The expressions of insulin-like growth factors, their receptors, and binding proteins are related to the mechanism regulating masseter muscle mass in the rat

Matsumoto, Tomo; Akutsu, Satonari; Wakana, N.; Morito, Mitsuhiko; Shimada, Akemi; Yamane, Akira

doi:10.1016/j.archoralbio.2006.01.003

Cited by 24 publications

(33 citation statements)

References 32 publications

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“…Gonçalves et al (19) found that clenbuterol did not change IGF-I levels in the soleus muscle. In contrast, clenbuterol has been reported to induce overexpression of IGF-I mRNA in the soleus and masseter muscles (1,45). Arthritis increased IGFBP-5 in a way similar to myogenin, where the highest expression was observed on day 12.…”

Section: Discussionmentioning

confidence: 79%

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Formoterol decreases muscle wasting as well as inflammation in the rat model of rheumatoid arthritis

Gómez-SanMiguel

Gómez-Moreira

Nieto-Bona

et al. 2016

American Journal of Physiology-Endocrinology and Metabolism

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Adjuvant-induced arthritis is an experimental model of rheumatoid arthritis that is associated with body weight loss and muscle wasting. β2-adrenergic receptor agonists are powerful anabolic agents that trigger skeletal muscle hypertrophy and have been proposed as a promising treatment for muscle wasting in human patients. The aim of this work was to determine whether formoterol, a selective β2-adrenoreceptor agonist, is able to ameliorate muscle wasting in arthritic rats. Arthritis was induced in male Wistar rats by intradermal injection of Freund's adjuvant. Control and arthritic rats were injected daily with 50 μg/kg sc formoterol or saline for 12 days. Body weight change, food intake, and arthritis index were analyzed. After euthanasia, in the gastrocnemius mRNA was analyzed by PCR, and proteins were analyzed by Western blotting. Arthritis decreased gastrocnemius weight, cross-sectional area, and myofiber size, whereas formoterol increased those variables in both arthritic and control rats. Formoterol decreased the external signs of arthritis as well as NF-κB(p65) activation, TNFα, and COX-2 levels in the gastrocnemius of arthritic and control rats. Those effects of formoterol were associated with a decreased expression of myostatin, atrogin-1, and MuRF1 and in LC3b lipidation. Arthritis increased the expression of MyoD, myogenin, IGF-I, and IGFBP-3 and -5 in the gastrocnemius. In control and in arthritic rats, treatment with formoterol increased Akt phosphorylation and myogenin levels, whereas it decreased IGFBP-3 expression in the gastrocnemius. These data suggest that formoterol has an anti-inflammatory effect and decreases muscle wasting in arthritic rats through increasing Akt activity and myogenin and decreasing myostatin, the p-NF-κB(p65)/TNF pathway, and IGFBP-3.

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Section: Discussionmentioning

confidence: 79%

“…An inhibitory effect of clenbuterol on IGFBP-3 expression has been reported previously in the masseter muscle (45). IGFBP-3 is able to suppress myoblast proliferation through an IGF-I-independent mechanism (51).…”

Section: Discussionmentioning

confidence: 86%

Formoterol decreases muscle wasting as well as inflammation in the rat model of rheumatoid arthritis

Gómez-SanMiguel

Gómez-Moreira

Nieto-Bona

et al. 2016

American Journal of Physiology-Endocrinology and Metabolism

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“…Matsumoto et al (22) suggested that one hypothesis to explain the skeletal muscle hypertrophy induced by clenbuterol is the stimulated production of peptide growth factors such as insulin-like growth factors. However, these studies differ in regard to doses, including low and large doses.…”

Section: Discussionmentioning

confidence: 99%

The effect of a low dose of clenbuterol on rat soleus muscle submitted to joint immobilization

