期刊
MOLECULAR METABOLISM
卷 5, 期 7, 页码 472-479出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.molmet.2016.05.006
关键词
Akt; Lipodystrophy; Insulin signaling; Insulin resistance
资金
- NCI NIH HHS [P01 CA098101] Funding Source: Medline
- NIDDK NIH HHS [R01 DK093959, F30 DK100123, P30 DK050306, P30 DK019525, R01 DK056886, P01 DK049210] Funding Source: Medline
Objective: Adipose depot mass is tightly regulated to maintain energy homeostasis. AKT is a critical kinase in the insulin-signaling cascade that is required for the process of adipogenesis in vitro. However, the role of AKT in the maintenance and/or function of mature adipocytes in vivo had not been examined. Methods: To study this, we deleted Akt1 and Akt2 in adipocytes of mice using the AdipoQ-Cre driver. Results: Strikingly, mice lacking adipocyte AKT were severely lipodystrophic, having dramatically reduced gonadal adipose and no discernible subcutaneous or brown adipose tissue. As a result, these mice developed severe insulin resistance accompanied by fatty liver, hepatomegaly and with enlarged islets of Langerhans. Conclusions: These data reveal the critical role of adipocyte AKT and insulin signaling for maintaining adipose tissue mass. (C) 2016 The Author(s). Published by Elsevier GmbH.
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