Dissociation of diabetes and obesity in mice lacking orphan nuclear receptor small heterodimer partner
DC Field | Value | Language |
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dc.contributor.author | Park, Young Joo | - |
dc.contributor.author | Kim, Seong Chul | - |
dc.contributor.author | Kim, Jeehee | - |
dc.contributor.author | Anakk, Sayeepriyadarshini | - |
dc.contributor.author | Lee, Jae Man | - |
dc.contributor.author | Tseng, Hsiu-Ting | - |
dc.contributor.author | Yechoor, Vijay | - |
dc.contributor.author | Park, Junchol | - |
dc.contributor.author | Choi, June-Seek | - |
dc.contributor.author | Jang, Hak Chul | - |
dc.contributor.author | Lee, Ki-Up | - |
dc.contributor.author | Novak, Colleen M. | - |
dc.contributor.author | Moore, David D. | - |
dc.contributor.author | Lee, Yoon Kwang | - |
dc.date.accessioned | 2021-09-07T05:31:57Z | - |
dc.date.available | 2021-09-07T05:31:57Z | - |
dc.date.created | 2021-06-19 | - |
dc.date.issued | 2011-12 | - |
dc.identifier.issn | 0022-2275 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/110998 | - |
dc.description.abstract | Mixed background SHP(-/-) mice are resistant to diet-induced obesity due to increased energy expenditure caused by enhanced PGC-1 alpha expression in brown adipocytes. However, congenic SHP(-/-) mice on the C57BL/6 background showed normal expression of PGC-1 alpha and other genes involved in brown adipose tissue thermogenesis. Thus, we reinvestigated the impact of small heterodimer partner (SHP) deletion on diet-induced obesity and insulin resistance using congenic SHP(-/-) mice. Compared with their C57BL/6 wild-type counterparts, SHP(-/-) mice subjected to a 6 month challenge with a Western diet (WestD) were leaner but more glucose intolerant, showed hepatic insulin resistance despite decreased triglyceride accumulation and increased beta-oxidation, exhibited alterations in peripheral tissue uptake of dietary lipids, maintained a higher respiratory quotient, which did not decrease even after WestD feeding, and displayed islet dysfunction. Hepatic mRNA expression analysis revealed that many genes expressed higher in SHP(-/-) mice fed WestD were direct peroxisome proliferator-activated receptor alpha (PPAR alpha) targets. Indeed, transient transfection and chromatin immunoprecipitation verified that SHP strongly repressed PPAR alpha-mediated transactivation. SHP is a pivotal metabolic sensor controlling lipid homeostasis in response to an energy-laden diet through regulating PPAR alpha-mediated transactivation. The resultant hepatic fatty acid oxidation enhancement and dietary fat redistribution protect the mice from diet-induced obesity and hepatic steatosis but accelerate development of type 2 diabetes.-Park, Y. J., S. C. Kim, J. Kim, S. Anakk, J. M. Lee, H-T. Tseng, V. Yechoor, J. Park, J-S. Choi, H. C. Jang, K-U. Lee, C. M. Novak, D. D. Moore, and Y. K. Lee. Dissociation of diabetes and obesity in mice lacking orphan nuclear receptor small heterodimer partner. J. Lipid Res. 2011. 52: 2234-2244. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC | - |
dc.subject | DIET-INDUCED OBESITY | - |
dc.subject | NEGATIVE FEEDBACK-REGULATION | - |
dc.subject | INDUCED INSULIN-RESISTANCE | - |
dc.subject | FATTY-ACID OXIDATION | - |
dc.subject | SKELETAL-MUSCLE | - |
dc.subject | LIPID-METABOLISM | - |
dc.subject | SIGNALING PATHWAYS | - |
dc.subject | RETINOIC ACID | - |
dc.subject | BIRTH-WEIGHT | - |
dc.subject | LIVER | - |
dc.title | Dissociation of diabetes and obesity in mice lacking orphan nuclear receptor small heterodimer partner | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Choi, June-Seek | - |
dc.identifier.doi | 10.1194/jlr.M016048 | - |
dc.identifier.scopusid | 2-s2.0-81855217508 | - |
dc.identifier.wosid | 000296923300011 | - |
dc.identifier.bibliographicCitation | JOURNAL OF LIPID RESEARCH, v.52, no.12, pp.2234 - 2244 | - |
dc.relation.isPartOf | JOURNAL OF LIPID RESEARCH | - |
dc.citation.title | JOURNAL OF LIPID RESEARCH | - |
dc.citation.volume | 52 | - |
dc.citation.number | 12 | - |
dc.citation.startPage | 2234 | - |
dc.citation.endPage | 2244 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.subject.keywordPlus | DIET-INDUCED OBESITY | - |
dc.subject.keywordPlus | NEGATIVE FEEDBACK-REGULATION | - |
dc.subject.keywordPlus | INDUCED INSULIN-RESISTANCE | - |
dc.subject.keywordPlus | FATTY-ACID OXIDATION | - |
dc.subject.keywordPlus | SKELETAL-MUSCLE | - |
dc.subject.keywordPlus | LIPID-METABOLISM | - |
dc.subject.keywordPlus | SIGNALING PATHWAYS | - |
dc.subject.keywordPlus | RETINOIC ACID | - |
dc.subject.keywordPlus | BIRTH-WEIGHT | - |
dc.subject.keywordPlus | LIVER | - |
dc.subject.keywordAuthor | hepatic steatosis | - |
dc.subject.keywordAuthor | beta-oxidation | - |
dc.subject.keywordAuthor | oxygen consumption | - |
dc.subject.keywordAuthor | respiratory quotient | - |
dc.subject.keywordAuthor | insulin sensitivity | - |
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