Adipose tissue is a primary site of obesity-induced inflammation, which is emerging as an important contributor to obesity-related diseases. The factors influencing adipose tissue-induced inflammation and the resulting pathologies remain poorly understood. However, dietary fiber diets appear to be protective, suggesting a cross-talk between the colonic metabolism and adipose tissue-induced inflammation. Short-chain fatty acids, e.g. propionic acid (PA), are the principal products of the dietary fiber fermentation by microbiota.
Materials and methods
Human omental and subcutaneous adipose tissue explants were obtained from gynaecological patients who underwent surgery. Explants were incubated for 24 h with propionic acid. Human THP-1 monocytic cells were differentiated to macrophages and incubated with LPS in the presence and absence of propionic acid. Cytokine and chemokine production were determined by multiplex ELISA, and mRNA expression of metabolic and macrophages genes was determined by RT-PCR.
Here we showed that the treatment of human adipose tissue with PA resulted in a significant downregulation of several inflammatory parameters (e.g. TNF-α and CCL5). Furthermore, PA positively influenced factors associated with insulin sensitivity, lipogenesis and glucose uptake (e.g. lipoprotein lipase and GLUT4). Similar effects on cytokine and chemokine production by macrophages were also observed. PA mediated its effects via G-protein coupled receptor signaling pathways (Gi/o-dependent and –independent pathways).
Propionic acid, normally produced in the colon, may have a direct beneficial effect on adipose tissue, such as reducing obesity-associated inflammation and increasing lipogenesis and glucose uptake. Effects on adipose tissue as a whole are at least partially explained by effects on macrophages but likely also adipocytes are involved. This suggests that, in vivo, propionic acid and dietary fibres may have potential in preventing obesity-related inflammation and associated diseases.