Up-Regulation of Adiponectin Expression in Antigravitational Soleus Muscle in Response to Unloading Followed by Reloading, and Functional Overloading in Mice

Goto, Ayumi; Ohno, Yoshitaka; Ikuta, Akihiro; Suzuki, Miho; Ohira, Tetsuya; Egawa, Tatsuro; Sugiura, T.; Yoshioka, Toshitada; Ohira, Yoshinobu; Goto, Katsumasa

doi:10.1371/journal.pone.0081929

Cited by 31 publications

(41 citation statements)

References 51 publications

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“…Moreover, as only a slight and non-significant difference in body weight and food intake was observed between trained and control mice, it is conceivable to attribute AdipoR1 up-regulation to exercise training itself. This hypothesis is reinforced by the study of Goto et al which observed a down-regulation of AdipoR1 mRNA in atrophied soleus muscle after a 2-week hindlimb suspension [65]. This alteration is no longer observed after a 2-week ambulation recovery protocol.…”

Section: Discussionmentioning

confidence: 94%

Interactions of exercise training and high-fat diet on adiponectin forms and muscle receptors in mice

et al. 2016

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BackgroundMetabolic syndrome (MetS) is characterized by systemic disturbances that increase cardiovascular risk. Adiponectin (Ad) exhibits a cardioprotective function because of its anti-inflammatory and anti-atherosclerotic properties. In the bloodstream, this adipocytokine circulates on multimers (Admer), among which high molecular weight (HMW) are the most active forms. Because alterations of Ad plasmatic levels, Admer distribution and receptor (AdipoR) expression have been described in murine models and obese patients, strategies that aim to enhance Ad production or its effect on target tissues are the subject of intense investigations. While exercise training is well known to be beneficial for reducing cardiovascular risk, the contribution of Ad is still controversial. Our aim was to evaluate the effect of exercise training on Ad production, Admer distribution and AdipoR muscle expression in a murine model of MetS.MethodsAt 6 weeks of age, mice were submitted to a standard (SF) or high-fat high-sugar (HF) diet for 10 weeks. After 2 weeks, the SF- and HF-fed animals were randomly assigned to a training program (SFT, HFT) or not (SFC, HFC). The trained groups were submitted to sessions of running on a treadmill 5 days a week.Results and conclusionsThe HF mice presented the key problems associated with MetS (increased caloric intake, body weight, glycemia and fat mass), a change in Admer distribution in favor of the less-active forms and increased AdipoR2 expression in muscle. In contrast, exercise training reversed some of the adverse effects of a HF diet (increased glucose tolerance, better caloric intake control) without any modifications in Ad production and Admer distribution. However, increased AdipoR1 muscle expression was observed in trained mice, but this effect was hampered by HF diet. These data corroborate a recent hypothesis suggesting a functional divergence between AdipoR1 and AdipoR2, with AdipoR1 having the predominant protective action on metabolic function.Electronic supplementary materialThe online version of this article (doi:10.1186/s12986-016-0138-2) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 94%

Interactions of exercise training and high-fat diet on adiponectin forms and muscle receptors in mice

et al. 2016

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“…The hindlimb suspension rodent model was developed to mimic spaceflight-associated skeletal muscle atrophy. Furthermore, antigravitational slow-twitch soleus muscle has been used the most frequently in the experiment of unloading (22,43,71,81) because it is comprised of more than 50% slow-twitch fiber (78), which is more affected by reduced weight-bearing. The molecular profiling of soleus muscle in response to hindlimb suspension has significance for understanding the underlying mechanism of unloading-and disuseassociated muscle atrophy.…”

Section: Discussionmentioning

confidence: 99%

Involvement of AMPK in regulating slow-twitch muscle atrophy during hindlimb unloading in mice

