Short-chain fatty acids regulate systemic bone mass and protect from pathological bone loss, 2018, Zaiss et al

Andy

Retired committee member
Abstract

Microbial metabolites are known to modulate immune responses of the host. The main metabolites derived from microbial fermentation of dietary fibers in the intestine, short-chain fatty acids (SCFA), affect local and systemic immune functions. Here we show that SCFA are regulators of osteoclast metabolism and bone mass in vivo. Treatment of mice with SCFA as well as feeding with a high-fiber diet significantly increases bone mass and prevents postmenopausal and inflammation-induced bone loss.

The protective effects of SCFA on bone mass are associated with inhibition of osteoclast differentiation and bone resorption in vitro and in vivo, while bone formation is not affected. Mechanistically, propionate (C3) and butyrate (C4) induce metabolic reprogramming of osteoclasts resulting in enhanced glycolysis at the expense of oxidative phosphorylation, thereby downregulating essential osteoclast genes such as TRAF6 and NFATc1. In summary, these data identify SCFA as potent regulators of osteoclast metabolism and bone homeostasis.
Open access at https://www.nature.com/articles/s41467-017-02490-4

Article based on study - https://www.fau.eu/2018/01/12/news/research/can-muesli-help-against-arthritis/
In the latest article published in Nature Communications, FAU researchers show that it is not the intestinal bacteria themselves, but rather their metabolites which affect the immune system and therefore have a knock-on effect on autoimmune diseases such as rheumatoid arthritis. How intestinal bacteria and the immune system communicate is still unclear, and scientists are still unsure about what may be done to have a positive effect on the bacteria. The researchers focussed on the short-chain fatty acids propionate and butyrate, which are formed during the fermentation processes caused by intestinal bacteria. These fatty acids can be found, for example, in the joint fluid and it is assumed that they have an important effect on the functionality of joints.
 
This looks like nonsense again to me. Metabolites from germs in mice are not 'regulators' of bone mass. They may affect bone mass in highly artificial circumstances. But the regulators of our bone mass are our regulatory feedback based hormonal systems. It is a bit like saying ice cream is a regulator of body weight in camels.

And there is no evidence whatever for bacterial products being relevant to rheumatoid arthritis. This is just Chinese fairly stories being whispered around by people who like fairy stories.
 
This looks like nonsense again to me. Metabolites from germs in mice are not 'regulators' of bone mass. They may affect bone mass in highly artificial circumstances. But the regulators of our bone mass are our regulatory feedback based hormonal systems. It is a bit like saying ice cream is a regulator of body weight in camels.

And there is no evidence whatever for bacterial products being relevant to rheumatoid arthritis. This is just Chinese fairly stories being whispered around by people who like fairy stories.
Perhaps illustrates the gulf between theory and evidence.
 
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