Serum adipocyte fatty acid-binding protein in the critically ill

Abstract

Sepsis due to unabated inflammation is common. Increased production of pro-inflammatory cytokines, free radicals, and eicosanoids has been detected in sepsis and other critical illnesses but could also be due to decreased synthesis and release of anti-inflammatory molecules. Increased serum adipose-fatty acid-binding protein (A-FABP) levels can cause insulin resistance and have been reported in the critically ill, serve as a marker of prognosis, and thus link metabolic homeostasis and inflammation. A-FABP can be linked to the expression of Toll-like receptors, macrophage activation, synthesis and release of pro-inflammatory cytokines interleukin-6 and tumor necrosis factor-alpha, activation of cyclooxygenase 2 (COX-2) expression, and eicosanoid synthesis, events that can cause insulin resistance and initiation and progression of inflammation and sepsis. Unsaturated fatty acids and their anti-inflammatory products, such as lipoxins, resolvins, and protectins, may suppress A-FABP expression, inhibit macrophage and COX-2 activation, and decrease production of pro-inflammatory cytokines and ultimately could lead to a decrease in insulin resistance and resolution of inflammation and recovery from sepsis. Serial measurement of these pro- and anti-inflammatory molecules and correlation of their levels to the progression to or recovery from (or both) sepsis and other inflammatory processes may form a new approach to predict prognosis in inflammatory conditions and eventually could lead to the development of new therapeutic strategies.

Serum Fatty Acid‐Binding Protein 4 is Increased in Patients with Psoriasis

“…The gene encoding this adipokine is located on chromosome 8q21. Elevated levels of FABP4 are closely linked with the development of obesity, IR, DM, hypertension, CAD and atherosclerosis [10, 14, 15]. Studies in humans have shown that a genetic variant at the FABP4 locus reduced the risk for atherosclerosis, diabetes and coronary heart disease [16, 17], and reduced FABP4 expression in adipose tissue was related to lower risk for CAD and DM [16].…”

“…Studies in humans have shown that a genetic variant at the FABP4 locus reduced the risk for atherosclerosis, diabetes and coronary heart disease [16, 17], and reduced FABP4 expression in adipose tissue was related to lower risk for CAD and DM [16]. Several studies have proved that increased circulating FABP4 levels are a promising biomarker predicting heart failure, stroke, and prognosis and mortality in patients with end-stage renal disease, CAD or other critical illnesses [6, 14, 15, 20, 21]. …”

Albumin infusion for the critically ill – is it beneficial and, if so, why and how?

“…Adipose-fatty acid binding protein (A-FABP), which induces insulin resistance and whose levels are increased in the critically ill [ 18 ], is a carrier of fatty acids and is expressed primarily in adipocytes and macrophages. A-FABP regulates systemic insulin sensitivity and lipid and glucose metabolism [ 19 ]. Mice deficient in A-FABP are resistant to the development of hyperinsulinemia, hyperglycemia and insulin resistance [ 18 ].…”

Cannabis Sativa Revisited—Crosstalk between microRNA Expression, Inflammation, Oxidative Stress, and Endocannabinoid Response System in Critically Ill Patients with Sepsis

“…A very important aspect is that the CD4+ T helper cells use the major histocompatibility complex class II (MHC II) for antigen recognition [24][25][26]. Following the biomacromolecular and cellular reactions, increased amounts of proinflammatory cytokines are released, such as tumor necrosis factor alpha (TNF-α), interleukin-1 (IL-1), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6) [27][28][29]. The released pro-inflammatory mediators enter a vicious circle, leading to the activation and proliferation of leucocytes, the overexpression of the endothelial adhesion molecules, the activation of the complement system, and to the overproduction of tissue factors and free radicals (FR) [30].…”