Taurine Attenuates Catabolic Processes Related to the Onset of Sarcopenia

Abstract

Sarcopenia that occurs with advancing age is characterized by a gradual loss of muscle protein component due to the activation of catabolic pathways, increased level of inflammation, and mitochondrial dysfunction. Experimental evidence demonstrates that several physio-pathological processes involved in the onset of sarcopenia may be counteracted by the intake of specific amino acids or antioxidant molecules, suggesting that diet may represent an effective strategy for improving the anabolic response of muscle during aging. The non-essential amino acid taurine is highly expressed in several mammalian tissues, including skeletal muscle where it is involved in the ion channel regulation, in the modulation of intracellular calcium concentration, and where it plays an important role as an antioxidant and anti-inflammatory factor. Here, with the purpose to reproduce the chronic low-grade inflammation characteristics of senescent muscle in an in vitro system, we exploited the role of Tumor Necrosis Factor α (TNF) and we analyzed the effect of taurine in the modulation of different signaling pathways known to be dysregulated in sarcopenia. We demonstrated that the administration of high levels of taurine in myogenic L6 cells stimulates the differentiation process by downregulating the expression of molecules involved in inflammatory pathways and modulating processes such as autophagy and apoptosis. Although further studies are currently ongoing in our laboratory to better elucidate the molecular mechanisms responsible for the positive effect of taurine on myogenic differentiation, this study suggests that taurine supplementation may represent a strategy to delay the loss of mass and functionality characteristic of senescent muscles.

The Role of Taurine in Skeletal Muscle Functioning and Its Potential as a Supportive Treatment for Duchenne Muscular Dystrophy

“…Furthermore, it was suggested that taurine delays muscle-specific senescence including sarcopenia in tumor necrosis factor (TNF)-α stimulated L6 myogenic rat cells. In evidence, differences in the regulation of inflammation, autophagy, and apoptosis have been reported upon taurine treatment [17]. In addition, TNF-α stimulation of L6 myogenic rat cells hampered muscle differentiation which could be restored by taurine.…”

“…In addition, TNF-α stimulation of L6 myogenic rat cells hampered muscle differentiation which could be restored by taurine. Presumably this effect was mediated through the PI3/AKT signaling pathway since myocyte enhancer factor-2 (MEF-2), a transcription factor involved in myogenic differentiation, was markedly decreased after knockdown of AKT [17]. Furthermore, expression of TauT increased during muscle differentiation and was even further enhanced upon binding of MEF-2 to the promotor region of TauT [18].…”

Integrating untargeted and targeted metabolomics coupled with pathway analysis reveals muscle disorder in osteoporosis on orchiectomized mice

“…At the same time, the reduction of carnosine and anserine level provide absent of anti-oxidative process, where oxidative stress is aggravated and the risk of necrosis was hastened. [38][39][40] . The activation of detailed key factors, including IL37, NFkB, or Mapk, provides more danger hidden in OP cases 16,38,[41][42][43] .…”

“…All the 31 detected significant metabolites regulate these three elements directly or indirectly. Obviously, the aggravation of any one element brings far-reaching disturbance on the other two elements [38][39][40] . Taking a close look at the metabolites that contribute to the activation of key factors including IL37, NFkB, or Mapk, more danger was hidden in OP cases 16,38,[41][42][43] .…”

Musculoskeletal Aging and Sarcopenia in the Elderly

“…Taurine, a non-essential amino acid abundant in nuts, shellfish, eggs, meat, and dairy products, is another promising nutrient that might be supplemented to promote muscle health and counteract sarcopenia [ 12 ]. The administration of taurine to myogenic L6 cells was shown to stimulate cell differentiation by downregulating the expression inflammatory molecules and through modulating autophagy and apoptosis [ 12 ].…”