The influence of senescent associated secretory phenotype on glucose homeostasis in C2C12 muscle cells: insights into potential p38 inhibitor interventions.

Karan S Rana, Mandeep K Marwah, Farah N S Raja, Irundika Dias, Yukta Sameer Hindalekar, Mohamad Anas Al Tahan, James E Brown, Srikanth Bellary

School of Biosciences, College of Health and Life, Aston University, Birmingham, UK.School of Biosciences, College of Health and Life, Aston University, Birmingham, UK. · pubmed

Paper

Abstract

Increased accumulation of senescent cells with aging is associated with reduced ability of insulin-target tissues to utilize glucose, resulting in increased insulin resistance and glucotoxicity. We investigated the role of the senescent-associated secretory phenotype (SASP) within C2C12, skeletal muscle cells on glucose homeostasis and if such effects could be reduced by blocking pro-inflammatory pathways. C2C12 myotubes were treated with 40% conditioned media from senescent fibroblasts. Indirect glucose uptake and glycogen content were measured. The effect of SASP on the generation of reactive oxygen species [1] and mitochondrial function was also measured. The experiments above were repeated with a p38 inhibitor. 40% SASP treatment significantly decreased glucose utilization and glycogen storage within myotubes (

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Research summary

The paper claims that the senescent-associated secretory phenotype (SASP) negatively impacts glucose homeostasis in muscle cells, and that this effect can be mitigated by p38 inhibitor interventions. This research addresses the mechanisms of aging-related insulin resistance, which is a significant aspect of age-related metabolic dysfunction.

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