Mechanism of action of gut microbiota and probiotic Lactobacillus rhamnosus GG on skeletal remodeling in mice

Abstract

IntroductionGut microbiota (GM) is the collection of small organisms such as bacteria, fungi, bacteriophages and protozoans living in the intestine in symbiotics relation within their host. GM regulates host metabolism by various mechanisms.MethodsThis review aims to consolidate current information for physicians on the effect of GM on bone health. For this, an online search of the literature was conducted using the keywords gut microbiota, bone mass, osteoporosis, Lactobacillus and sex steroid.Results and ConclusionsThere is a considerable degree of variation in bone mineral density (BMD) within populations, and it is estimated that a significant component of BMD variability is due to genetics. However, the remaining causes of bone mass variance within populations remain largely unknown. A well‐recognized cause of phenotypic variation in bone mass is the composition of the microbiome. Studies have shown that germ‐free (GF) mice have higher bone mass compared to conventionally raised (CR) mice. Furthermore, GM dysbiosis, also called dysbacteriosis, is defined as any alteration in the composition of the microbial community that has been colonized in the host intestine and associated with the development of bone diseases. For instance, postmenopausal osteoporosis (PMO) and diabetes. GM can be modulated by several factors such as genetics, age, drugs, food habits and probiotics. Probiotics are defined as viable bacteria that confer health benefits by modulating GM when administered in adequate quantity. Lactobacillus rhamnosus GG (LGG) is a great example of such a probiotic. LGG has been shown to regulate bone mass in healthy mice as well as ovariectomized (OVX) mice via two different mechanisms. This review will focus on the literature regarding the mechanism by which GM and probiotic LGG regulate bone mass in healthy mice as well as in OVX mice, a model of PMO.

Genus_Ruminococcus and order_Burkholderiales affect osteoporosis by regulating the microbiota-gut-bone axis

“…Additionally, when fecal transplants from conventional mice are administered, germ-free mice show a decrease in bone mass (Sjogren et al, 2012). This trend is also observed in germ-free mice after drug castration, suggesting that gut bacteria may play a role in bone growth and development through certain mechanisms (Li et al, 2016;Tyagi, 2023); however, the differences in regulation may be closely related to differences in mouse gender, mouse species, cage conditions, and feed used. This relationship between gut microbes and bone metabolism is known as the microbiota-gut-bone axis or gut-bone axis (Tu et al, 2021).…”

The Influence of Ketogenic Diet on Gut Microbiota: Potential Benefits, Risks and Indications

“…LGG or butyrate has been linked to the expansion of T-regulatory cells (T-reg) in both the gut and bone marrow, leading to the upregulation of osteogenic stimulus mediated by CD8+ T-cells. Wnt10b may promote bone formation by activating Wnt signaling in osteoblasts [84,85]. Interestingly, SCFAs, including butyrate, have been associated with T-reg and CD8+ T-cell-mediated bone anabolic activity, although SCFAs' antiresorptive activity may be T cell-independent [81,86].…”