Effects of telmisartan on TNFα induced PPARγ phosphorylation and insulin resistance in adipocytes
| Autor: | Guangkuo Li, Guangwei Li, Fengshi Tian, Tao Fang, Na Shen, Yun Xie, Li Yonghui, Yanbo Di, Xiaoxu Cui, Peiqi Xi |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty medicine.medical_treatment Glucose uptake Biophysics Peroxisome proliferator-activated receptor 030204 cardiovascular system & hematology Biochemistry 03 medical and health sciences Mice 0302 clinical medicine Insulin resistance Internal medicine 3T3-L1 Cells medicine Adipocytes Animals Adiponectin secretion Telmisartan Phosphorylation Molecular Biology chemistry.chemical_classification biology Adiponectin Chemistry Tumor Necrosis Factor-alpha Insulin Cell Biology medicine.disease PPAR gamma 030104 developmental biology Endocrinology biology.protein Insulin Resistance Angiotensin II Type 1 Receptor Blockers GLUT4 medicine.drug |
| Zdroj: | Biochemical and biophysical research communications. 503(4) |
| ISSN: | 1090-2104 |
| Popis: | Background Telmisartan is an angiotensin II receptor blocker (ARB) and a partial agonist of peroxisome proliferator activated receptor γ (PPARγ). It has been shown to significantly enhance insulin sensitivity in clinical studies and in vitro experiments. However, the effect of telmisartan on PPARγ in adipocytes remains unknown. Methods 3T3-L1 adipocytes were incubated with tumor necrosis factor α (TNFα) to simulate growth under an inflammatory condition. On this basis, adipocytes were treated with telmisartan at different concentrations for 1 h. Then, the phosphorylation level of PPARγ, glucose uptake, mRNA levels of PPARγ downstream genes and adiponectin secretion of adipocytes were analyzed. Results Telmisartan reduced the phosphorylation level of PPARγ, altered mRNA expressions of adiponectin, adipsin, leptin, FABP4, GLUT4 and CAP, and promoted the secretion of adiponectin. Furthermore, telmisartan treatment restored the decrease of cellular glucose uptake due to TNFα stimulation. Conclusions Telmisartan regulated PPARγ phosphorylation and its downstream gene expressions, promoted glucose uptake and acted as an overall insulin sensitizing agent in adipocytes. The specific phosphorylation site of PPARγ affected by telmisartan, the mechanism of telmisartan in regulating PPARγ phosphorylation, and whether the effects of telmisartan in adipocytes is responsible for its whole-body insulin sensitizing effect require further exploration. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect