Abstract
The interplay between adipose tissue and skeletal muscle and the impact on mobility and aging remain enigmatic. The progressive decline in mobility promoted by aging has been previously attributed to the loss of skeletal mass and function and more recently linked to changes in body fat composition and quantity. Regardless of body size, visceral and intermuscular adipose depots increase with aging and are associated with adverse health outcomes. However, the quality of adipose tissue, in particular abdominal subcutaneous as it is the largest depot, likely plays a significant role in aging outcomes, such as mobility decline, though its communication with other tissues such as skeletal muscle. In this review, we discuss the age-associated development of a pro-inflammatory profile, cellular senescence, and metabolic inflexibility in abdominal subcutaneous adipose tissue. Collectively, these facets of adipose tissue quality influence its secretory profile and crosstalk with skeletal muscle and likely contribute to the development of muscle atrophy and disability. Therefore, the identification of the key structural and functional components of adipose tissue quality—including necrosis, senescence, inflammation, self-renewal, metabolic flexibility—and adipose tissue-secreted proteins that influence mobility via direct effects on skeletal muscle are necessary to prevent morbidity/mortality in the aging population.
Highlights
Addressing the needs of the rapidly expanding aging population has become one of most daunting challenges of our time
While redistribution occurs in all adipose depots during aging, this review focuses on abdominal subcutaneous adipose tissue as it is the largest adipose tissue depot in the human body and its overall contribution to systemic phenotypes may be greater than visceral adipose tissue (VAT), even if the magnitude of effects per unit mass is smaller
This study demonstrates that peri-muscular adipose tissue deposition accelerates aging-induced muscle atrophy factors related to proteolysis and senescence in muscle and induce a progressive loss of skeletal muscle mass and function [78]
Summary
Addressing the needs of the rapidly expanding aging population has become one of most daunting challenges of our time. There is some evidence about secreted factors such as a secretory-associated senescent phenotype secreted by senescent cells within the adipose tissue with the ability to reduce expressions of contractile proteins and induce insulin resistance in human muscle cells [14], suggesting a potentially important role for adipose tissue and adipose tissue-secreted factors in mediating declines in muscle function and mobility with aging. Adipose tissue is a highly dynamic organ with the potential to influence muscle function and whole-body metabolism during aging. FOR PEER[21]; REVIEW this review emphasizes how the adipose tissue quality and 3 of its secretory profile impacts skeletal muscle function and mobility in aging. SASP,influence secretory-associated free fatty acids; M1, inter-organ including2.skeletal muscle pathology. SASP, secretory-associated senescent macrophagepathology, 1; M2, macrophage phenotype; FFAs, free fatty acids; M1, macrophage 1; M2, macrophage 2
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