Chromium supplement inhibits skeletal muscle atrophy in hindlimb-suspended mice

Dong, Feng; Hua, Yinan; Zhao, Peng; Ren, Jun; Du, Min; Nair, Sreejayan

doi:10.1016/j.jnutbio.2008.09.006

Cited by 15 publications

(7 citation statements)

References 47 publications

(60 reference statements)

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“…Moreover, similar to Mstn, the rapid and transient increase in Murf1 mRNA levels observed in the SOL of TS+V‐ and TS+T‐treated mice was not paralleled by changes in protein expression levels. The expression of MAFbx/Atrogin‐1 and MuRF1 protein has been investigated during hindlbimb unloading, and discrepancies between Murf1 mRNA and MuRF1 protein levels have been described in paraplegic rat muscle and human bed‐rest models . Lack of associations between gene and protein expression levels is not uncommon and can be explained by different factors.…”

Section: Discussionmentioning

confidence: 99%

Effects of tail suspension on serum testosterone and molecular targets regulating muscle mass

et al. 2015

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TS produced an increase followed by a transient drop in testosterone levels. Muscle atrophy was associated with downregulation of Igf1 and upregulation of Mstn, Redd1, Atrogin-1, and MuRF1 mRNA with clear differences in Igf1, Mstn, and MAFbx/Atrogin-1 gene expression between SOL and EDL. Testosterone supplementation did not affect muscle mass or protein expression levels during TS. Conclusions The known anabolic effects of testosterone are not sufficient to ameliorate loss of muscle mass during TS.

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Section: Discussionmentioning

confidence: 99%

Effects of tail suspension on serum testosterone and molecular targets regulating muscle mass

et al. 2015

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“…Mouse C2C12 myoblasts (ATCC, Manassas, VA) were cultured and differentiated to myotubes as reported previously [16]. Fully, differentiated myotubes were rendered quiescent in the presence of serum-free media and were treated with or without Cr( d -Phe) 3 (0-100 μM) and/or palmitate (0-2 mM).…”

Section: Methodsmentioning

confidence: 99%

Chromium (d-Phenylalanine)3 alleviates high fat-induced insulin resistance and lipid abnormalities

Kandadi

Unnikrishnan

Warrier

et al. 2011

Journal of Inorganic Biochemistry

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High-fat diet has been implicated as a major cause of insulin resistance and dyslipidemia. The objective of this study was to evaluate the impact of dietary-supplementation of chromium (Dphenylalanine) 3 [Cr(D-Phe) 3 ] on -glucose and -insulin tolerance in high-fat diet fed mice. C57BL/ 6-mice were randomly assigned to orally receive vehicle or Cr(D-Phe) 3 (45 μg of elemental chromium/kg/day) for 8-weeks. High-fat-fed mice exhibited impaired whole-body -glucose andinsulin tolerance and elevated serum triglyceride levels compared to normal chow-fed mice. Insulin-stimulated glucose up-take in the gastrocnemius muscles, assessed as 2-[ 3 Hdeoxyglucose] incorporation was markedly diminished in high-fat fed mice compared to control mice. Treatment with chromium reconciled the high-fat diet-induced alterations in carbohydrate and lipid metabolism. Treatment of cultured, differentiated myotubes with palmitic acid evoked insulin resistance as evidenced by lower levels of insulin-stimulated Akt-phosphorylation, elevated JNK-phosphorylation, (assessed by Western blotting), attenuation of phosphoinositol-3-kinase activity (determined in the insulin-receptor substrate-1-immunoprecipitates by measuring the extent of phosphorylation of phosphatidylinositol by γ-32 P-ATP), and impairment in cellular glucose up-take, all of which were inhibited by Cr(D-Phe) 3 . These results suggest a beneficial effect of chromium-supplementation in insulin resistant conditions. It is likely that these effects of chromium may be mediated by augmenting downstream insulin signaling.

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“…Flavone ( 2 : purity 98%, Wako Pure Chemical Industries, Ltd., Osaka, Japan) or N -acetyl- l -cysteine (purity 98%, Wako) was also mixed with the vehicle and injected into the gastrocnemius muscle in a similar manner (2.5 pmol/leg) as above. After 24 h, half of the mice were subjected to tail suspension . Their tails were suspended to keep their rear legs off the ground (tail-suspension group).…”

Section: Methodsmentioning

confidence: 99%

Quercetin Prevents Unloading-Derived Disused Muscle Atrophy by Attenuating the Induction of Ubiquitin Ligases in Tail-Suspension Mice

et al. 2010

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The effects of quercetin (1) were investigated on disused muscle atrophy using mice that underwent tail suspension. Periodic injection of 1 into the gastrocnemius muscle suppressed muscle weight loss and ubiquitin ligase expression. Compound 1 reduced the enhancement of lipid peroxidation in the muscle. Injection of N-acetyl-l-cysteine, but not flavone (2), also prevented muscle weight loss and enhancement of lipid peroxidation. These findings demonstrate that 1 can prevent disused muscle atrophy by attenuating the expression of ubiquitin ligases and that such prevention originates from its antioxidant activity.

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Chromium supplement inhibits skeletal muscle atrophy in hindlimb-suspended mice

Cited by 15 publications

References 47 publications

Effects of tail suspension on serum testosterone and molecular targets regulating muscle mass

Effects of tail suspension on serum testosterone and molecular targets regulating muscle mass

Chromium (d-Phenylalanine)3 alleviates high fat-induced insulin resistance and lipid abnormalities

Quercetin Prevents Unloading-Derived Disused Muscle Atrophy by Attenuating the Induction of Ubiquitin Ligases in Tail-Suspension Mice

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