The Effect of Nutritional Regimes Upon Collagen Concentration and Survival of Rats

Deyl, Z.; Juřicová, M.; Stuchlíková, E.

doi:10.1007/978-1-4757-0731-1_31

Cited by 7 publications

(7 citation statements)

References 5 publications

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“…Conversely, BW of both the DEX and CB+DEX groups was significantly lower than that in the Control group (DEX (n = 8): 279 + 4.0 g, CB+DEX (n = 8): 283 + 4.6 g, both P < 0.01 vs. Control) [ 30 , 31 ].…”

Section: Resultsmentioning

confidence: 99%

Protective Effects of Clenbuterol against Dexamethasone-Induced Masseter Muscle Atrophy and Myosin Heavy Chain Transition

et al. 2015

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BackgroundGlucocorticoid has a direct catabolic effect on skeletal muscle, leading to muscle atrophy, but no effective pharmacotherapy is available. We reported that clenbuterol (CB) induced masseter muscle hypertrophy and slow-to-fast myosin heavy chain (MHC) isoform transition through direct muscle β2-adrenergic receptor stimulation. Thus, we hypothesized that CB would antagonize glucocorticoid (dexamethasone; DEX)-induced muscle atrophy and fast-to-slow MHC isoform transition.MethodologyWe examined the effect of CB on DEX-induced masseter muscle atrophy by measuring masseter muscle weight, fiber diameter, cross-sectional area, and myosin heavy chain (MHC) composition. To elucidate the mechanisms involved, we used immunoblotting to study the effects of CB on muscle hypertrophic signaling (insulin growth factor 1 (IGF1) expression, Akt/mammalian target of rapamycin (mTOR) pathway, and calcineurin pathway) and atrophic signaling (Akt/Forkhead box-O (FOXO) pathway and myostatin expression) in masseter muscle of rats treated with DEX and/or CB.Results and ConclusionMasseter muscle weight in the DEX-treated group was significantly lower than that in the Control group, as expected, but co-treatment with CB suppressed the DEX-induced masseter muscle atrophy, concomitantly with inhibition of fast-to-slow MHC isoforms transition. Activation of the Akt/mTOR pathway in masseter muscle of the DEX-treated group was significantly inhibited compared to that of the Control group, and CB suppressed this inhibition. DEX also suppressed expression of IGF1 (positive regulator of muscle growth), and CB attenuated this inhibition. Myostatin protein expression was unchanged. CB had no effect on activation of the Akt/FOXO pathway. These results indicate that CB antagonizes DEX-induced muscle atrophy and fast-to-slow MHC isoform transition via modulation of Akt/mTOR activity and IGF1 expression. CB might be a useful pharmacological agent for treatment of glucocorticoid-induced muscle atrophy.

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Section: Resultsmentioning

confidence: 99%

Protective Effects of Clenbuterol against Dexamethasone-Induced Masseter Muscle Atrophy and Myosin Heavy Chain Transition

et al. 2015

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“…Consistent with the findings from GSEA, the majority of the coexpression modules consisted of genes down‐regulated in response to MR or CR. For MR, we identified 4 separate modules, 2 of which consisted entirely of down‐regulated genes (modules 1, 2), while the other 2 contained only one up‐regulated module in each of them (modules 3, 4). Module 1 contained pathways related to inflammatory response, cell migration, and cell communication (nodes connected by solid lines showing higher correlations than those connected by dashed lines).…”

Section: Resultsmentioning

confidence: 99%

“…C alorie restriction (CR) to 60% of ad libitum intake produces a robust and reproducible extension of mean and maximal life span across species (1–3). CR is recognized as the gold standard for life span extension, but the difficulty of adhering to this dietary regimen has spurred the search for CR mimetics that extend life without imposition of severe food intake restriction.…”

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confidence: 99%

“…Obesity‐induced inflammation is comparable to the inflammation that accompanies aging, including increased production of reactive oxygen species and inflammatory cytokines (12). Given that chronic CR and dietary MR produce comparable extensions in rodent life span (1, 2, 4, 5), we recently examined the transcriptional effect of the two dietary regimens on the systems biology of systemic inflammation (13). Despite comparable reductions in adiposity, the two dietary regimens produced fundamentally different anti‐inflammatory responses in liver and adipose tissue.…”

