Aging is associated with a decline in lean muscle mass and development of metabolic dysfunction. Skeletal muscle-derived, exercise-induced “myokines” are believed to have anti-inflammatory effects and substantially regulate glucose and fatty acid metabolism. To better understand the linkage between aging associated metabolic dysfunctions and aberrant myokine signaling, we use the MILLIPLEX® map Mouse Myokine Panel and the Mouse Aging Panel (under development) to measure circulating myokine and aging related biomarkers in youth and elderly C57BL/6 mice (Youth: ∼8 weeks old, n=16; Elderly: ∼48 weeks old, n=16). Impaired regenerative capacity and reduction of myokine secretion are hallmarks of aged skeletal muscle. In the elderly group, the myokine SPARC concentrations were 40% that of the youth group and the myogenesis inhibitor GDF8 concentrations were 7-fold higher in the elderly vs. youth. Interestingly, a 21-fold higher level of EPO and a 3-fold higher level of OSTN were observed in the elderly vs. youth groups suggesting a possible compensation effect in these aged mice. We observed the novel type 2 diabetes associated chemokine fractalkine level is 604-fold higher in elderly vs. youth groups. In addition, 41-fold higher IL-6 and 2-fold higher CCL27 in elderly vs. youth coincide with the theory of aberrant glucose metabolism being associated with elevated adipocyte inflammation in elderly populations. Body composition change, and aberrant energy sensing are pervasive features of aging. We found the starvation hormone FGF-21 level was 23-fold higher in elderly mice vs. youth, while the satiety hormone leptin was 3-fold higher. In brief, we measured multiple novel myokines and geriatric related metabolic biomarkers using the MILLIPLEX® map quantitative immunoassay platform. Analytical validation revealed excellent assay performance well suited for biomarker monitoring in mouse models of age-related disease research.
L. Zeng: None.
