Sleep deprivation affects inflammatory marker expression in adipose tissue

<p>Abstract</p> <p/> <p>Sleep deprivation has been shown to increase inflammatory markers in rat sera and peripheral blood mononuclear cells. Inflammation is a condition associated with pathologies such as obesity, cancer, and cardiovascular diseases. We investigated changes in the pro and anti-inflammatory cytokines and adipokines in different depots of white adipose tissue in rats. We also assessed lipid profiles and serum levels of corticosterone, leptin, and adiponectin after 96 hours of sleep deprivation.</p> <p>Methods</p> <p>The study consisted of two groups: a control (C) group and a paradoxical sleep deprivation by 96 h (PSD) group. Ten rats were randomly assigned to either the control group (C) or the PSD. Mesenteric (MEAT) and retroperitoneal (RPAT) adipose tissue, liver and serum were collected following completion of the PSD protocol. Levels of interleukin (IL)-6, interleukin (IL)-10 and tumour necrosis factor (TNF)-α were analysed in MEAT and RPAT, and leptin, adiponectin, glucose, corticosterone and lipid profile levels were analysed in serum.</p> <p>Results</p> <p>IL-6 levels were elevated in RPAT but remained unchanged in MEAT after PSD. IL-10 protein concentration was not altered in either depot, and TNF-α levels decreased in MEAT. Glucose, triglycerides (TG), VLDL and leptin decreased in serum after 96 hours of PSD; adiponectin was not altered and corticosterone was increased.</p> <p>Conclusion</p> <p>PSD decreased fat mass and may modulate the cytokine content in different depots of adipose tissue. The inflammatory response was diminished in both depots of adipose tissue, with increased IL-6 levels in RPAT and decreased TNF-α protein concentrations in MEAT and increased levels of corticosterone in serum.</p

EDS spectra of dead biomass of <i>R. mucilaginosa</i>.

<p>(A) before exposure to copper solution and (B) after exposure to the metal confirming the presence of copper.</p

First and second-order adsorption rate constants.

<p>First and second-order adsorption rate constants.</p

Transmission electron micrograph of <i>R. mucilaginosa</i> sections.

<p>(A) Control (without copper) and (B) Section of the yeast showing intracellular localization of copper NPs (arrow).</p

SEM-EDS analysis of the surface of dead biomass of <i>R. mucilaginosa</i>.

<p>(A) Before adsorption of copper ion and (B) after adsorption of copper ion.</p

Adsorption isotherm parameters for Cu (II) ions with live and dead biomass of <i>R. mucilaginosa</i>.

<p>Adsorption isotherm parameters for Cu (II) ions with live and dead biomass of <i>R. mucilaginosa</i>.</p

XRD analysis.

<p>Structural function S (Q) compared to the XRD patterns of the metallic copper and CuO.</p

Biosorption isotherm models and biosorption kinetics of <i>H. lixii</i>.

<p>Langmuir plots for live (A), dried (B) and dead (C) biomass. Pseudo second-order models for live (D), dried (E) and dead (F) biomass.</p

TEM micrographs of <i>H. lixii</i> sections.

<p>(A) Control (without copper), (B) Section of the fungus showing extracellular localization of copper nanoparticles and (C) Copper nanoparticles.</p