How fat cells damage muscles and lead to wasting and weakness

  • In a previous research paper presentation on this website, we reported that fat cells accumulating in muscle tissue undermine the muscle tissue, leading to weakness and wasting.
  • Now a new paper published in the journal diabetes shows how visceral fat (deep stomach fat, also known as "beer belly" or just "belly fat") also undermines muscle tissue throughout the body.
  • Specifically it was found that in obesity, visceral adipocytes (fat cells) secrete inflammatory proteins (IL-6 and IL-1β) that reduce the contractile proteins in muscles, leading to muscle weakness and muscle wasting. Superficial fat tissue (basically, fat under the skin) was much less potent in that respect.
  • In summary, this paper shows that belly fat is not only a risk factor for diabetes and cardiovascular disease but also for muscle weakness and muscle loss.
  • Stress, alcohol, a high carb diet and inactivity are the main reasons for the accumulation of visceral / stomach fat



  • Journal: Diabetes
  • Paper: Human adipocytes induce inflammation and atrophy in muscle cells during obesity
  • 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.
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