Endotoxin stimulates lipolysis in bovine adipocytes

As cows progress from pregnancy to lactation, the adipose tissues (AT) undergo adaptations characterized by the mobilization of free fatty acids (FFA) through lipolysis to address energy deficiencies. Typically, in clinically healthy cows, the intensity of lipolysis decreases during lactation. However, when the release of FFA surpasses tissue requirements, it leads to the accumulation of lipid-derived products, heightening the susceptibility of cows to metabolic and infectious diseases. A second factor correlated to disease incidence in dairy cows is the presence of bacterial endotoxins in blood. The last is implicated in AT lipolysis and dysfunction in mammals. However, the mechanisms by which endotoxin activates lipolysis and affects the formation of lipid derived products in bovine adipocyte remains unknown. We hypothesize that endotoxin triggers AT dysfunction by increasing the synthesis and release of lipid-derived products with proinflammatory potential. Preadipocytes were obtained from subcutaneous AT of multiparous Holstein cows (n=9). Adipogenesis was induced for 7 d and cells were incubated with endotoxin [lipopolysaccharide 1µg/mL (LPS)] for up to 7 h. Beta-adrenergic receptor agonist isoproterenol (ISO; 1 µM) was used as an activator of canonical lipolysis. The antilipolytic effect of insulin was evaluated alone or in combination with LPS. Lipolysis was evaluated by the release of glycerol in the media. RNA from adipocytes was sequenced in Illumina NextSeqData, and Differential Expressed Genes (DEG) identified. Enrichment and network analyses were performed in Ingenuity Pathways (IPA). Our findings provide evidence supporting the higher abundance of lipid-derived products with proinflammatory activity and dysfunction related to inflammatory activation. Overall design: To investigate the proinflammatory effect of endotoxins in bovine adipocytes and its role on the formation of lipid-derived products