalence of obesity has increased explosively over the last several decades, associated metabolic disorders, including type 2 diabetes, dyslipidemia, hypertension, and cardiovascular diseases, have been also increased. Thus, new strategies for preventing and treating them are needed. The nuclear peroxisome proliferator-activated receptors (PPARs) are involved fundamentally in regulating energy homeostasis; thus, they have been considered attractive drug targets for addressing metabolic disorders. Among the PPARs, PPARγ is a master regulator of gene expression for metabolism, inflammation, and other pathways in many cell types, especially adipocytes. It is a physiological receptor of the potent anti-diabetic drugs of the thiazolidinediones (TZDs) class, including rosiglitazone (Avandia). However, TZDs have undesirable and severe side effects, such as weight gain, fluid retention, and cardiovascular dysfunction. Recently, many reports have suggested that PPARγ could be modulated by post-translational modifications (PTMs), and modulation of PTM has been considered as novel approaches for treating metabolic disorders with fewer side effects than the TZDs. In this review, we discuss how PTM of PPARγ may be regulated and issues to be considered in making novel anti-diabetic drugs that can modulate the PTM of PPARγ. |
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| AbstractList | As the prevalence of obesity has increased explosively over the last several decades, associated metabolic disorders, including type 2 diabetes, dyslipidemia, hypertension, and cardiovascular diseases, have been also increased. Thus, new strategies for preventing and treating them are needed. The nuclear peroxisome proliferator-activated receptors (PPARs) are involved fundamentally in regulating energy homeostasis; thus, they have been considered attractive drug targets for addressing metabolic disorders. Among the PPARs, PPARγ is a master regulator of gene expression for metabolism, inflammation, and other pathways in many cell types, especially adipocytes. It is a physiological receptor of the potent anti-diabetic drugs of the thiazolidinediones (TZDs) class, including rosiglitazone (Avandia). However, TZDs have undesirable and severe side effects, such as weight gain, fluid retention, and cardiovascular dysfunction. Recently, many reports have suggested that PPARγ could be modulated by post-translational modifications (PTMs), and modulation of PTM has been considered as novel approaches for treating metabolic disorders with fewer side effects than the TZDs. In this review, we discuss how PTM of PPARγ may be regulated and issues to be considered in making novel anti-diabetic drugs that can modulate the PTM of PPARγ. As the prevalence of obesity has increased explosively overthe last several decades, associated metabolic disorders,including type 2 diabetes, dyslipidemia, hypertension, andcardiovascular diseases, have been also increased. Thus, newstrategies for preventing and treating them are needed. Thenuclear peroxisome proliferator-activated receptors (PPARs)are involved fundamentally in regulating energy homeostasis;thus, they have been considered attractive drug targets foraddressing metabolic disorders. Among the PPARs, PPARγ is amaster regulator of gene expression for metabolism,inflammation, and other pathways in many cell types,especially adipocytes. It is a physiological receptor of thepotent anti-diabetic drugs of the thiazolidinediones (TZDs)class, including rosiglitazone (Avandia). However, TZDs haveundesirable and severe side effects, such as weight gain, fluidretention, and cardiovascular dysfunction. Recently, manyreports have suggested that PPARγ could be modulated bypost-translational modifications (PTMs), and modulation ofPTM has been considered as novel approaches for treatingmetabolic disorders with fewer side effects than the TZDs. Inthis review, we discuss how PTM of PPARγ may be regulatedand issues to be considered in making novel anti-diabeticdrugs that can modulate the PTM of PPARγ. KCI Citation Count: 29 As the prevalence of obesity has increased explosively over the last several decades, associated metabolic disorders, including type 2 diabetes, dyslipidemia, hypertension, and cardiovascular diseases, have been also increased. Thus, new strategies for preventing and treating them are needed. The nuclear peroxisome proliferator-activated receptors (PPARs) are involved fundamentally in regulating energy homeostasis; thus, they have been considered attractive drug targets for addressing metabolic disorders. Among the PPARs, PPARγ is a master regulator of gene expression for metabolism, inflammation, and other pathways in many cell types, especially adipocytes. It is a physiological receptor of the potent anti-diabetic drugs of the thiazolidinediones (TZDs) class, including rosiglitazone (Avandia). However, TZDs have undesirable and severe side effects, such as weight gain, fluid retention, and cardiovascular dysfunction. Recently, many reports have suggested that PPARγ could be modulated by post-translational modifications (PTMs), and modulation of PTM has been considered as novel approaches for treating metabolic disorders with fewer side effects than the TZDs. In this review, we discuss how PTM of PPARγ may be regulated and issues to be considered in making novel anti-diabetic drugs that can modulate the PTM of PPARγ. [BMB Reports 2014; 47(11): 599-608] |
| Author | Park, Jiyoung Choi, Sun-Sil Choi, Jang Hyun |
| AuthorAffiliation | Department of Biological Science, School of Life Sciences, Ulsan National Institute of Science and Technology (UNIST), Ulsan 689-798, Korea |
| AuthorAffiliation_xml | – name: Department of Biological Science, School of Life Sciences, Ulsan National Institute of Science and Technology (UNIST), Ulsan 689-798, Korea |
| Author_xml | – sequence: 1 givenname: Sun-Sil surname: Choi fullname: Choi, Sun-Sil – sequence: 2 givenname: Jiyoung surname: Park fullname: Park, Jiyoung – sequence: 3 givenname: Jang Hyun surname: Choi fullname: Choi, Jang Hyun |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25154720$$D View this record in MEDLINE/PubMed https://www.kci.go.kr/kciportal/ci/sereArticleSearch/ciSereArtiView.kci?sereArticleSearchBean.artiId=ART001929867$$DAccess content in National Research Foundation of Korea (NRF) |
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| SubjectTerms | Antidiuretic Agents - therapeutic use Energy Metabolism Humans Insulin Resistance Metabolic Diseases - drug therapy Metabolic Diseases - metabolism Obesity - drug therapy PPAR gamma - agonists PPAR gamma - metabolism Protein Processing, Post-Translational Review Thiazolidinediones - adverse effects Thiazolidinediones - therapeutic use 화학 |
| Title | Revisiting PPARγ as a target for the treatment of metabolic disorders |
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