Mild Electrical Stimulation with Heat Shock Ameliorates Insulin Resistance via Enhanced Insulin Signaling

Morino, Saori; Kondo, Tatsuya; Sasaki, Kazunari; Adachi, Hironori; Suico, Mary Ann; Sekimoto, Erika; Matsuda, Tomoko; Shuto, Tsuyoshi; Araki, Eiichi; Kai, Hirofumi

doi:10.1371/journal.pone.0004068

Cited by 73 publications

(142 citation statements)

References 51 publications

(66 reference statements)

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“…The intra-articular temperature was sufficiently raised by direct heat conduction using electrodes made of special rubber that conducts electricity and emits heat. In addition, we previously confirmed that MES þ HS treatment (10 min per session; twice/week for 16 weeks) had no observable adverse effects in mice, 16 and that MES did not induce cell toxicity in vitro.…”

Section: Discussionsupporting

confidence: 54%

“…1A). 16 The electrodes were connected to a BioMetronome TM (Tsuchiya Gum Co., Ltd., Kumamoto, Japan), that can apply MES. Electrical stimulation for cells was delivered using 5 V (55 pulses per second [pps]) of direct current with individual pulse duration of 0.1 ms.…”

Section: Chondrocytesmentioning

confidence: 99%

“…12,13 In recent years, we have shown that MES increases HSP70 via the inhibition of protein degradation by the ubiquitin-proteasome pathway in A549 cells, 14 and that MES increases glucose uptake in the skeletal rat muscle (L6) cells. 15 Moreover, we previously reported that combination treatment with MES and HS ameliorated the diabetic phenotype in mice, 16,17 and attenuated hepatic ischemia/reperfusion injury in mice, 18 suggesting that MES and HS may have broad protective effects. However, the effect of MES and HS on articular cartilage remains unclear.…”

mentioning

confidence: 96%

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Mild electrical stimulation with heat stimulation increase heat shock protein 70 in articular chondrocyte

Hiraoka

Takahashi

Mazda

et al. 2013

Journal Orthopaedic Research

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The objective of this study is to investigate the effects of mild electrical stimulation (MES) and heat stress (HS) on heat shock protein 70 (HSP70), that protects chondrocytes and enhances cartilage matrix metabolism, in chondrocyte and articular cartilage. Rabbit articular chondrocytes were treated with MES and/or HS. The safeness was assessed by LDH assay and morphology. HSP70 protein, ubiquitinated proteins and HSP70 mRNA were examined by Western blotting and real-time PCR. Rat knee joints were treated with MES and/or HS. HSP70 protein, ubiquitinated proteins, HSP70 mRNA and proteoglycan core protein (PG) mRNA in articular cartilage were investigated. In vitro, HS increased HSP70 mRNA and HSP70 protein. MES augmented ubiquitinated protein and HSP70 protein, but not HSP70 mRNA. MES þ HS raised HSP70 mRNA and ubiquitinated protein, and significantly increased HSP70 protein. In vivo, HS and MES þ HS treatment augmented HSP70 mRNA. HS modestly augmented HSP70 protein. MES þ HS significantly increased HSP70 protein and ubiquitinated proteins. PG mRNA was markedly raised by MES þ HS. This study demonstrated that MES, in combination with HS, increases HSP70 protein in chondrocytes and articular cartilage, and promotes cartilage matrix metabolism in articular cartilage. MES in combination with HS can be a novel physical therapy for osteoarthritis by inducing HSP70 in articular cartilage. ß

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Section: Discussionsupporting

confidence: 54%

Section: Chondrocytesmentioning

confidence: 99%

mentioning

confidence: 96%

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Mild electrical stimulation with heat stimulation increase heat shock protein 70 in articular chondrocyte

Hiraoka

Takahashi

Mazda

et al. 2013

Journal Orthopaedic Research

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“…HSPs act as molecular chaperones, and the expression can increase in response to physical and chemical stressors as well as oxidative stress. Several laboratories (21,35) have demonstrated that induction of HSPs by heat treatment can protect against obesity-related insulin resistance and that an increased expression of HSP70 and HSP25 plays a significant role in protecting SM from the development of age-related insulin resistance (20). Moreover, the small HSPs especially protect against ROS and stress situations such as ATP depletion (1).…”

Section: E500mentioning

confidence: 99%

Skeletal muscle uncoupling-induced longevity in mice is linked to increased substrate metabolism and induction of the endogenous antioxidant defense system

