Oxidative stress, inflammation, and glycometabolism disorder-induced erythrocyte hemolysis in selenium-deficient exudative diathesis broilers.

Selenium (Se) deficiency causes injury of diversified tissues and cells, including livers, hearts, skeletal muscles, and erythrocytes. The aim of the present study is to explore the molecular mechanism of erythrocyte hemolysis due to Se deficiency in broilers. One hundred and eighty broilers (male/female, 1 day old) were randomly divided into two groups and fed with either a normal Se content diet (C group, 0.2 mg Se/kg) or a Se-deficient diet (ED group, 0.008 mg Se/kg) for 45 days. During the trial period of 15-30 days, biological properties such as osmotic fragility, fluidity, phospholipid components of cell membrane, adenosine triphosphatase activities, and antioxidant function of erythrocytes in broilers were examined. Moreover, the messenger RNA (mRNA) expressions of genes associated with inflammation, glycometabolism, and avian uncoupling protein (avUCP) were detected. We found that compared with the C group, hemolysis rate, degree of polarization, and microviscosity of erythrocytes were increased in broilers of the ED group. The composition of erythrocyte membrane lipids was changed. Meanwhile, the antioxidant function of erythrocytes was weakened and mRNA levels of inflammatory genes were stimulated by Se deficiency (p < 0.05). In addition, mRNA expressions of rate-limiting enzymes in glycometabolism were effected and avUCP mRNA level was downregulated (p < 0.05) in the ED group. It has been concluded from the results that oxidative stress, inflammatory response, and glycometabolism disorder lead to erythrocyte hemolysis by changing the structure and function of erythrocyte membrane in ED broilers suffered from Se deficiency.

H2S promotes a glycometabolism disorder by disturbing the Th1/Th2 balance during LPS-induced inflammation in the skeletal muscles of chickens.

Hydrogen sulfide (H2S) is a common environmental pollutant. In humans, H2S enters the body and is transported to different tissues and organs, inducing various types of damage such as chronic inflammatory reactions. Glucose metabolism disorders have been shown to be closely associated with chronic inflammation. The goal of the present study was to investigate the effects and mechanisms of H2S on glycometabolism disorders and chronic inflammatory responses. A chronic inflammation model in the skeletal muscles of chickens was induced using lipopolysaccharide (LPS), after which the animals were exposed to exogenous H2S. Subsequently, the glucose metabolism and the pathways associated with chronic inflammation were analyzed. The pathological analysis showed that significant inflammatory injury to skeletal muscles occurred after animals exposed to H2S. The Th1/Th2 ratio imbalance was exacerbated after exposure to H2S with IFNγ downregulated and IL-1, IL-4, and IL-6 upregulated. In addition, the level of IκBα was suppressed and induced the expression of NF-κB, significantly activating the inflammatory pathway, while the expression of heat shock proteins was elevated. In addition, glucose metabolism factors were analyzed. IRS1 phosphorylation was inhibited in animals exposed to H2S, and the expression of insulin-like growth factor (IGF) signaling pathway-related factors was upregulated to promote insulin resistance, causing glucose metabolism disorders. The results of this study revealed that H2S can trigger changes in the ratio of Th1/Th2 to produce more proinflammatory cytokines that disturb the insulin signaling pathway, causing glycometabolism disorders during the inflammatory response in the skeletal muscles of chickens.

Comparison of different substitution fluid for hemofiltration in patients with dysfunction of glycometabolism and MODS caused by trauma / 中华急诊医学杂志

Objective To find a better composition substitution fluid for continuous venovenous hemofiltration (CWH) comparing with the Port's composition substitution fluid,and to evaluate its efficiency and prognosis on patients with dysfunction of glycometabolism and multiple organ dysfunction syndrome (MODS) caused by trauma. Method Totol of 134 patients in the Firist Affiliated Hospotal of the Fourth Miliatary Medicial University,with glycometabolism dysfunction and MODS caused by trauma between Janurary 2001 and December 2006 were treated with CVVH.They were divided into two groups:the Port's composition substitution fluid which glucose concentration was 59.1 mmoL/L (group A,59 cases) and the new substitution fluid which glucose concentration is 11.8 mmol/L (group B,75 cases).The changes of electrolytes,arterial blood gas analysis,blood glucose and osmolarity during CVVH were observed.Results The mortality in group A was significantly higher than that in group B (64.4 % vs 40.0 %,P = 0.005).Before treated with CVVH,there was no significant differences of APACHEⅡscores between group A and group B.Either in the survival patients or in non-survivors,the APACHEⅡscores in group B were significantly higher than that in group A (P