title: Physiological Aging: Links Among Adipose Tissue Dysfunction, Diabetes, and Frailty.
abstract: Advancing age is associated with progressive declines in physiological function that lead to overt chronic disease, frailty, and eventual mortality. Importantly, age-related physiological changes occur in cellularity, insulin-responsiveness, secretory profiles, and inflammatory status of adipose tissue, leading to adipose tissue dysfunction. Although the mechanisms underlying adipose tissue dysfunction are multifactorial, the consequences result in secretion of proinflammatory cytokines and chemokines, immune cell infiltration, an accumulation of senescent cells, and an increase in senescence-associated secretory phenotype (SASP). These processes synergistically promote chronic sterile inflammation, insulin resistance, and lipid redistribution away from subcutaneous adipose tissue. Without intervention, these effects contribute to age-related systemic metabolic dysfunction, physical limitations, and frailty. Thus adipose tissue dysfunction may be a fundamental contributor to the elevated risk of chronic disease, disability, and adverse health outcomes with advancing age.
authors.affiliation: Department of Nutritional Sciences, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma.|Reynolds Oklahoma Center on Aging, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma.
authors.forename: Michael B
authors.initials: MB
authors.lastname: Stout
authors.affiliation: Department of Internal Medicine-Geriatrics, Sticht Center on Aging, Wake Forest School of Medicine, Winston-Salem, North Carolina; and.
authors.forename: Jamie N
authors.initials: JN
authors.lastname: Justice
authors.affiliation: Department of Internal Medicine-Geriatrics, Sticht Center on Aging, Wake Forest School of Medicine, Winston-Salem, North Carolina; and.
authors.forename: Barbara J
authors.initials: BJ
authors.lastname: Nicklas
authors.affiliation: Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota.
authors.forename: James L
authors.initials: JL
authors.lastname: Kirkland
mesh_terms: D017667:Adipocytes / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism* / Q000503:physiopathology; D000375:Aging; D000818:Animals; D016922:Cellular Senescence; D002908:Chronic Disease; D016207:Cytokines / Q000378:metabolism; D003920:Diabetes Mellitus / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000378:metabolism*; D007333:Insulin Resistance; D009765:Obesity / Q000378:metabolism / Q000503:physiopathology
chemical_list: D016207:Cytokines