Lipid oxidation dysregulation: an emerging player in the pathophysiology of sepsis

Abstract

Sepsis is a life-threatening organ dysfunction caused by abnormal host response to infection. Millions of people are affected annually worldwide. Derangement of the inflammatory response is crucial in sepsis pathogenesis. However, metabolic, coagulation, and thermoregulatory alterations also occur in patients with sepsis. Fatty acid mobilization and oxidation changes may assume the role of a protagonist in sepsis pathogenesis. Lipid oxidation and free fatty acids (FFAs) are potentially valuable markers for sepsis diagnosis and prognosis. Herein, we discuss inflammatory and metabolic dysfunction during sepsis, focusing on fatty acid oxidation (FAO) alterations in the liver and muscle (skeletal and cardiac) and their implications in sepsis development.

Impact of critical illness on cholesterol and fatty acids: insights into pathophysiology and therapeutic targets

“…2 ) [ 62 ]. FFAs are first dissociated from albumin or liberated from lipoproteins by lipoprotein lipase, and afterwards taken up by a complex array of proteins, among which the receptor cluster of differentiation 36 (CD36) is one of the most extensively researched [ 63 ]. The observed hypertriglyceridemia during critical illness may indirectly indicate decreased cellular uptake, but post-mortem biopsies from adipose tissue indicated increased uptake of FFAs [ 16 , 17 , 64 ].…”