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Updated: Apr 23, 2026

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance
Published on: February 17, 2023
Phosphatase and tension homolog overexpression in insulin resistant diabetic adipose tissue
Jing-bo Zeng1, Yun Zhang2, Qi Sun2
1Department of Endocrinology, Key Laboratory of Endocrinology of the Ministry of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China; Department of Endocrinology, Fuxing Hospital Affiliated to Capital University of Medical Sciences, Beijing 100038, China.
Objective:
To investigate the expression of phosphatase and tension homolog (PTEN) in adipose tissue of KKAy diabetic mice, a mouse model of type 2 diabetes.
Methods:
KKAy diabetic mice were fed with high fat diet for 4 weeks. After blood glucose met the criteria of diabetes (over 16.7 mmol/L), mice were randomly divided into 3 groups: a control group (without any treatment), a rosiglitazone group (treated with rosiglitazone 12.5 mg/kg.d once per day), and a metformin group (treated with metformin 3 g/kg.d twice daily). After 4 weeks, we then determined the expression of PTEN and phosphoserine 473-Akt (pS473-Akt) in the epididymal adipose tissue with Western blots. The mice in each group were further divided into the insulin (-) subgroup and insulin (+) subgroup, which were intraperitoneally injected with saline and insulin (5 mU/g body weight), respectively.
Results:
The expression of PTEN was elevated in the epididymal adipose tissue obtained from KKAy diabetic mice compared with that from the C57BL/6J mice (P<0.001). In accordance with the enhanced expression of PTEN, the level of pS473-Akt stimulated by insulin was decreased in the adipose tissue of KKAy mice compared to the C57BL/6J mice (P<0.001). Treatment with the insulin-sensitizing agents, rosiglitazone and metformin did not inhibit the elevated expression of PTEN in adipose tissue of KKAy diabetic mice.
Conclusion:
PTEN may play an important role in the development of insulin resistance in adipose tissue of type 2 diabetes mice model.
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