Circulating GDF11 levels are decreased with age but are unchanged with obesity and type 2 diabetes

• Published in: Aging (Albany, NY.) Vol. 11; no. 6; pp. 1733 - 1744
• Main Authors: Añón-Hidalgo, Juan, Catalán, Victoria, Rodríguez, Amaia, Ramírez, Beatriz, Silva, Camilo, Galofré, Juan C., Salvador, Javier, Frühbeck, Gema, Gómez-Ambrosi, Javier
• Format: Journal Article
• Language: English
• Published: United States Impact Journals 21.03.2019
• Subjects: Adult; Aged; Aging - blood; Animals; Body Composition; Bone Morphogenetic Proteins - blood; Cross-Sectional Studies; Diabetes Mellitus, Type 2 - blood; Enzyme-Linked Immunosorbent Assay; Female; Growth Differentiation Factors - blood; Humans; Male; Mice; Middle Aged; Obesity - blood; Research Paper; GDF11; fat-free mass; type 2 diabetes; aging; obesity
• ISSN: 1945-4589; 1945-4589
• DOI: 10.18632/aging.101865

Growth differentiation factor 11 (GDF11) is a member of the transforming growth factor β (TGFβ) superfamily which declines with age and exerts anti-aging regenerative effects in skeletal muscle in mice. However, recent data in humans and mice are conflicting casting doubts about its true functional actions. The aim of the present study was to compare the circulating concentrations of GDF11 in individuals of different ages as well as body weight and glycemic status. Serum concentrations of GDF11 were measured by ELISA in 319 subjects. There was a significant increase in GDF11 concentrations in people in the 41-50 y group and a decline in the elder groups (61-70 and 71-80 y groups, =0.008 for the comparison between all age groups). However, no significant correlation between fat-free mass index (FFMI), a formula used to estimate the amount of muscle mass in relation to height, and logGDF11 was observed ( =0.08, =0.197). Moreover, no significant differences in circulating concentrations of GDF11 regarding obesity or glycemic status were found. Serum GDF11 concentrations in humans decrease in older ages being unaltered in obesity and T2D. Further studies should determine the exact pathophysiological role of GDF11 in aging.