Elevation of muscle temperature stimulates muscle glucose uptake in vivo and in vitro

Koshinaka, Keiichi; Kawamoto, Emi; Abe, Natsuki; Koji, Takehiko; Nakazato, Masamitsu; Kawanaka, Kentaro

doi:10.1007/s12576-013-0278-3

Cited by 25 publications

(30 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Therapeutic effects of heat stress on insulin resistance have been reported in type 2 diabetes of rodents (hindlimb hot bathing, 41ºC, 20 min) 5) and patients (Hot tub bathing, 37.8-41.0ºC, 30 min/ day, 6 days/week, 3 weeks) 6) , mediated by up-regulated glucose uptake in skeletal muscles, based on a mechanistic study investigating isolated skeletal muscle (42ºC, 30 min) 7) . In addition to glucose metabolism, several lines of evidence demonstrated various adaptabilities of mitochondria-centered oxidative metabolism by heat stress.…”

Section: Brief History Of Research On Heat Stress In Skeletal Musclementioning

confidence: 99%

Heat stress induces mitochondrial adaptations in skeletal muscle

Tamura

Hatta

2017

JPFSM

View full text Add to dashboard Cite

PURPOSE The purposes of present study were to investigate i) the chronic effects of whole‐body heat stress (WHS) on adaptation of mitochondrial enzyme activity and ii) the acute effects of WHS on kinase phosphorylation known to mediate mitochondrial biogenesis in mice skeletal muscle. METHODS ICR mice were divided into sedentary or WHS group. Mice in WHS group were exposed to hot environment chamber (30 × 20 × 13 cm, ambient temperature: 40 °C) for 30 min on each experiment day. In chronic experiment, we examined the effects of 3 weeks (Frequency: 5 days/week) WHS on maximal citrate synthase (CS) and 3‐Hydroxyacyl‐CoA dehydrogenase (3‐HAD) activities in plantaris muscle. In acute experiment, we studied the effects of a single WHS on phosphorylation of AMP activated protein kinase (AMPK), p38 mitrogen activated protein kinase (p38 MAPK) and calcium/calmodulin‐dependent protein kinase II (CaMK II) in plantaris muscle. RESULTS In chronic experiment, both maximal CS and 3‐HAD activities were increased in WHS group (CS: +35%, P<0.01, 3‐HAD: +49%, P<0.01). In acute experiment, phosphorylation of AMPK in WHS group was decreased (−43%, P<0.05). Phosphorylation of p38 MAPK was increased in WHS group (+252%, P<0.05). Phosphorylation of CaMK II was not different between groups. CONCLUSION Chronic whole‐body heat stress increased mitochondrial enzyme activities.

show abstract

Section: Brief History Of Research On Heat Stress In Skeletal Musclementioning

confidence: 99%

Heat stress induces mitochondrial adaptations in skeletal muscle

Tamura

Hatta

2017

JPFSM

View full text Add to dashboard Cite

show abstract

“…Short-term HS at 41°C for 20 min enhanced insulin-dependent glucose uptake in rat skeletal muscles 6) . Furthermore, HS at approximately 42°C for approximately 30 min stimulated insulin-independent glucose uptake, which was accompanied by energy depletion in rat skeletal muscles 7,8) . This HS-induced stimulation of glucose uptake was abrogated by an AMPK inhibitor 7,8) .…”

Section: Introductionmentioning

confidence: 93%

“…Furthermore, HS at approximately 42°C for approximately 30 min stimulated insulin-independent glucose uptake, which was accompanied by energy depletion in rat skeletal muscles 7,8) . This HS-induced stimulation of glucose uptake was abrogated by an AMPK inhibitor 7,8) . Therefore, these results suggested that HS enhances skeletal muscle glucose utilization via an AMPK-dependent mechanism.…”

