Diet-induced obesity alters skeletal muscle fiber types of male but not female mice

DeNies, Maxwell S.; Johnson, Jordan; Maliphol, Amanda B.; Bruno, Michael A.; Kim, Annabelle; Rizvi, Abbas; Rustici, Kevyn; Medler, Scott

doi:10.1002/phy2.204

Cited by 74 publications

(79 citation statements)

References 49 publications

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“…A significant increase in genioglossus electromyogram (EMGgg) was found in the postmenopausal group re-examined after hormone therapy2930. Denies and colleagues investigated the long-term effects of a high-fat diet and subsequent obesity on muscle fiber type composition and found that the high-fat diet was associated with a significantly lower proportion of slow, type I fibers in the soleus muscle of male, but not female, mice31. The critical pathophysiological feature of OSAS is sleep-related pharyngeal collapse of the UA, which is partly determined by the properties of different muscle fiber types.…”

Section: Discussionmentioning

confidence: 99%

Estrogen/ERR-α signaling axis is associated with fiber-type conversion of upper airway muscles in patients with obstructive sleep apnea hypopnea syndrome

Chen¹,

Lu²,

Guan³

et al. 2016

Sci Rep

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Estrogen is related with the low morbidity associated with obstructive sleep apnea hypopnea syndrome (OSAS) in women, but the underlying mechanisms remain largely unknown. In this study, we examined the relationship between OSAS and estrogen related receptor-α (ERR-α). We found that the expression levels of ERR-α and Myh7 were both downregulated in palatopharyngeal tissues from OSAS patients. In addition, we report that ERR-α is dynamically expressed during differentiation of C2C12 myoblasts. Knockdown of ERR-α via instant siRNA resulted in reduced expression of Myh7, but not Myh4. Furthermore, differentiation of C2C12 cells under 3% chronic intermittent hypoxia, a model resembling human OSAS, was impaired and accompanied by a obvious reduction in Myh7 expression levels. Moreover, activation of ERR-α with 17β-estradiol (E2) increased the expression of Myh7, whereas pretreatment with the ERR-α antagonist XCT790 reversed the E2-induced slow fiber-type switch. A rat ovariectomy model also demonstrated the switch to fast fiber type. Collectively, our findings suggest that ERR-α is involved in estrogen-mediated OSAS by regulating Myhc-slow expression. The present study illustrates an important role of the estrogen/ERR-α axis in the pathogenesis of OSAS, and may represent an attractive therapeutic target, especially in postmenopausal women.

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Section: Discussionmentioning

confidence: 99%

Estrogen/ERR-α signaling axis is associated with fiber-type conversion of upper airway muscles in patients with obstructive sleep apnea hypopnea syndrome

Chen¹,

Lu²,

Guan³

et al. 2016

Sci Rep

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“…For example, DNA microarray analysis in skeletal muscle revealed 35 differentially expressed transcripts between male and female rats following a HF diet. 21 Similarly, compared to their male counterparts, female rats elevate mitochondrial content to a lesser extent 20 and do not show changes in fiber type 22 following a HF diet. More importantly, gender-related differences in both apoptosis 69,70 and autophagy 69,71,72 have been noted in the literature.…”

Section: Discussionmentioning

confidence: 99%

“…Given that there are fiber/muscle differences in apoptotic 17 as well as autophagic 18,19 signaling and protein expression, a concurrent evaluation of these pathways within skeletal muscles of different fiber composition would provide novel insight regarding this relationship following HF feeding. Additionally, despite evidence that some physiological responses to HF feeding are sex-dependent, [20][21][22] much of the current literature has been conducted using male animals. 10,[23][24][25][26][27][28][29][30][31][32] Recently, calls to eliminate gender bias in animal research have been made; 33,34 making an examination of the muscle-specific adaptations to HF feeding in a female model timely.…”

Section: Introductionmentioning

confidence: 99%

High-fat feeding does not induce an autophagic or apoptotic phenotype in female rat skeletal muscle

Campbell

Mitchell

McMillan

et al. 2014

Exp Biol Med (Maywood)

