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Diabetes. 2015 Feb 18. pii: db140796. [Epub ahead of print]
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Human adipocytes induce inflammation and atrophy in muscle cells during obesity.
Pellegrinelli V 1, Rouault C 2, Rodriguez-Cuenca S 3, Albert V 2, Edom-Vovard F 4, Vidal-Puig A 3, Clément K 2, Butler-Browne G 4, Lacasa D 2.
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Cited by: Really? No one cited it yet. Is it a very recent publication?
Abstract
Inflammation and lipid accumulation are hallmarks of muscular pathologies resulting from metabolic diseases such as obesity and type II diabetes. During obesity, the hypertrophy of visceral adipose tissue (VAT) contributes to muscle dysfunctions particularly through dysregulated production of adipokines.We have investigated the crosstalk 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 co-culture 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 co-cultured cells of cytokines and chemokines with IL-6 and IL-1β as key contributors. Moreover, we gathered evidence showing that obese subcutaneous adipocytes were less potent than VAT adipocytes in inducing these myotubes dysfunctions. Interestingly, the atrophy induced by visceral adipocytes was corrected by IGF-II/IGFBP-5. Finally, we observed that 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 the muscle phenotype that could contribute to muscle wasting associated with metabolic disorders.
© 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
copy
Human adipocytes induce inflammation and atrophy in muscle cells during obesity.
Pellegrinelli V 1, Rouault C 2, Rodriguez-Cuenca S 3, Albert V 2, Edom-Vovard F 4, Vidal-Puig A 3, Clément K 2, Butler-Browne G 4, Lacasa D 2.
Author information
Cited by: Really? No one cited it yet. Is it a very recent publication?
Abstract
Inflammation and lipid accumulation are hallmarks of muscular pathologies resulting from metabolic diseases such as obesity and type II diabetes. During obesity, the hypertrophy of visceral adipose tissue (VAT) contributes to muscle dysfunctions particularly through dysregulated production of adipokines.We have investigated the crosstalk 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 co-culture 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 co-cultured cells of cytokines and chemokines with IL-6 and IL-1β as key contributors. Moreover, we gathered evidence showing that obese subcutaneous adipocytes were less potent than VAT adipocytes in inducing these myotubes dysfunctions. Interestingly, the atrophy induced by visceral adipocytes was corrected by IGF-II/IGFBP-5. Finally, we observed that 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 the muscle phenotype that could contribute to muscle wasting associated with metabolic disorders.
© 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
