FADS2 inhibition in essential fatty acid deficiency induces hepatic lipid accumulation via impairment of very low-density lipoprotein (VLDL) secretion.

Fatty acid desaturase 2 (FADS2) is responsible for the first desaturation reaction in the synthesis of highly unsaturated fatty acids (HUFAs), such as arachidonic acid (20:4n-6) and eicosapentaenoic acid (20:5n-3), and is involved in Mead acid (20:3n-9) production during essential fatty acid deficiency (EFAD). In this study, an obvious hepatic lipid accumulation was observed in EFAD mice treated with a FADS2 inhibitor. FADS2 inhibition in the EFAD state reduced secretion of very low-density lipoprotein (VLDL) and markedly diminished Mead acid in phosphatidylcholine (PC) in the liver and plasma.

Amadori-modified glycated albumin predominantly induces E-selectin expression on human umbilical vein endothelial cells through NADPH oxidase activation.

Background: Protein glycation is closely linked to endothelial-cell dysfunction and vascular complications in diabetes. Glycated albumin is reported to induce cellular signaling similar to advanced glycation endoproducts (AGEs), however, cellular signaling remains obscure.

Method: We stimulated human umbilical vein endothelial cells (HUVECs) by glycated human serum albumin (Glc-HSA), determined E-selectin expression by real-time PCR and immunometric methods, and estimated cellular signaling by using various signaling molecule inhibitors and confocal microscopy.