Section: Introductionmentioning

confidence: 93%

“…The energy depletion triggers an activation of a cellular energy sensor AMPK. In fact, short-term HS has been shown to activate AMPK in skeletal muscle accompanied by decreased ATP, phosphocreatine, and glycogen levels 7,8) . It is accepted that AMPK negatively regulates protein synthesis through inhibiting mTOR/p70S6K signaling in skeletal muscle.…”

Section: Fig 2 Changes In Buffer Ph During Incubationmentioning

confidence: 99%

See 1 more Smart Citation

The effect of short-term heat stress on protein synthesis signaling in isolated rat skeletal muscle

Goto

Sekine

Oshima

et al. 2018

JPFSM

View full text Add to dashboard Cite

Heat stress (HS) is a potent stimulus for activating glucose metabolism in skeletal muscles. However, the effect of short-term HS on protein turnover in skeletal muscles is unclear. This study aimed to investigate the effect of short-term HS on protein synthesis and protein degradation in skeletal muscles. The epitrochlearis muscle was isolated from male Sprague-Dawley rats weighing 150-160 grams (g) and incubated with or without HS at 42°C for 10 or 30 min in alpha minimum essential medium. HS for 30 min significantly decreased phosphorylation of 70-kDa ribosomal protein S6 kinase at Thr 389 and 4E-binding protein 1 at Thr 37/46 . Correspondingly, HS for 30 min decreased the rate of protein synthesis. In contrast, HS had no effect on the expression of autophagy-related proteins, including microtubule-associated protein light chain 3 and p62, or on the mRNA expression of muscle-specific ubiquitin ligases, including muscle RING-finger 1 (MuRF1) and atrogin-1/MAFbx. These findings suggested that short-term HS for approximately 30 min is a physiologically relevant stimulus that suppresses protein synthesis signaling in skeletal muscles.

show abstract

“…An elegant study demonstrated in animal models that the simple increase of skeletal muscle temperature is able to stimulate glucose uptake through the activations of AMPK and Akt, which were partially reversed after the use of pharmacological inhibitors of these proteins, such as compound C and Wortmannin, respectively 60 . Other studies also suggested that the increased glucose uptake, which occurs because of increase in muscle temperature, is due to the increased production of reactive oxygen species (ROS) that regulates the activity of NOS (promoting NO production) favoring the formation of RNS (as a result of the reaction of NO with ROS previously exposed).…”

Section: Muscle Temperature and Glucose Uptakementioning

confidence: 99%

Molecular mechanisms of glucose uptake in skeletal muscle at rest and in response to exercise

Pereira

Moura

Muñoz

et al. 2017

Motriz: rev. educ. fis.

View full text Add to dashboard Cite

-Glucose uptake is an important phenomenon for cell homeostasis and for organism health. Under resting conditions, skeletal muscle is dependent on insulin to promote glucose uptake. Insulin, after binding to its membrane receptor, triggers a cascade of intracellular reactions culminating in activation of the glucose transporter 4, GLUT4, among other outcomes. This transporter migrates to the plasma membrane and assists in glucose internalization. However, under special conditions such as physical exercise, alterations in the levels of intracellular molecules such as ATP and calcium act to regulate GLUT4 translocation and glucose uptake in skeletal muscle, regardless of insulin levels. Regular physical exercise, due to stimulating pathways related to glucose uptake, is an important non-pharmacological intervention for improving glycemic control in obese and diabetic patients. In this mini-review the main mechanisms involved in glucose uptake in skeletal muscle in response to muscle contraction will be investigated.

show abstract

Elevation of muscle temperature stimulates muscle glucose uptake in vivo and in vitro

Cited by 25 publications

References 33 publications

Heat stress induces mitochondrial adaptations in skeletal muscle

Heat stress induces mitochondrial adaptations in skeletal muscle

The effect of short-term heat stress on protein synthesis signaling in isolated rat skeletal muscle

Molecular mechanisms of glucose uptake in skeletal muscle at rest and in response to exercise

Contact Info

Product

Resources

About