Impact of serum amyloid A on cellular cholesterol efflux to serum in type 2 diabetes mellitus

Effect of Rosuvastatin on Cholesterol Efflux Capacity and Endothelial Function in Type 2 Diabetes Mellitus and Dyslipidemia

“…One study found that the CE of HDL in patients with a long duration of DM (>10 years) was lower than that in nondiabetic controls. 32 Similarly, in the present study, baseline CE capacity of patients was impaired compared with that of healthy controls.…”

Serum amyloid A links endotoxaemia to weight gain and insulin resistance in mice

“…In adipocytes, macrophages and leucocytes, SAA stimulates the production of cytokines promoting inflammation and a positive feedback on SAA production. An additional hypothesis from our data suggests that SAA also participates in (B) the LPS passage from the gut lumen into the bloodstream, increasing gut permeability, and in (C) LPS maintenance in serum, impairing SR-BI [18,20], one of the receptors responsible for LPS clearance manuscript. RAF and AC contributed to the study conception and design, analysis and interpretation of data, and writing and editing of the manuscript.…”

“…When complexed with HDL [44], LPS is cleared by SR-BI in hepatocytes [45] and in other cell types such as macrophages and monocytes, as recently described [46]. The clearance of LPS through SR-BI efficiently determines the magnitude of the inflammatory response, and it has already been shown that SAA is associated with impairment of SR-BI [20]. Thus, the authors suggest that the reduction in SAA serum levels due to the ASO SAA treatment could decrease gut permeability to LPS and also improve SR-BI-mediated LPS clearance, leading to decreased endotoxaemia.…”

“…However, liver-derived SAA has been implicated not only in the regulation of inflammatory responses [13][14][15] but also in the control of cell proliferation [16][17][18] and metabolic profile [18][19][20]. Although mainly secreted by the liver, SAA has also been reported as being produced by adipocytes, macrophages and several other cell types [21,22], with levels positively correlated with obesity grade, as well as increased expression under hypoxic conditions [22,23].…”

“…SAA is an endogenous ligand to TLR-4 [13] and TLR-2 [24] and was recently described as causing impairment to the scavenger receptor BI (SR-BI) [20]. All these receptors are admittedly associated with the inflammatory response and also related to lipopolysaccharide (LPS) responsiveness [13,24,25].…”