Egawa

Goto

Ohno

et al. 2015

American Journal of Physiology-Endocrinology and Metabolism

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-AMPK is considered to have a role in regulating skeletal muscle mass. However, there are no studies investigating the function of AMPK in modulating skeletal muscle mass during atrophic conditions. In the present study, we investigated the difference in unloading-associated muscle atrophy and molecular functions in response to 2-wk hindlimb suspension between transgenic mice overexpressing the dominant-negative mutant of AMPK (AMPK-DN) and their wild-type (WT) littermates. Male WT (n ϭ 24) and AMPK-DN (n ϭ 24) mice were randomly divided into two groups: an untreated preexperimental control group (n ϭ 12 in each group) and an unloading (n ϭ 12 in each group) group. The relative soleus muscle weight and fiber cross-sectional area to body weight were decreased by ϳ30% in WT mice by hindlimb unloading and by ϳ20% in AMPK-DN mice. There were no changes in puromycin-labeled protein or Akt/70-kDa ribosomal S6 kinase signaling, the indicators of protein synthesis. The expressions of ubiquitinated proteins and muscle RING finger 1 mRNA and protein, markers of the ubiquitin-proteasome system, were increased by hindlimb unloading in WT mice but not in AMPK-DN mice. The expressions of molecules related to the protein degradation system, phosphorylated forkhead box class O3a, inhibitor of B␣, microRNA (miR)-1, and miR-23a, were decreased only in WT mice in response to hindlimb unloading, and 72-kDa heat shock protein expression was higher in AMPK-DN mice than in WT mice. These results imply that AMPK partially regulates unloading-induced atrophy of slow-twitch muscle possibly through modulation of the protein degradation system, especially the ubiquitin-proteasome system. AMP-activated protein kinase; protein degradation; autophagy; ubiquitin-proteasome; microRNA; heat shock protein SKELETAL MUSCLE IS THE LARGEST TISSUE IN THE BODY, accounting for ϳ40% of the total body mass, and has a crucial role in metabolism as well as locomotion. Skeletal muscle has a high ability to adapt to multiple stimuli. Increased loading, such as resistance training and mechanical stretching, leads to skeletal muscle hypertrophy (18,75). In contrast, aging, poor nutrition, several diseases such as diabetes, cancer, sepsis, and chronic renal failure, and decreased loading, such as inactivity, lead to skeletal muscle atrophy (23,34,39). Skeletal muscle atrophy occurs as a result of changes in protein turnover: decreased protein synthesis, increased protein degradation, or a combination of both (17). The coordination of protein turnover in the atrophic process is regulated by complicated molecular responses, and the molecular mechanism involved in this process in skeletal muscle is not yet completely understood and remains to be elucidated.5=-AMP-activated protein kinase (AMPK) is well established as a metabolic sensor that helps maintain cellular energy homeostasis by modulating glucose, lipid, and protein metabolism (16,26,28). AMPK is a heterotrimeric kinase comprising a catalytic ␣-subunit and two regulatory subunits, the ␤-and ␥-subunits. Two ...

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“…Exercise was associated with increased adiponectin levels compared to high‐fat‐sedentary and control animals, with potential effect in preventing bone loss . Furthermore, mechanical loading up‐regulated adiponectin and its receptors in skeletal muscle . Adiponectin stimulated osteoclast proliferation and mineralization, via p38 MAPK signaling pathway and bone morphogenetic protein (BMP)‐2, but contradictory results showed inhibition of osteoclast differentiation and promotion of apoptosis .…”

Section: Adiponectinmentioning

confidence: 99%

Biomechanics, obesity, and osteoarthritis. The role of adipokines: When the levee breaks

Francisco

Pérez

Pino

et al. 2017

Journal Orthopaedic Research

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Osteoarthritis is a high-incidence painful and debilitating disease characterized by progressive degeneration of articular joints, which indicates a breakdown in joint homeostasis favoring catabolic processes. Biomechanical loading, associated with inflammatory and metabolic imbalances of joint, strongly contributes to the initiation and progression of the disease. Obesity is a primary risk factor for disease onset, and mechanical factors increased the risk for disease progression. Moreover, inflammatory mediators, in particular, adipose tissue-derived cytokines (better known as adipokines) play a critical role linking obesity and osteoarthritis. The present article summarizes the knowledge about the role of adipokines in cartilage and bone function, highlighting their contribution to the imbalance of joint homeostasis and, consequently, pathogenesis of osteoarthritis. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:594-604, 2018.

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Up-Regulation of Adiponectin Expression in Antigravitational Soleus Muscle in Response to Unloading Followed by Reloading, and Functional Overloading in Mice

Cited by 31 publications

References 51 publications

Interactions of exercise training and high-fat diet on adiponectin forms and muscle receptors in mice

Interactions of exercise training and high-fat diet on adiponectin forms and muscle receptors in mice

Involvement of AMPK in regulating slow-twitch muscle atrophy during hindlimb unloading in mice

Biomechanics, obesity, and osteoarthritis. The role of adipokines: When the levee breaks

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