1. Nutritional factors of inflammation induction or lipid mechanism of endotoxin transport
- Author
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G. G. Enuchidze, M. Y. Yakovlev, M. V. Meshkov, A. A. Melamud, M. M. Yakovleva, I. A. Anychovskaya, S. I. Lazareva, P. L. Okorokov, and I. M. Salachov
- Subjects
Starvation ,medicine.medical_specialty ,Lipopolysaccharide ,Physiology ,Arbitrary unit ,Inflammation ,Lipid metabolism ,Anorexia ,Biology ,Orlistat ,chemistry.chemical_compound ,Endocrinology ,Blood serum ,chemistry ,Physiology (medical) ,Internal medicine ,medicine ,medicine.symptom ,medicine.drug - Abstract
Integral parameters of bacterial lipopolysaccharide concentration and antiendotoxin immunity activity were determined in the blood serum of subjects with two extreme variants of eating disorders: obesity and anorexia nervosa (in its clinical model, long-term starvation). The results of the study showed that obese patients had initially higher endotoxin concentrations (2.41 ± 0.11 vs 1.13 ± 0.05 EU/mL in the control), which significantly decreased as a result taking a course of orlistat or after starvation (for no longer than 20 days) (to 1.34 ± 0.04 and 1.01 ± 0.09 EU/mL, respectively). The decrease in the endotoxin serum level was associated with an increase in the concentration of high-density lipoproteins (HDLs) and a decrease in the concentration of low-density lipoproteins (LDLs). This allowed us to assume that the complex of the latter with the endotoxin is the LDL fraction that may function as a depot of the hydrophobic form of the lipopolysaccharide molecule in the bloodstream. Long-term starvation (starting from day 20) led to the appearance of symptoms characteristic of septic states, which was preceded by a twofold increase in the concentration of the endotoxin and antibodies against the enterobacterial common antigen and subsequent increase in the level of anti-glycolipid antibodies (from 133.2 ± 2.6 to 355.6 ± 15.0 optical density arbitrary units) starting from day 25โ27 of starvation, which is characteristic for the initial phase of the systemic inflammatory response syndrome.
- Published
- 2012
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