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Isolation and Differentiation of Stromal Vascular Cells to Beige/Brite Cells
Published on: March 28, 2013
Telmisartan ameliorates adipoR1 and adipoR2 expression via PPAR-γ activation in the coronary artery and VSMCs
Xuhua Shen1, Hongwei Li1, Weiping Li1
1Department of Cardiology, Beijing Friendship Hospital, Capital Medical University, 95 Yong An Road, West district, Beijing 100050, China.
Abstract:
The effects of telmisartan on insulin-resistant properties and expression of adiponectin receptors (AdipoRs) were investigated. A diabetic rat model was established using a high-fat diet and streptozotocin (25mg/kg) and primary rat coronary vascular smooth muscle cells (VSMCs) were used to elucidate the underlying mechanisms. The diabetic rats were insulin-resistant and exhibited weight gain, elevated blood pressures, and increased plasma triglyceride levels. These manifestations were ameliorated by elmisartan treatment. Four-week telmisartan therapy increased plasma adiponectin and decreased TNF-α expression in the coronary artery. Moreover, telmisartan significantly decreased AdipoR1 and AdipoR2 expression. Using high glucose-treated rat coronary VSMCs, telmisartan and PPAR-γ agonist GW1929 prominently stimulated PPAR-γ and decreased TNF-α expression. Interestingly, telmisartan or GW1929 also prevented hyperglycemia-induced downregulation of AdipoR1 and AdipoR2 expression. Additionally, GW9662 (PPAR-γ antagonist) significantly decreased the effects of telmisartan on AdipoR1 and AdipoR2 expression. These results demonstrated that telmisartan effectively ameliorated coronary insulin resistance and inflammation in diabetic rats and upregulated AdipoR1/R2 expression via activation of PPAR-γ in the coronary artery and VSMCs.
Insights
Telmisartan treatment improved insulin resistance and reduced inflammation in diabetic rats. It upregulated adiponectin receptors (AdipoRs) in the coronary artery and vascular smooth muscle cells by activating PPAR-γ.
Area of Science:
- Cardiovascular Pharmacology
- Metabolic Syndrome Research
Background:
- Coronary artery disease is a common complication of diabetes, characterized by insulin resistance and inflammation.
- Adiponectin receptors (AdipoRs) play a crucial role in regulating glucose and lipid metabolism, and their dysregulation is implicated in insulin resistance.
Purpose of the Study:
- To investigate the effects of telmisartan on insulin resistance and adiponectin receptor expression in a diabetic rat model.
- To elucidate the underlying mechanisms involving peroxisome proliferator-activated receptor-gamma (PPAR-γ) in the coronary artery and vascular smooth muscle cells.
Main Methods:
- A diabetic rat model was induced using a high-fat diet and streptozotocin.
- Primary rat coronary vascular smooth muscle cells (VSMCs) were treated with high glucose.
- Telmisartan, GW1929 (PPAR-γ agonist), and GW9662 (PPAR-γ antagonist) were administered to assess their effects on insulin resistance, inflammation markers (TNF-α), and AdipoR1/R2 expression.
Main Results:
- Telmisartan treatment ameliorated insulin resistance, weight gain, hypertension, and hypertriglyceridemia in diabetic rats.
- Telmisartan increased plasma adiponectin and decreased TNF-α expression in the coronary artery.
- Telmisartan and GW1929 upregulated AdipoR1 and AdipoR2 expression in VSMCs, an effect blocked by GW9662, indicating PPAR-γ activation.
Conclusions:
- Telmisartan effectively ameliorates coronary insulin resistance and inflammation in diabetic rats.
- Telmisartan upregulates AdipoR1 and AdipoR2 expression via PPAR-γ activation in the coronary artery and VSMCs.
- These findings highlight telmisartan's potential therapeutic role in managing diabetic cardiovascular complications.
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