Caveolin-3 is involved in the protection of resveratrol against high-fat-diet-induced insulin resistance by promoting GLUT4 translocation to the plasma membrane in skeletal muscle of ovariectomized rats

Tan, Zhi; Zhou, Lijun; Mu, Panwei; Liu, Shuiping; Chen, Sijuan; Fu, Xiaodong; Wang, Tinghuai

doi:10.1016/j.jnutbio.2011.12.003

Cited by 58 publications

(39 citation statements)

References 40 publications

(52 reference statements)

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“…Furthermore, the finding that antioxidant treatment enhanced STAT3 activation in the heart of diabetic rats through APN signaling (9) suggests that malfunction of APN might be a key mechanism that rendered the diabetic heart less or not responsive to IPo cardioprotection. In addition, cardioprotective effects of APN were diminished in high-fat diet-induced diabetes (10,11), in which Cav3 is downregulated (12). This, together with our recent finding that Cav3 is disrupted (13) and STAT3 inactivated (9), which deranged eNOS signaling in diabetic myocardium with concomitantly reduced APN (9), indicates that APN signaling (e.g., AdipoR1/Cav3) is impaired in diabetes.…”

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confidence: 56%

Hyperglycemia Abrogates Ischemic Postconditioning Cardioprotection by Impairing AdipoR1/Caveolin-3/STAT3 Signaling in Diabetic Rats

Yao

Liu

et al. 2015

Diabetes

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Signal transducer and activator of transcription 3 (STAT3) activation is key for ischemic postconditioning (IPo) to attenuate myocardial ischemia-reperfusion injury (MIRI), but IPo loses cardioprotection in diabetes in which cardiac STAT3 activation is impaired and adiponectin (APN) reduced. We found that IPo increased postischemic cardiomyocyte-derived APN, activated mitochondrial STAT3 (mitoSTAT3), improved mitochondrial function, and attenuated MIRI in wild-type but not in APN knockout (Adipo 2/2 ) mice subjected to 30 min coronary occlusion, followed by 2 or 24 h of reperfusion. Hypoxic postconditioning-induced protection against hypoxia/reoxygenation injury was lost in Adipo 2/2 cardiomyocytes but restored by recombinant APN, but this APN beneficial effect was abolished by specific STAT3 or APN receptor 1 (AdipoR1) gene knockdown, or caveolin-3 (Cav3) disruption. APN activated cardiac STAT3 and restored IPo cardioprotection in 4-week diabetic rats where AdipoR1 and Cav3 were functionally interactive but not in 8-week diabetic rats whose cardiac Cav3 was severely reduced and AdipoR1/Cav3 signaling impaired. We concluded that IPo activates mitoSTAT3 through APN/AdipoR1/Cav3 pathway to confer cardioprotection, whereas in diabetes, IPo loses cardioprotection due to impaired APN/AdipoR1/Cav3 signaling. Therefore, effective means that may concomitantly activate APN and repair APN signaling (i.e., AdipoR1/Cav3) in diabetes may represent promising avenues in the treatment of MIRI in diabetes.

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mentioning

confidence: 56%

Hyperglycemia Abrogates Ischemic Postconditioning Cardioprotection by Impairing AdipoR1/Caveolin-3/STAT3 Signaling in Diabetic Rats

Yao

Liu

et al. 2015

Diabetes

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“…Moreover, the length of the intervention was shorter, which led to changes in HbA1c. Evidence from animal studies demonstrated that resveratrol enhances GLUT4 translocation to plasma membrane and also GLUT4 gene expression in insulin‐resistant animals (Chen, Zhang, et al, ; Deng, Hsieh, Huang, Lu, & Hung, ; Tan et al, ). Another resveratrol‐dependent mechanism is related to the changes in expression or activation of intracellular SIRT1 and AMPK.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Resveratrol Supplementation on Cardio‐Metabolic Risk Factors in Patients with Type 2 Diabetes: A Randomized, Double‐Blind Controlled Trial

Abdollahi

Salehi‐Abargouei

Toupchian

et al. 2019

Phytotherapy Research

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The aim of the present randomized controlled trial was to evaluate the effect of a micronized resveratrol supplement on glycemic status, lipid profile, and body composition in patients with type 2 diabetes mellitus (T2DM). A total of 71 overweight patients with T2DM (body mass index ranged 25–30) were randomly assigned to receive 1000 mg/day trans‐resveratrol or placebo (methyl cellulose) for 8 weeks. Anthropometric indices and biochemical indices including lipid and glycemic profile were measured before and after the intervention. In adjusted model (age, sex, and baseline body mass index), resveratrol decreased fasting blood sugar (−7.97±13.6 mg/dL, p=0.05) and increased high density lipoprotein (3.62±8.75 mg/dL, p=0.01) levels compared with placebo. Moreover, the mean difference in insulin levels reached significance (−0.97±1.91, μIU/mL, p= 0.02). However, no significant differences were observed for anthropometric measures. It was found that 8‐week resveratrol supplementation produced useful effects on some cardio‐metabolic parameters in patients with T2DM. More studies are needed to confirm these findings.

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“…Abnormal expression of CAV1 can not only cause insulin resistance and hyperglycemia, but also participates in formation of breast cancer and abnormal expression of metastasized CAV1. It is closely associated with the occurrence, progression, and prognosis of breast cancer (Tan et al, 2012;Ma et al, 2013). The mutation rate of the pre-menopausal CAV1 is higher than that of the post-menopausal CAV1, but the morbidity…”

Section: Discussionmentioning

confidence: 99%

Roles of microRNA-221/222 in type 2 diabetic patients with post-menopausal breast cancer

Pan

Qiu

2016

Genet. Mol. Res.

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ABSTRACT. The aim of the research was to examine the expression level of microRNA221/222 (miR-221/222) in the serum of patients with type 2 diabetes mellitus (T2DM) who are also diagnosed with post-menopausal breast cancer. We aimed to evaluate the differences in microRNA expression in patients with T2DM alone, patients with postmenopausal breast cancer alone, and patients with both T2DM and postmenopausal breast cancer. We selected 20 cases from a healthy control group, 30 cases from the group of patients with T2DM and obesity, 30 cases from the group of the patients with post-menopausal breast cancer, and 30 cases from the group of patients with both T2DM and post-menopausal breast cancer. The expression of miR-221/222 in the serum of the patients with post-menopausal breast cancer was higher than that of T2DM patients (P < 0.05), but lower than that of the T2DM patients who were also positive for post-menopausal breast cancer (P < 0.05); the expression of miR-221/222 in the serum of the T2DM patients was higher than that of the healthy controls (P < 0.05). BMI, HOMA-IR, HbA1c, and TG were positively correlated with the relative expression of miR-221/222 in the serum (P < 0.01). In conclusion, miR-

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Caveolin-3 is involved in the protection of resveratrol against high-fat-diet-induced insulin resistance by promoting GLUT4 translocation to the plasma membrane in skeletal muscle of ovariectomized rats

Cited by 58 publications

References 40 publications

Hyperglycemia Abrogates Ischemic Postconditioning Cardioprotection by Impairing AdipoR1/Caveolin-3/STAT3 Signaling in Diabetic Rats

Hyperglycemia Abrogates Ischemic Postconditioning Cardioprotection by Impairing AdipoR1/Caveolin-3/STAT3 Signaling in Diabetic Rats

The Effect of Resveratrol Supplementation on Cardio‐Metabolic Risk Factors in Patients with Type 2 Diabetes: A Randomized, Double‐Blind Controlled Trial

Roles of microRNA-221/222 in type 2 diabetic patients with post-menopausal breast cancer

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