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Serum selenoprotein P levels in patients with type 2 diabetes and prediabetes: implications for insulin resistance, inflammation, and atherosclerosis.

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OBJECTIVE The dysregulation of hepatokines may be associated with the pathogenesis of insulin resistance and type 2 diabetes. A recent study has suggested that selenoprotein P (SeP), a novel hepatokine, may play a role in the regulation of glucose metabolism and insulin sensitivity. We examined the

The Antagonistic Effect of Selenium on Cadmium-Induced Damage and mRNA Levels of Selenoprotein Genes and Inflammatory Factors in Chicken Kidney Tissue.

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Selenium (Se) is a necessary trace mineral in the diet of humans and animals. Cadmium (Cd) is a toxic heavy metal that can damage animal organs, especially the kidneys. Antagonistic interactions between Se and Cd have been reported in previous studies. However, little is known about the effects of

Polymorphisms in the selenoprotein S gene: lack of association with autoimmune inflammatory diseases.

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BACKGROUND Selenoprotein S (SelS) protects the functional integrity of the endoplasmic reticulum against the deleterious effects of metabolic stress. SEPS1/SelS polymorphisms have been involved in the increased release of pro-inflammatory cytokines interleukin (IL)-1beta, tumor necrosis factor

Selenoprotein S1: a novel inflammatory gene.

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Selenoprotein S1 (SEPS1), a novel gene involved in the stress response of endoplasmic reticulum and inflammation control. Recent results provide a direct mechanistic link between SEPS1 and the production of inflammatory cytokines, suggesting SEPS1 may play a major role in the mediation of

The role of selenoprotein W in inflammatory injury in chicken immune tissues and cultured splenic lymphocyte.

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Selenoprotein W (SelW) is mainly understood in terms of its antioxidant effects in the cellular defense system. Inflammation is an important indicator of animal tissue injury, and the inflammatory cells may trigger a sophisticated and well-orchestrated inflammatory cascade, resulting in exaggerated

A Reduction in Selenoprotein S Amplifies the Inflammatory Profile of Fast-Twitch Skeletal Muscle in the mdx Dystrophic Mouse.

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Excessive inflammation is a hallmark of muscle myopathies, including Duchenne muscular dystrophy (DMD). There is interest in characterising novel genes that regulate inflammation due to their potential to modify disease progression. Gene polymorphisms in Selenoprotein S (Seps1) are associated with

Impaired exercise performance is independent of inflammation and cellular stress following genetic reduction or deletion of Selenoprotein S.

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Selenoprotein S (Seps1) can be protective against oxidative, endoplasmic reticulum (ER) and inflammatory stress. Seps1 global knockout mice are less active, possess compromised fast muscle ex vivo strength and, depending on context, heightened inflammation. Oxidative, ER and inflammatory stress

The role of the selenoprotein S (SELS) gene -105G>A promoter polymorphism in inflammatory bowel disease and regulation of SELS gene expression in intestinal inflammation.

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Recently, a -105G>A promoter polymorphism coding for selenoprotein S (SELS) has been shown to increase proinflammatory cytokine expression. We, therefore, analyzed SELS expression and potential phenotypic consequences of the -105G>A polymorphism in patients with inflammatory bowel disease (IBD).

Activation of the selenoprotein SEPS1 gene expression by pro-inflammatory cytokines in HepG2 cells.

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SEPS1 (also called selenoprotein S, SelS) plays an important role in the production of inflammatory cytokines and its expression is activated by endoplasmic reticulum (ER) stress. In this report, we have identified two binding sites for the nuclear factor kappa B in the human SEPS1 promoter. SEPS1

Selenium Deficiency Affects the mRNA Expression of Inflammatory Factors and Selenoprotein Genes in the Kidneys of Broiler Chicks.

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The aim of this study was to investigate the influence of Se deficiency on the transcription of inflammatory factors and selenoprotein genes in the kidneys of broiler chicks. One hundred fifty 1-day-old broiler chicks were randomly assigned to two groups fed with either a low-Se diet (L group, 0.033

Possible correlation of selenoprotein W with inflammation factors in chicken skeletal muscles.

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The aim of the present study was to investigate the possible correlation of selenoprotein W (SelW) with inflammatory injury induced by dietary selenium (Se) deficiency in chicken. One-day-old male chickens were fed either a commercial diet or a Se-deficient diet for 55 days. Then, the expression

Selenium and selenoproteins in inflammatory bowel diseases and experimental colitis.

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Inadequate dietary intake of the essential trace element selenium (Se) is thought to be a risk factor for several chronic diseases associated with oxidative stress and inflammation. Biological actions of Se occur through low-molecular weight metabolites and through selenoproteins. Several key

Reducing selenoprotein P expression suppresses adipocyte differentiation as a result of increased preadipocyte inflammation.

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Oxidative stress and low-grade inflammation have been implicated in obesity and insulin resistance. As a selenium transporter, ubiquitously expressed selenoprotein P (SeP) is known to play a role in the regulation of antioxidant enzyme activity. However, SeP expression and regulation in adipose

Selenium Deficiency Influences the Expression of Selenoproteins and Inflammatory Cytokines in Chicken Aorta Vessels.

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Selenium deficiency is known to cause cardiovascular diseases. However, the role of Se deficiency in causing oxidative damage and inflammation injury to the aorta vessels of chickens is not well known. In the present study, 180 1-day-old chickens were randomly divided into two groups, a low-Se group

Selenomethionine Suppressed TLR4/NF-κB Pathway by Activating Selenoprotein S to Alleviate ESBL Escherichia coli-Induced Inflammation in Bovine Mammary Epithelial Cells and Macrophages

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Inflammation is the hallmark of extended-spectrum β-lactamase (ESBL)-producing Escherichia coli-induced bovine mastitis. Organic selenium can activate pivotal proteins in immune responses and regulate the immune system. The present study aimed to investigate whether selenomethionine (SeMet)

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