Over-expression of TLR4-CD14,pro-inflammatory cytokines,metabolic markers and NEFAs in obese non-diabetic Mexicans

Introduction: obesity is the world's most important public health problem. adipose tissue contributes significantly to increase pro-inflammatory mediators whose cascade begins with the union of tlr4 to its microbial ligands (tlr: toll like receptors). it has been reported recently that nefas (non-esterified fatty acids) bind to this receptor as agonists. the purpose of our study was to determine the levels of expression of tlr4-cd14,the pro-inflammatory cytokines,the metabolic markers and the nefas in a group of adult,non-diabetic obese mexicans. method: a group of 210 adult middle-class mexican non-diabetic obese patients was evaluated: 105 normal weight individuals,and 105 non-diabetic obese. on both groups,the following was tested in each patient: tlr4-cd14 receptors on monocytes in peripheral blood,inflammatory profile,homa-ir (homeostasis model assessment-insulin resistance),nefas and each individual's anthropometric profile. results: obesity is strongly associated with the expression of tlr4 (77%,mfi (mean fluorescence index) 7.70) and cd14 (86% mfi 1.61) with 66% double positives (p = 0.000). these figures contrast with those for the normal weight individuals that constituted the control group: tlr4 (70% mfi 6.41) and cd14 (84% mfi 1.25) with 59% double positives. as for cytokine concentration,non- diabetic obese individuals vs the normal weight/thin,the numbers were: il-1β = 2.0 vs 2.5 pg/ml (p=ns),il-6=36 vs 28 pg/ml (p = 0.030),il-8 = 27 vs 27 pg/ml (p=ns),il-10=8.4 vs 6.8 pg/ml (p = ns),tnf-α =31 vs 15 pg/ml (p = 0.000) respectively. insulin levels were 12.1 vs 19.7 mcu/ml (p = 0.000) and the nefas were much higher in the obese vs normal weight/thin individuals (p = 0.000). conclusion: adipose tissue used to be thought of as mere storage of fats and energy,but it has been revealed to be an important neuro-immune-endocrine organ. immune cells,stimulated by nefas,produce pro-inflammatory cytokines,which have a direct effect on oxidating radicals that directly target the release of noradrenalin. this in turn,reactivates the vicious cycle of low-grade chronic inflammation,as is now described in obesity. © 2014 de loera-rodriguez et al.