Keipert

Ost

Chadt

et al. 2013

American Journal of Physiology-Endocrinology and Metabolism

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Keipert S, Ost M, Chadt A, Voigt A, Ayala V, Portero-Otin M, Pamplona R, Al-Hasani H, Klaus S. Skeletal muscle uncouplinginduced longevity in mice is linked to increased substrate metabolism and induction of the endogenous antioxidant defense system. Am J Physiol Endocrinol Metab 304: E495-E506, 2013. First published December 31, 2012 doi:10.1152/ajpendo.00518.2012.-Ectopic expression of uncoupling protein 1 (UCP1) in skeletal muscle (SM) mitochondria increases lifespan considerably in high-fat diet-fed UCP1 Tg mice compared with wild types (WT). To clarify the underlying mechanisms, we investigated substrate metabolism as well as oxidative stress damage and antioxidant defense in SM of low-fatand high-fat-fed mice. Tg mice showed an increased protein expression of phosphorylated AMP-activated protein kinase, markers of lipid turnover (p-ACC, FAT/CD36), and an increased SM ex vivo fatty acid oxidation. Surprisingly, UCP1 Tg mice showed elevated lipid peroxidative protein modifications with no changes in glycoxidation or direct protein oxidation. This was paralleled by an induction of catalase and superoxide dismutase activity, an increased redox signaling (MAPK signaling pathway), and increased expression of stress-protective heat shock protein 25. We conclude that increased skeletal muscle mitochondrial uncoupling in vivo does not reduce the oxidative stress status in the muscle cell. Moreover, it increases lipid metabolism and reactive lipid-derived carbonyls. This stress induction in turn increases the endogenous antioxidant defense system and redox signaling. Altogether, our data argue for an adaptive role of reactive species as essential signaling molecules for health and longevity.uncoupling protein 1; AMP-activated protein kinase; oxidative stress; redox signaling; lipid metabolism AGING IS A VERY COMPLEX PROCESS driven by numerous molecular pathways and biochemical events. Regarding the relationship between energy metabolism and longevity, there is a hypothesis termed "uncoupling to survive," which suggests that increased mitochondrial uncoupling and thus increased energy expenditure might increase longevity by preventing the formation of reactive oxygen species (ROS) (6). Previously, we showed that transgenic (Tg) mice with an ectopic expression of the uncoupling protein 1 (UCP1) in skeletal muscle (UCP1 Tg mice) showed a delayed development of obesity, improved glucose tolerance, and a 42% increased median lifespan compared with their wild-type (WT) littermates when exposed to a high-fat diet (30). However, the molecular mechanisms for these beneficial health effects of skeletal muscle uncoupling are not yet clarified.One hallmark of UCP1 Tg mice is an increased insulin sensitivity independent of body weight. Insulin resistance plays a crucial part in the pathogenesis of the metabolic syndrome and is characterized by a reduced substrate metabolism and impaired defense against stress in skeletal muscle. Skeletal muscle (SM) uncoupling increases SM glucose uptake and activates the AMPactivated protein k...

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“…Gupte et al showed that a heat treatment improved glucose tolerance and insulin resistance in high-fat-fed rats [9]. We have shown that a combination of heat shock treatment (HS) and mild electrical stimulation (MES) [42°C pads and 12-V direct current (55 pulses/s with 0.1-ms duration) for 10 min, twice per week] could effectively induce HSP72 mRNA and protein in high-fat-fed mice, which resulted in improved insulin signaling and glycemic control with decreased visceral fat [10]. In this method, MES (12-V direct current, 55 pulses/s with 0.1-ms duration) enhances heat induction of HSP72 at least in part by a suppression of HSP72 degradation [11] and may also activate insulin signaling by modulating the membrane localization of the insulin receptor [12].…”

Section: Increased Expression Of Hsp72 Ameliorates Insulin Resistancementioning

confidence: 99%

Cellular stress response pathways and diabetes mellitus

2015

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Mild Electrical Stimulation with Heat Shock Ameliorates Insulin Resistance via Enhanced Insulin Signaling

Cited by 73 publications

References 51 publications

Mild electrical stimulation with heat stimulation increase heat shock protein 70 in articular chondrocyte

Mild electrical stimulation with heat stimulation increase heat shock protein 70 in articular chondrocyte

Skeletal muscle uncoupling-induced longevity in mice is linked to increased substrate metabolism and induction of the endogenous antioxidant defense system

Cellular stress response pathways and diabetes mellitus

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