34 replies to this topic

[ta5]

Bone Res. 2016 Jun 21;4:16012.

Relationship of serum GDF11 levels with bone mineral density and bone turnover markers in postmenopausal Chinese women.
Chen Y1, Guo Q2, Zhang M2, Song S3, et al.
Growth differentiation factor 11 (GDF11) is an important circulating factor that regulates aging. However, the role of GDF11 in bone metabolism remains unclear. The present study was undertaken to investigate the relationship between serum GDF11 level, bone mass, and bone turnover markers in postmenopausal Chinese women. Serum GDF11 level, bone turnover biochemical markers, and bone mineral density (BMD) were determined in 169 postmenopausal Chinese women (47-78 years old). GDF11 serum levels increased with aging. There were negative correlations between GDF11 and BMD at the various skeletal sites. After adjusting for age and body mass index (BMI), the correlations remained statistically significant. In the multiple linear stepwise regression analysis, age or years since menopause, BMI, GDF11, and estradiol were independent predictors of BMD. A significant negative correlation between GDF11 and bone alkaline phosphatase (BAP) was identified and remained significant after adjusting for age and BMI. No significant correlation was noted between cross-linked N-telopeptides of type I collagen (NTX) and GDF11. In conclusion, GDF11 is an independent negative predictor of BMD and correlates with a biomarker of bone formation, BAP, in postmenopausal Chinese women. GDF11 potentially exerts a negative effect on bone mass by regulating bone formation.
PMID: 27408764

[corb]

Bone Res. 2016 Jun 21;4:16012.

Relationship of serum GDF11 levels with bone mineral density and bone turnover markers in postmenopausal Chinese women.
Chen Y1, Guo Q2, Zhang M2, Song S3, et al.
Growth differentiation factor 11 (GDF11) is an important circulating factor that regulates aging. However, the role of GDF11 in bone metabolism remains unclear. The present study was undertaken to investigate the relationship between serum GDF11 level, bone mass, and bone turnover markers in postmenopausal Chinese women. Serum GDF11 level, bone turnover biochemical markers, and bone mineral density (BMD) were determined in 169 postmenopausal Chinese women (47-78 years old). GDF11 serum levels increased with aging. There were negative correlations between GDF11 and BMD at the various skeletal sites. After adjusting for age and body mass index (BMI), the correlations remained statistically significant. In the multiple linear stepwise regression analysis, age or years since menopause, BMI, GDF11, and estradiol were independent predictors of BMD. A significant negative correlation between GDF11 and bone alkaline phosphatase (BAP) was identified and remained significant after adjusting for age and BMI. No significant correlation was noted between cross-linked N-telopeptides of type I collagen (NTX) and GDF11. In conclusion, GDF11 is an independent negative predictor of BMD and correlates with a biomarker of bone formation, BAP, in postmenopausal Chinese women. GDF11 potentially exerts a negative effect on bone mass by regulating bone formation.
PMID: 27408764

 

Very interesting!

GDF11 has been observed as a regulator of bone formation before, or at least mice with GDF11 knockout have bone formation problems - you would have thought it's a positive regulator from that but it seems like it's not if you look at your study. Sometimes negative regulators are important as well, especially in development.

 

Either way, interesting.

[SearchHorizon]

A great thread.  

 

Corb's posts above suggest that, in GDF11 trials, inhibiting myostatin (due to supraphysiological levels of injected GDF11 competing against myostatin) was what led to improvements in biomarkers. In other words, what we should be looking for may be myostatin inhibitors.

 

One well-known myostatin inhibitor is follistatin.

 

I read that Conboy has experimented with TGF-beta blockers as well as follistatin. I would be VERY curious to find out the effects of follistatin on neuronal survival and differentiation. I have looked into this, but with little success. I know that follistatin induces hypertrophy. This does suggest that follistatin could have positive impact on other cell types, including hippocampal neurons.

 

 

[MikeDC]

GDF11 is very contraversal to say the least. Half of the studies say it rejuvenate and the other half say it make you older. From my understanding it is not an important factor in aging. NAD+ Decline plays a very big role in aging.

[corb]

GDF11 does not do anything positive as such.
If it helps, it helps through muscle atrophy which is impaired in aging like everything else.

I've seen papers that claim it clears senescent muscle cells from aged mice hearts but it does not seem to improve regeneration - like every other senescent cell clearing strategy I don't think it will be very helpful in isolation.

 

I don't think anything posted in this thread has been overturned or proven wrong so far, though I have to admit I lost interest in the topic a good time ago so I might be wrong on that account.