17β-Estradiol attenuates diet-induced insulin resistance and glucose intolerance through up-regulation of caveolin-3

Mu, Panwei; Tan, Zhi; Cui, Yu-Hong; Liu, H.; Xu, Xiequn; Huang, Qin; Wang, Tengyao

doi:10.1007/s11845-010-0594-z

Cited by 5 publications

(5 citation statements)

References 27 publications

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“…Insulin increases GLUT4 to plasma membrane fraction enriched by caveolae [9,38]. Our recent study has demonstrated that estrogen via its receptor improves glucose uptake by the up-regulation of CAV-3 expression in skeletal muscle cells [16]. In the present work, we showed that RSV up-regulated CAV-3 expression in HFD-induced insulin-resistant soleus muscles and in C2C12 myotubes.…”

Section: Discussionsupporting

confidence: 62%

“…More importantly, different groups have demonstrated insulin resistance in the skeletal muscle of CAV-3 knockout mice [14,15], suggesting that CVA-3 may be a critical intermediate for glucose uptake. Our previous work has also shown that estrogen via its receptor improved glucose uptake by up-regulation of CAV-3 expression in skeletal muscle cells [16]. Numerous studies have shown that RSV has molecular structure and pharmacologic properties similar to those of estradiol, so it mimics many roles of estrogen (for review, see Ref.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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

Zhou

et al. 2012

The Journal of Nutritional Biochemistry

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Section: Discussionsupporting

confidence: 62%

Section: Introductionmentioning

confidence: 99%

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

Zhou

et al. 2012

The Journal of Nutritional Biochemistry

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“…Phosphorylation of the regulatory light chain of myosin is estradiol sensitive (16,39,44), thus providing additional evidence for estradiol's critical role in modulating myosin-actin interactions in skeletal muscle, ultimately impacting how muscle contracts and produces force. Moreover, studies on both women and female rodents show that estradiol has regulatory roles in energy metabolism and mitochondrial function, which can also affect muscle contractility (13,21,32,37,49,50,61,62). What is less clear is whether estradiol mediates its effects on contractility through estrogen receptors (ERs) or via a non-receptormediated mechanism.…”

Section: Introductionmentioning

confidence: 99%

Deletion of estrogen receptor α in skeletal muscle results in impaired contractility in female mice

Collins

Mader

Cabelka

et al. 2018

Journal of Applied Physiology

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Estradiol deficiency in females can result in skeletal muscle strength loss, and treatment with estradiol mitigates the loss. There are three primary estrogen receptors (ERs), and estradiol elicits effects through these receptors in various tissues. Ubiquitous ERα-knockout mice exhibit numerous biological disorders, but little is known regarding the specific role of ERα in skeletal muscle contractile function. The purpose of this study was to determine the impact of skeletal muscle-specific ERα deletion on contractile function, hypothesizing that ERα is a main receptor through which estradiol affects muscle strength in females. Deletion of ERα specifically in skeletal muscle (skmERαKO) did not affect body mass compared with wild-type littermates (skmERαWT) until 26 wk of age, at which time body mass of skmERαKO mice began to increase disproportionally. Overall, skmERαKO mice had low strength demonstrated in multiple muscles and by several contractile parameters. Isolated extensor digitorum longus muscles from skmERαKO mice produced 16% less eccentric and 16-26% less submaximal and maximal isometric force, and isolated soleus muscles were more fatigable, with impaired force recovery relative to skmERαWT mice. In vivo maximal torque productions by plantarflexors and dorsiflexors were 16% and 12% lower in skmERαKO than skmERαWT mice, and skmERαKO muscles had low phosphorylation of myosin regulatory light chain. Plantarflexors also generated 21-32% less power, submaximal isometric and peak concentric torques. Data support the hypothesis that ablation of ERα in skeletal muscle results in muscle weakness, suggesting that the beneficial effects of estradiol on muscle strength are receptor mediated through ERα. NEW & NOTEWORTHY We comprehensively measured in vitro and in vivo skeletal muscle contractility in female estrogen receptor α (ERα) skeletal muscle-specific knockout mice and report that force generation is impaired across multiple parameters. These results support the hypothesis that a primary mechanism through which estradiol elicits its effects on strength is mediated by ERα. Evidence is presented that estradiol signaling through ERα appears to modulate force at the molecular level via posttranslational modifications of myosin regulatory light chain.

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“…Activated AKT promoted the translocation of GLUT-4 to the plasma membrane and enhanced glucose uptake. There is evidence that increased CAV-3 expression contributed to GLUT4 translocation and thus ameliorated high-fat-diet (HFD)-induced glucose intolerance and insulin resistance, which indicated a positive correlation between the alternation of glucose metabolism and the level of caveolin-3 [ 93 , 101 ]. Conversely, decreased expression levels of CAV-3 were observed in diabetes animal models [ 102 ].…”

Section: Caveolin-3 and Metabolic Perturbationmentioning

confidence: 99%

Caveolin-3 and Arrhythmias: Insights into the Molecular Mechanisms

Qiu

Wang

et al. 2022

JCM

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Caveolin-3 is a muscle-specific protein on the membrane of myocytes correlated with a variety of cardiovascular diseases. It is now clear that the caveolin-3 plays a critical role in the cardiovascular system and a significant role in cardiac protective signaling. Mutations in the gene encoding caveolin-3 cause a broad spectrum of clinical phenotypes, ranging from persistent elevations in the serum levels of creatine kinase in asymptomatic humans to cardiomyopathy. The influence of Caveolin-3(CAV-3) mutations on current density parallels the effect on channel trafficking. For example, mutations in the CAV-3 gene promote ventricular arrhythmogenesis in long QT syndrome 9 by a combined decrease in the loss of the inward rectifier current (IK1) and gain of the late sodium current (INa-L). The functional significance of the caveolin-3 has proved that caveolin-3 overexpression or knockdown contributes to the occurrence and development of arrhythmias. Caveolin-3 overexpression could lead to reduced diastolic spontaneous Ca2+ waves, thus leading to the abnormal L-Type calcium channel current-induced ventricular arrhythmias. Moreover, CAV-3 knockdown resulted in a shift to more negative values in the hyperpolarization-activated cyclic nucleotide channel 4 current (IHCN4) activation curve and a significant decrease in IHCN4 whole-cell current density. Recent evidence indicates that caveolin-3 plays a significant role in adipose tissue and is related to obesity development. The role of caveolin-3 in glucose homeostasis has attracted increasing attention. This review highlights the underlining mechanisms of caveolin-3 in arrhythmia. Progress in this field may contribute to novel therapeutic approaches for patients prone to developing arrhythmia.

show abstract

17β-Estradiol attenuates diet-induced insulin resistance and glucose intolerance through up-regulation of caveolin-3

Abstract: Caveolin-3 plays an important role in the mechanism by which E(2) attenuates diet-induced glucose intolerance.

Cited by 5 publications

References 27 publications

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

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

Deletion of estrogen receptor α in skeletal muscle results in impaired contractility in female mice

Caveolin-3 and Arrhythmias: Insights into the Molecular Mechanisms

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