Sex dimorphic actions of rosiglitazone in generalised peroxisome proliferator-activated receptor-gamma (PPAR-gamma)-deficient mice
文献类型：期刊论文
| 作者 | Duan, ShengZhong（段胜仲） ; Usher, M. G.; Foley, E. L.; Milstone, D. S.; Brosius, F. C., III; Mortensen, R. M.
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| 刊名 | DIABETOLOGIA
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| 出版日期 | 2010 |
| 卷号 | 53期号:7页码:1493-1505 |
| 关键词 | Adipose tissue Insulin resistance Macrophage PPAR-gamma Rosiglitazone |
| 英文摘要 | The aim of this study was to determine the dependency on peroxisome proliferator-activated receptor-gamma (PPAR-gamma) of insulin sensitisation and glucose homeostasis by thiazolidinediones using a global Ppar-gamma (also known as Pparg)-knockout mouse model. Global Mox2-Cre-Ppar-gamma-knockout (MORE-PGKO) mice were treated with rosiglitazone and analysed for insulin sensitivity and glucose metabolism. Metabolic and hormonal variables were determined. Adipose and other tissues were measured and analysed for gene expression. Rosiglitazone induced regrowth of fat in female but not male MORE-PGKO mice, and only in specific depots. Insulin sensitivity increased but, surprisingly, was not associated with the typical changes in adipokines, plasma NEFA or tissue triacylglycerol. However, increases in alternatively activated macrophage markers, which have been previously associated with metabolic improvement, were observed in the regrown fat. Rosiglitazone improved glucose homeostasis but not insulin sensitivity in male MORE-PGKO mice, with further increase of insulin associated with an apparent expansion of pancreatic islets. Stimulating fat growth by rosiglitazone is sufficient to improve insulin sensitivity in female mice with 95% PPAR-gamma deficiency. This increase in insulin sensitivity is not likely to be due to changes typically seen in adipokines or lipids but may involve changes in macrophage polarisation that occur independent of PPAR-gamma. In contrast, rosiglitazone improves glucose homeostasis in male mice with similar PPAR-gamma deficiency by increasing insulin production independent of changes in adiposity. Further, the insulin-sensitising effect of rosiglitazone is dependent on PPAR-gamma in this male lipodystrophic model. |
| 类目[WOS] | Endocrinology & Metabolism |
| 研究领域[WOS] | Endocrinology & Metabolism |
| 关键词[WOS] | CAUSES INSULIN-RESISTANCE ; A-ZIP/F-1 FATLESS MICE ; PPAR-GAMMA ; ADIPOSE-TISSUE ; ALTERNATIVE ACTIVATION ; MACROPHAGE ACTIVATION ; C57BL/KSJ-DB/DB MICE ; PANCREATIC-ISLETS ; SKELETAL-MUSCLE ; SENSITIVITY |
| 收录类别 | SCI |
| 语种 | 英语 |
| WOS记录号 | WOS:000278118700027 |
| 公开日期 | 2015-09-22 |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.144/handle/331004/175]  |
| 专题 | 中国科学院上海生命科学研究院营养科学研究所_核受体与代谢和疾病研究组 |
| 推荐引用方式 GB/T 7714 | Duan, ShengZhong,Usher, M. G.,Foley, E. L.,et al. Sex dimorphic actions of rosiglitazone in generalised peroxisome proliferator-activated receptor-gamma (PPAR-gamma)-deficient mice[J]. DIABETOLOGIA,2010,53(7):1493-1505. |
| APA | Duan, ShengZhong,Usher, M. G.,Foley, E. L.,Milstone, D. S.,Brosius, F. C., III,&Mortensen, R. M..(2010).Sex dimorphic actions of rosiglitazone in generalised peroxisome proliferator-activated receptor-gamma (PPAR-gamma)-deficient mice.DIABETOLOGIA,53(7),1493-1505. |
| MLA | Duan, ShengZhong,et al."Sex dimorphic actions of rosiglitazone in generalised peroxisome proliferator-activated receptor-gamma (PPAR-gamma)-deficient mice".DIABETOLOGIA 53.7(2010):1493-1505. |
入库方式： OAI收割
来源：上海营养与健康研究所
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