One major discovery of the last decade in the field of metabolic diseases is that the microorganisms comprising the gut microbiota are now considered a metabolic "organ", modulating multiple functions of the host, such as intestinal immune system maturation, adiposity, cardiac metabolism, liver triglyceride storage, and brain development and behaviour. The corresponding mechanisms involve increased energy harvesting through the production by microbiota of short-chain fatty acids for use by the host, and the release of pro-inflammatory compounds, such as lipopolysaccharide (LPS), flagellin and peptidoglycan. In particular, a high-fat diet (HFD) modifies gut microbiota, resulting in an increase of plasma LPS levels known as "metabolic endotoxaemia", a major driver of the onset of metabolic diseases through a CD14-dependent mechanism. The LPS-sensitive cell types can be seen within bone marrow-derived cells (BMC), which are involved in the development of inflammation in the adipose tissue of obese and type 2 diabetic mice. Furthermore, the expression of LPS receptor/cofactor CD14 cells from the stromal vascular fraction of adipose depots can also be directly targeted by LPS to initiate precursor cell development and adiposity. Moreover, data from the literature also indicate an impact of gut microbiota on intestinal stem cells. Thus, this mini review presents the experimental evidence supporting a relationship between gut microbiota and stem cells as a new axis of metabolic homoeostasis control.
Keywords: Gut microbiota; High-fat diet; Metabolic diseases; Omics; Stem cells.
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