I guess this used too high of a dose:
Basic Res Cardiol. 2017 Jul;112(4):48. doi: 10.1007/s00395-017-0639-9. Epub 2017 Jun 24.
Zimmers TA1,2,3,4,5, Jiang Y6, Wang M6, Liang TW6, et al.
Growth differentiation factor 11 (GDF11), a TGF-beta superfamily member, is highly homologous to myostatin and essential for embryonic patterning and organogenesis. Reports of GDF11 effects on adult tissues are conflicting, with some describing anti-aging and pro-regenerative activities on the heart and skeletal muscle while others opposite or no effects. Herein, we sought to determine the in vivo cardiac and skeletal muscle effects of excess GDF11. Mice were injected with GDF11 secreting cells, an identical model to that used to initially identify the in vivo effects of myostatin. GDF11 exposure in mice induced whole body wasting and profound loss of function in cardiac and skeletal muscle over a 14-day period. Loss of cardiac mass preceded skeletal muscle loss. Cardiac histologic and echocardiographic evaluation demonstrated loss of ventricular muscle wall thickness, decreased cardiomyocyte size, and decreased cardiac function 10 days following initiation of GDF11 exposure. Changes in skeletal muscle after GDF11 exposure were manifest at day 13 and were associated with wasting, decreased fiber size, and reduced strength. Changes in cardiomyocytes and skeletal muscle fibers were associated with activation of SMAD2, the ubiquitin-proteasome pathway and autophagy. Thus, GDF11 over administration in vivo results in cardiac and skeletal muscle loss, dysfunction, and death. Here, serum levels of GDF11 by Western blotting were 1.5-fold increased over controls. Although GDF11 effects in vivo are likely dose, route, and duration dependent, its physiologic changes are similar to myostatin and other Activin receptors ligands. These data support that GDF11, like its other closely related TGF-beta family members, induces loss of cardiac and skeletal muscle mass and function.
PMID: 28647906
Clin Sci (Lond). 2017 Jun 13. pii: CS20171028. doi: 10.1042/CS20171028.
Yang R1, Fu S1, Zhao L2, Zhen B2, Ye L1, Niu X1, Li X1, Zhang P2, Bai J3.
GDF-11 has been implicated in reverse effects of aging on the central nervous system of humans. β2-MG has been reported to negatively regulate cognitive. However, there is a lot of controversy about the role of GDF-11 and β2-MG in ageing and cognitive regulation. Objective: To examine the involvement of GDF-11 and β2-MG in the aging process and cognitive dysfunction. Methods: A total of 51 healthy subjects and 41 elderly patients with different degrees of age-related cognitive impairment participated in the study. We measured plasma GDF-11 and β2-MG levels using ELISA and immunoturbidimetry, respectively. The results were statistically analyzed to evaluate the associations between levels of GDF-11 and β2-MG and aging and cognitive impairments. Results: Circulating GDF-11 levels did not decline with age or correlate with aging in healthy Chinese males. We did not detect differences in circulating GDF-11 levels among the healthy advanced age and 4 cognitive impairment groups. β2-MG levels increased with age, but there was no significant difference between healthy elderly males and advanced age males. Increased levels of β2-MG were observed in the dementia group compared with the healthy advanced age group. Conclusion: Our results suggest that circulating GDF-11 may not exert a protective effect during the aging process or on cognitive function, and β2-MG may play a role in ageing and cognitive impairment. However, it is possible that the relatively small sample size in this study affected the quality of the statistical analysis, and future studies are needed to further validate our findings.
PMID: 28611236
Edited by ta5, 30 June 2017 - 02:21 PM.