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confidence: 99%

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A systems biology analysis of the unique and overlapping transcriptional responses to caloric restriction and dietary methionine restriction in rats

et al. 2014

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Dietary methionine restriction (MR) and calorie restriction (CR) each improve metabolic health and extend life span. We used comprehensive transcriptome profiling and systems biology analysis to interrogate the unique and overlapping molecular responses in rats provided these dietary regimens for 20 mo after weaning. Microarray analysis was conducted on inguinal white adipose (IWAT), brown adipose tissue (BAT), liver, and skeletal muscle. Compared to controls, CR-induced transcriptomic responses (absolute fold change ≥1.5 and P≤0.05) were comparable in IWAT, BAT, and liver (~800 genes). MR-induced effects were largely restricted to IWAT and liver (~2400 genes). Pathway enrichment and gene-coexpression analyses showed that induction of fatty acid synthesis in IWAT was common to CR and MR, whereas immunity and proinflammatory signaling pathways were specifically down-regulated in MR-treated IWAT and liver (FDR≤0.07-0.3). BAT demonstrated consistent down-regulation of PPAR-signaling under CR and MR, whereas muscle was largely unaffected. Interactome analysis identified CR-specific down-regulation of cytoskeletal matrix components in IWAT and MR-specific up-regulation of ribosomal genes in liver (FDR≤0.001). Transcriptomic down-regulation of inflammation genes by MR in IWAT was consistent with upstream inhibition of STAT3. Together, these results provide an integrated picture of the breadth of transcriptional responses to MR and CR among key metabolic tissues.

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“…7,8 Calorie restriction to 40% of ad libitum intake (DR) also produces a robust extension of mean and maximal life span across species, 17–19 along with the expected reduction in fat accumulation. In addition to comparable effects on longevity and adiposity, DR and MR share other beneficial outcomes including increased insulin sensitivity and a comprehensive improvement in biomarkers of metabolic health.…”

Section: Anti-inflammatory Responses To Dietary Methionine Restricmentioning

confidence: 99%

The Impact of Dietary Methionine Restriction on Biomarkers of Metabolic Health

Orgeron

Stone

Wanders

et al. 2014

Progress in Molecular Biology and Translational Science

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Calorie restriction without malnutrition, commonly referred to as dietary restriction (DR), results in a well-documented extension of life span. DR also produces significant, long-lasting improvements in biomarkers of metabolic health that begin to accrue soon after its introduction. The improvements are attributable in part to the effects of DR on energy balance, which limit fat accumulation through reduction in energy intake. Accumulation of excess body fat occurs when energy intake chronically exceeds the energy costs for growth and maintenance of existing tissue. The resulting obesity promotes the development of insulin resistance, disordered lipid metabolism, and increased expression of inflammatory markers in peripheral tissues. The link between the life-extending effects of DR and adiposity is the subject of an ongoing debate, but it is clear that decreased fat accumulation improves insulin sensitivity and produces beneficial effects on overall metabolic health. Over the last 20 years, dietary methionine restriction (MR) has emerged as a promising DR mimetic because it produces a comparable extension in life span, but surprisingly, does not require food restriction. Dietary MR also reduces adiposity but does so through a paradoxical increase in both energy intake and expenditure. The increase in energy expenditure fully compensates for increased energy intake and effectively limits fat deposition. Perhaps more importantly, the diet increases metabolic flexibility and overall insulin sensitivity and improves lipid metabolism while decreasing systemic inflammation. In this chapter, we describe recent advances in our understanding of the mechanisms and effects of dietary MR and discuss the remaining obstacles to implementing MR as a treatment for metabolic disease.

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The Effect of Nutritional Regimes Upon Collagen Concentration and Survival of Rats

Cited by 7 publications

References 5 publications

Protective Effects of Clenbuterol against Dexamethasone-Induced Masseter Muscle Atrophy and Myosin Heavy Chain Transition

Protective Effects of Clenbuterol against Dexamethasone-Induced Masseter Muscle Atrophy and Myosin Heavy Chain Transition

A systems biology analysis of the unique and overlapping transcriptional responses to caloric restriction and dietary methionine restriction in rats

The Impact of Dietary Methionine Restriction on Biomarkers of Metabolic Health

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