Advanced glycation end‐products induce skeletal muscle atrophy and dysfunction in diabetic mice via a <scp>RAGE</scp>‐mediated, <scp>AMPK</scp>‐down‐regulated, Akt pathway

Chiu, Chen‐Yuan; Yang, Rong‐Sen; Sheu, Meei-Ling; Chan, Ding‐Cheng; Yang, Ting‐Hua; Tsai, Keh–Sung; Chiang, Chih‐Kang; Liu, Shing‐Hwa

doi:10.1002/path.4674

Cited by 125 publications

(157 citation statements)

References 49 publications

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“…Histological examination was assessed by using haematoxylin and eosin staining. For assessment of the collagen deposition during muscle regeneration, the paraffin‐embedded soleus muscle sections were stained with Masson's trichrome as described previously . Immunohistochemistry was performed on fixed soleus muscle sections for Atrogin‐1 and SIRT‐3 staining with anti‐mouse Atrogin‐1 rabbit polyclonal antibody and anti‐mouse SIRT‐3 rabbit polyclonal antibody (Abcam, Cambridge, UK).…”

Section: Methodsmentioning

confidence: 99%

“…Human tissue sampling of the present study was reviewed and approved by the National Taiwan University Hospital Institutional Review Board for clinical investigation and collected after written informed consent from all participating subjects. The process of isolation and culture of primary HSMPCs was described previously . Briefly, human skeletal muscle biopsies (~0.2 g) were collected from 10 rectus muscles of patients under orthopaedic surgery (mean age, 64 years; range, 34 to 81 years, both male and female).…”

Section: Methodsmentioning

confidence: 99%

“…Immunoblotting was performed as described previously . Briefly, cell protein concentration was quantified with the Pierce BCA Protein Assay Kit (Thermo Fisher Scientific, Waltham, MA, USA).…”

Section: Methodsmentioning

confidence: 99%

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Preventing muscle wasting by osteoporosis drug alendronate in vitro and in myopathy models via sirtuin‐3 down‐regulation

Chiu

Yang

et al. 2018

J cachexia sarcopenia muscle

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Background A global consensus on the loss of skeletal muscle mass and function in humans refers as sarcopenia and cachexia including diabetes, obesity, renal failure, and osteoporosis. Despite a current improvement of sarcopenia or cachexia with exercise training and supportive therapies, alternative and specific managements are needed to discover for whom are unable or unwilling to embark on these treatments. Alendronate is a widely used drug for osteoporosis in the elderly and postmenopausal women. Osteopenic menopausal women with 6 months of alendronate therapy have been observed to improve not only lumbar bone mineral density but also handgrip strength. However, the effect and mechanism of alendronate on muscle strength still remain unclear. Here, we investigated the therapeutic potential and the molecular mechanism of alendronate on the loss of muscle mass and strength in vitro and in vivo. Methods Mouse myoblasts and primary human skeletal muscle-derived progenitor cells were used to assess the effects of low-dose alendronate (0.1-1 μM) combined with or without dexamethasone on myotube hypertrophy and myogenic differentiation. Moreover, we also evaluated the effects of low-dose alendronate (0.5 and 1 mg/kg) by oral administration on the limb muscle function and morphology of mice with denervation-induced muscle atrophy and glycerol-induced muscle injury. Results Alendronate inhibited dexamethasone-induced myotube atrophy and myogenic differentiation inhibition in mouse myoblasts and primary human skeletal muscle-derived progenitor cells. Alendronate significantly abrogated dexamethasone-up-regulated sirtuin-3 (SIRT3), but not SIRT1, protein expression in myotubes. Both SIRT3 inhibitor AKG7 and SIRT3-siRNA transfection could also reverse dexamethasone-up-regulated atrogin-1 and SIRT3 protein expressions. Animal studies showed that low-dose alendronate by oral administration ameliorated the muscular malfunction in mouse models of denervation-induced muscle atrophy and glycerol-induced muscle injury with a negative regulation of SIRT3 expression. Conclusions The putative mechanism by which muscle atrophy was improved with alendronate might be through the SIRT3 down-regulation. These findings suggest that alendronate can be a promising therapeutic strategy for management of muscle wasting-related diseases and sarcopenia.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Preventing muscle wasting by osteoporosis drug alendronate in vitro and in myopathy models via sirtuin‐3 down‐regulation