Cancelliero

Durigan

Silva

et al. 2008

Braz J Med Biol Res

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The aim of the present study was to evaluate the effect of joint immobilization on morphometric parameters and glycogen content of soleus muscle treated with clenbuterol. Male Wistar (3-4 months old) rats were divided into 4 groups (N = 6 for each group): control, clenbuterol, immobilized, and immobilized treated with clenbuterol. Immobilization was performed with acrylic resin orthoses and 10 µg/kg body weight clenbuterol was administered subcutaneously for 7 days. The following parameters were measured the next day on soleus muscle: weight, glycogen content, cross-sectional area, and connective tissue content. The clenbuterol group showed an increase in glycogen (81.6%, 0.38 ± 0.09 vs 0.69 ± 0.06 mg/100 g; P < 0.05) without alteration in weight, cross-sectional area or connective tissue compared with the control group. The immobilized group showed a reduction in muscle weight (34.2%, 123.5 ± 5.3 vs 81.3 ± 4.6 mg; P < 0.05), glycogen content (31.6%, 0.38 ± 0.09 vs 0.26 ± 0.05 mg/100 mg; P < 0.05) and cross-sectional area (44.1%, 2574.9 ± 560.2 vs 1438.1 ± 352.2 µm 2 ; P < 0.05) and an increase in connective tissue (216.5%, 8.82 ± 3.55 vs 27.92 ± 5.36%; P < 0.05). However, the immobilized + clenbuterol group showed an increase in weight (15.9%; 81.3 ± 4.6 vs 94.2 ± 4.3 mg; P < 0.05), glycogen content (92.3%, 0.26 ± 0.05 vs 0.50 ± 0.17 mg/100 mg; P < 0.05), and cross-sectional area (19.9%, 1438.1 ± 352.2 vs 1724.8 ± 365.5 µm 2 ; P < 0.05) and a reduction in connective tissue (52.2%, 27.92 ± 5.36 vs 13.34 ± 6.86%; P < 0.05). Statistical analysis was performed using Kolmogorov-Smirnov and homoscedasticity tests. For the muscle weight and muscle glycogen content, two-way ANOVA and the Tukey test were used. For the crosssectional area and connective tissue content, Kruskal-Wallis and Tukey tests were used. This study emphasizes the importance of anabolic pharmacological protection during immobilization to minimize skeletal muscle alterations resulting from disuse.

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“…[11][12][13] The underlying mechanism of the therapeutic action of clenbuterol might be related to insulin-like growth factor (IGF)-1-mediated muscle hypertrophy, which has been correlated with increased CI-MPR (also known as IGF-2 receptor) expression. 14 In the present study, we evaluated a combination of anti-CD4 mAb and clenbuterol to induce immune tolerance and to increase CI-MPR-mediated uptake and trafficking of GAA, respectively. A single injection of anti-CD4 mAb blocked anti-GAA antibody formation, which was provoked by ubiquitous GAA expression with an AAV vector in GAA-KO mice.…”

Section: Introductionmentioning

confidence: 99%

Synergistic Efficacy from Gene Therapy with Coreceptor Blockade and a β₂-Agonist in Murine Pompe Disease

Han

Bird

et al. 2015

Human Gene Therapy

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The expressions of insulin-like growth factors, their receptors, and binding proteins are related to the mechanism regulating masseter muscle mass in the rat

Cited by 24 publications

References 32 publications

Formoterol decreases muscle wasting as well as inflammation in the rat model of rheumatoid arthritis

Formoterol decreases muscle wasting as well as inflammation in the rat model of rheumatoid arthritis

The effect of a low dose of clenbuterol on rat soleus muscle submitted to joint immobilization

Synergistic Efficacy from Gene Therapy with Coreceptor Blockade and a β₂-Agonist in Murine Pompe Disease

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The expressions of insulin-like growth factors, their receptors, and binding proteins are related to the mechanism regulating masseter muscle mass in the rat

Cited by 24 publications

References 32 publications

Formoterol decreases muscle wasting as well as inflammation in the rat model of rheumatoid arthritis

Formoterol decreases muscle wasting as well as inflammation in the rat model of rheumatoid arthritis

The effect of a low dose of clenbuterol on rat soleus muscle submitted to joint immobilization

Synergistic Efficacy from Gene Therapy with Coreceptor Blockade and a β2-Agonist in Murine Pompe Disease

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Synergistic Efficacy from Gene Therapy with Coreceptor Blockade and a β₂-Agonist in Murine Pompe Disease