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Apoptosis and autophagy are critical in normal skeletal muscle homeostasis; however, dysregulation can lead to muscle atrophy and dysfunction. Lipotoxicity and/or lipid accumulation may promote apoptosis, as well as directly or indirectly influence autophagic signaling. Therefore, the purpose of this study was to examine the effect of a 16-week high-fat diet on morphological, apoptotic, and autophagic indices in oxidative and glycolytic skeletal muscle of female rats. High-fat feeding resulted in increased fat pad mass, altered glucose tolerance, and lower muscle pAKT levels, as well as lipid accumulation and reactive oxygen species generation in soleus muscle; however, muscle weights, fiber type-specific cross-sectional area, and fiber type distribution were not affected. Moreover, DNA fragmentation and LC3 lipidation as well as several apoptotic (ARC, Bax, Bid, tBid, Hsp70, pBcl-2) and autophagic (ATG7, ATG4B, Beclin 1, BNIP3, p70 s6k, cathepsin activity) indices were not altered in soleus or plantaris following high-fat diet. Interestingly, soleus muscle displayed small increases in caspase-3, caspase-8, and caspase-9 activity, as well as higher ATG12-5 and p62 protein, while both soleus and plantaris muscle showed dramatically reduced Bcl-2 and X-linked inhibitor of apoptosis protein (XIAP) levels. In conclusion, this work demonstrates that 16 weeks of high-fat feeding does not affect tissue morphology or induce a global autophagic or apoptotic phenotype in skeletal muscle of female rats. However, high-fat feeding selectively influenced a number of apoptotic and autophagic indices which could have implications during periods of enhanced muscle stress.

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“…Ectopic lipid storage in muscle (i.e., within muscle cells and/or in adipocytes located between muscle fibers) represents a negative risk factor for the development of type 2 diabetes related to muscle insulin resistance (10)(11)(12)(13). Moreover, skeletal muscle of obese subjects also displays an impairment in oxidative capacity (14) and abnormal muscle fiber organization (15,16). An increased amount of VAT in obesity has been proposed to link obesity and muscle metabolic alterations, such as insulin resistance.…”

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confidence: 99%

Human Adipocytes Induce Inflammation and Atrophy in Muscle Cells During Obesity

et al. 2015

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Inflammation and lipid accumulation are hallmarks of muscular pathologies resulting from metabolic diseases such as obesity and type 2 diabetes. During obesity, the hypertrophy of visceral adipose tissue (VAT) contributes to muscle dysfunction, particularly through the dysregulated production of adipokines. We have investigated the cross talk between human adipocytes and skeletal muscle cells to identify mechanisms linking adiposity and muscular dysfunctions. First, we demonstrated that the secretome of obese adipocytes decreased the expression of contractile proteins in myotubes, consequently inducing atrophy. Using a three-dimensional coculture of human myotubes and VAT adipocytes, we showed the decreased expression of genes corresponding to skeletal muscle contractility complex and myogenesis. We demonstrated an increased secretion by cocultured cells of cytokines and chemokines with interleukin (IL)-6 and IL-1b as key contributors. Moreover, we gathered evidence showing that obese subcutaneous adipocytes were less potent than VAT adipocytes in inducing these myotube dysfunctions. Interestingly, the atrophy induced by visceral adipocytes was corrected by IGF-II/insulin growth factor binding protein-5. Finally, we observed that the skeletal muscle of obese mice displayed decreased expression of muscular markers in correlation with VAT hypertrophy and abnormal distribution of the muscle fiber size. In summary, we show the negative impact of obese adipocytes on muscle phenotype, which could contribute to muscle wasting associated with metabolic disorders.During obesity, hypertrophy of white adipose tissue (WAT) is associated with fibro-inflammation and cell dysfunction. However, visceral depot (visceral adipose tissue [VAT]) differs from subcutaneous adipose tissue (SAT) by its inflammatory status because of its high infiltration with immune cells such as macrophages, T lymphocytes, and mast cells (1,2). Hence, VAT hypertrophy is considered an important contributor to obesityrelated metabolic and cardiovascular diseases (3). In obese subjects, hypertrophied adipocytes display abnormal secretion of leptin and adiponectin and increased production of numerous inflammatory cytokines and chemokines, leading to a disrupted interorgan communication between VAT and important metabolic peripheral tissues such as liver and skeletal muscle (4). These organs are particularly exposed to free fatty acids and cytokines, mostly interleukin (IL)-6, which are increasingly released by the visceral fat of obese subjects (5,6). Skeletal muscles are one of the major metabolic tissues of the body, playing a pivotal role in glucose and lipid metabolism. There is a growing body of evidence showing the effects of obesity on skeletal muscle dysfunction, such as the development of insulin resistance, as attested to by numerous studies performed

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Diet-induced obesity alters skeletal muscle fiber types of male but not female mice

Cited by 74 publications

References 49 publications

Estrogen/ERR-α signaling axis is associated with fiber-type conversion of upper airway muscles in patients with obstructive sleep apnea hypopnea syndrome

Estrogen/ERR-α signaling axis is associated with fiber-type conversion of upper airway muscles in patients with obstructive sleep apnea hypopnea syndrome

High-fat feeding does not induce an autophagic or apoptotic phenotype in female rat skeletal muscle

Human Adipocytes Induce Inflammation and Atrophy in Muscle Cells During Obesity

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