Chiu

Yang

et al. 2018

J cachexia sarcopenia muscle

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“…42 Muscle atrophy is length dependent with more distal muscle areas showing greater losses. 34 Skeletal muscle atrophy may be related to increased advanced glycation end products and receptors 55 or reduced insulin signaling in skeletal muscle. 56 Adipose tissue in the muscle is increased in DPN, in particular in the posterior leg.…”

Section: The Effects Of Dpn On Skeletal Muscle Functionmentioning

confidence: 99%

Declining Skeletal Muscle Function in Diabetic Peripheral Neuropathy

Parasoglou

Rao

Slade

2017

Clinical Therapeutics

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Purpose In this review, we highlight the current concepts in the effects of diabetic peripheral neuropathy (DPN) in skeletal muscle. We discuss the lack of effective pharmacological treatments and the role of physical exercise intervention in limb protection and symptom reversal. We also highlight the importance of Magnetic Resonance Imaging (MRI) techniques in providing a mechanistic understanding of the disease and helping develop targeted treatments. Methods This review provides a comprehensive reporting on the effects of DPN in the skeletal muscle of diabetic patients. It also provides an update on the most recent trials of exercise intervention targeting DPN pathology. Lastly, we report on emerging MRI techniques that have shown promise in providing a mechanistic understanding of DPN and can help improve the design and implementation of clinical trials in the future. Findings Impairments in lower limb muscles reduce functional capacity and contribute to altered gait, increased fall risk, and impaired balance in patients with DPN. This is an important concern for DPN patients as their falls are very likely to be injurious, and lead to bone fractures, poorly healing wounds, and chronic infections that may require amputation. Preliminary studies have shown that moderate intensity exercise programs are well tolerated by patients with DPN. They can improve their cardiorespiratory function and can partially reverse some of the DPN symptoms. MRI has the potential to bring new mechanistic insights into the effects of DPN as well as to objectively measure small changes in DPN pathology as a result of intervention. Implications Non-invasive exercise intervention is particularly valuable in DPN due to its safety, low cost, and potential to augment pharmacological interventions. As we gain a better mechanistic understanding of the disease, more targeted and effective interventions can be designed.

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“…Khalil et al demonstrated that this manifests as through significant weight loss, muscle mass atrophy and increased rate of degradation of contractile proteins . In relation specifically to skeletal muscle, this atrophy is accompanied by pronounced muscular weakness and physical incapacity .…”

Section: Introductionmentioning

confidence: 99%

Effects of mesenchymal stromal cells on motor function and collagen in the skeletal muscles of rats with type I diabetes

Luna

Russo

Sabadine

et al. 2019

Int J Experimental Path

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Summary The present study aimed to evaluate the effects of mesenchymal stromal cell (MSC) transplantation on motor function and collagen organization in the muscles of rats with type 1 diabetes mellitus. Male Wistar rats were randomly assigned to three groups: control (C), diabetic (DM) and diabetic treated with MSCs (DM‐MSCs). Diabetes was induced by streptozotocin (50 µg/kg). Bone marrow cells were isolated from the tibia and femur. After 10 weeks of DM induction, the DM‐MSC rats received four i.p. injections of MSCs (1 × 106). Ten weeks after MSC transplantation, motor performance was evaluated by the rotarod test and the anterior tibial (TA) muscles were collected for morphometric and quantification of collagen birefringence by polarizing microscopy analysis. Motor performance of the DM group was significantly reduced when compared to the C group and increased significantly in the DM + MSC group. The TA muscle mass was significantly reduced in the DM and DM + MSC groups compared to the C group. The connective tissue increased in the DM group compared to the C group and decreased in the DM + MSC group. The percentage collagen birefringence decreased significantly in the DM group when compared to the C group and increased in the DM + MSC group. Motor performance was positively correlated with collagen birefringence and negatively correlated with percentage of connective tissue. The results indicate that MSC transplantation improves both motor function and the collagen macromolecular organization in type 1 DM.

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Advanced glycation end‐products induce skeletal muscle atrophy and dysfunction in diabetic mice via a RAGE‐mediated, AMPK‐down‐regulated, Akt pathway

Cited by 125 publications

References 49 publications

Preventing muscle wasting by osteoporosis drug alendronate in vitro and in myopathy models via sirtuin‐3 down‐regulation

Preventing muscle wasting by osteoporosis drug alendronate in vitro and in myopathy models via sirtuin‐3 down‐regulation

Declining Skeletal Muscle Function in Diabetic Peripheral Neuropathy

Effects of mesenchymal stromal cells on motor function and collagen in the skeletal muscles of rats with type I diabetes

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