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Leptin Deficiency and Beta-Cell Dysfunction Underlie Type 2 Diabetes in Compound Akt Knockout Mice
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Chen, William S. | - |
dc.contributor.author | Peng, Xiao-Ding | - |
dc.contributor.author | Wang, Yong | - |
dc.contributor.author | Xu, Pei-Zhang | - |
dc.contributor.author | Chen, Mei-Ling | - |
dc.contributor.author | Luo, Yongmei | - |
dc.contributor.author | Jeon, Sang-Min | - |
dc.contributor.author | Coleman, Kevin | - |
dc.contributor.author | Haschek, Wanda M. | - |
dc.contributor.author | Bass, Joseph | - |
dc.contributor.author | Philipson, Louis H. | - |
dc.contributor.author | Hay, Nissim | - |
dc.date.accessioned | 2024-05-02T06:23:42Z | - |
dc.date.available | 2024-05-02T06:23:42Z | - |
dc.date.created | 2023-04-15 | - |
dc.date.created | 2023-04-15 | - |
dc.date.created | 2023-04-15 | - |
dc.date.issued | 2009-06 | - |
dc.identifier.citation | Molecular and Cellular Biology, Vol.29 No.11, pp.3151-3162 | - |
dc.identifier.issn | 0270-7306 | - |
dc.identifier.uri | https://hdl.handle.net/10371/200704 | - |
dc.description.abstract | Phenotypic analyses of mice null for the individual Akt isoforms suggested that they are functionally distinct and that only Akt2 plays a role in diabetes. We show here that Akt isoforms play compensatory and complementary roles in glucose homeostasis and diabetes. Insulin resistance in Akt2(-/-) mice was inhibited by haplodeficiency of Pten, suggesting that other Akt isoforms can compensate for Akt2 function. Haplodeficiency of Akt1 in Akt2(-/-) mice, however, converts prediabetes to overt type 2 diabetes, which is also reversed by haplodeficiency of Pten. Akt3 does not appear to contribute significantly to diabetes. Overt type 2 diabetes in Akt1(+/-) Akt2(-/-) mice is manifested by hyperglycemia due to beta-cell dysfunction combined with impaired glucose homeostasis due to markedly decreased leptin levels. Restoring leptin levels was sufficient to restore normal blood glucose and insulin levels in Akt1(+/-) Akt2(-/-) and Akt2(-/-) mice, suggesting that leptin-deficiency is the predominant cause of diabetes in these mice. These results uncover a new mechanism linking Akt to diabetes, provide a therapeutic strategy, and show that diabetes induced as a consequence of cancer therapy, via Akt inhibition, could be reversed by leptin therapy. | - |
dc.language | 영어 | - |
dc.publisher | American Society for Microbiology | - |
dc.title | Leptin Deficiency and Beta-Cell Dysfunction Underlie Type 2 Diabetes in Compound Akt Knockout Mice | - |
dc.type | Article | - |
dc.identifier.doi | 10.1128/MCB.01792-08 | - |
dc.citation.journaltitle | Molecular and Cellular Biology | - |
dc.identifier.wosid | 000266006500019 | - |
dc.identifier.scopusid | 2-s2.0-66349106496 | - |
dc.citation.endpage | 3162 | - |
dc.citation.number | 11 | - |
dc.citation.startpage | 3151 | - |
dc.citation.volume | 29 | - |
dc.description.isOpenAccess | Y | - |
dc.contributor.affiliatedAuthor | Jeon, Sang-Min | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | KINASE-B-GAMMA | - |
dc.subject.keywordPlus | INSULIN-RESISTANCE | - |
dc.subject.keywordPlus | PROTEIN-KINASE | - |
dc.subject.keywordPlus | GLUCOSE-HOMEOSTASIS | - |
dc.subject.keywordPlus | IN-VIVO | - |
dc.subject.keywordPlus | HEPATIC GLUCONEOGENESIS | - |
dc.subject.keywordPlus | ADIPOSE-TISSUE | - |
dc.subject.keywordPlus | BODY-WEIGHT | - |
dc.subject.keywordPlus | OB/OB MICE | - |
dc.subject.keywordPlus | METABOLISM | - |
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