Sentences with phrase «tissue necrosis factor»

In Lyme, white blood cells that attack germs produce inflammatory cytokines like interleukin - 6 and tissue necrosis factor alpha.

Not exact matches

Reactivation of HBV may occur with chemotherapy, organ and tissue transplantation, High dose corticosteroids, and biologicals targeting tumor necrosis factor - alpha (TNF - α), Anti-TNF medications are used in treating rheumatic diseases, such as rheumatoid arthritis, digestive conditions that include Crohn's and colitis, and dermatologic conditions, such as psoriasis.

Abbreviations: ASC, apoptosis - associated speck - like protein containing a caspase - recruitment domain; ATM, adipose - tissue - resident macrophage; BAT, brown adipose tissue; CCR2, CC chemokine receptor 2; CHOP, C / EBP (CCAAT / enhancer - binding protein)- homologous protein; DHA, docosahexaenoic acid; EPA, eicosapentaenoic acid; ER, endoplasmic reticulum; GPCR, G - protein - coupled receptor; HIF, hypoxia - inducible factor; IFNγ, interferon γ; IKK, inhibitor of nuclear factor κB kinase; IL, interleukin; IRS - 1, insulin receptor substrate - 1; JNK, c - Jun N - terminal kinase; LDL, low - density lipoprotein; Ldlr, LDL receptor; LXR, liver X receptor; MCP - 1, monocyte chemoattractant protein 1; miRNA, microRNA; mTOR, mammalian target of rapamycin; NAFLD, non-alcoholic fatty liver disease; NF - κB, nuclear factor κB; NLRP3, NLR (nucleotide - binding - domain - and leucine - rich - repeat - containing) family, pyrin - domain - containing 3; oxLDL, oxidized LDL; PKR, double - stranded RNA - dependent protein kinase; PPAR, peroxisome - proliferator - activated receptor; STAT6, signal transducer and activator of transcription 6; SVF, stromal vascular fraction; TLR, Toll - like receptor; TNFα, tumour necrosis factor α; UPR, unfolded protein response; WAT, white adipose tissue

Liposuction did not significantly alter the insulin sensitivity of muscle, liver, or adipose tissue (assessed by the stimulation of glucose disposal, the suppression of glucose production, and the suppression of lipolysis, respectively); did not significantly alter plasma concentrations of C - reactive protein, interleukin - 6, tumor necrosis factor alpha, and adiponectin; and did not significantly affect other risk factors for coronary heart disease (blood pressure and plasma glucose, insulin, and lipid concentrations) in either group.

One theory proposes that once the storage capacity of subcutaneous adipose tissue (SAT) depots is exceeded under conditions of energy excess, either as a result of impaired expandability and / or excessive hypertrophic growth, fat deposition within visceral depots and non-adipose tissues including the liver, skeletal muscle and pancreas can ensue.93 This can subsequently lead to the development of systemic IR and a series of associated cardiometabolic disorders including dyslipidaemia, dysglycaemia, hyperinsulinaemia and hypertension.3 Expression of pro-inflammatory mediators including interleukins 1 (IL - 1), 6 (IL - 6), tumour necrosis factor alpha (TNF - α) and resistin, are also increased which can further potentiate IR and promote atherosclerosis.

Instead, researchers measure a variety of inflammatory chemical markers in the blood or tissue, notably interleukin - 6, tumor necrosis factor (TNF), C - reactive protein, prostaglandins, and leukotrienes.

C3G significantly upregulated the glucose transporter 4 (Glut4) and downregulated RBP4 in the white adipose tissue, which is accompanied by downregulation of the inflammatory adipocytokines (monocyte chemoattractant protein - 1 and tumor necrosis factor - alpha) in the white adipose tissue of the C3G group.

White adipose tissue messenger RNA levels and serum concentrations of inflammatory cytokines (tumor necrosis factor - α, interleukin - 6, and monocyte chemoattractant protein - 1) were reduced by C3G, as did macrophage infiltration in adipose tissue.

For example, KBs were recently reported to act as neuroprotective agents by raising ATP levels and reducing the production of reactive oxygen species in neurological tissues, 80 together with increased mitochondrial biogenesis, which may help to enhance the regulation of synaptic function.80 Moreover, the increased synthesis of polyunsaturated fatty acids stimulated by a KD may have a role in the regulation of neuronal membrane excitability: it has been demonstrated, for example, that polyunsaturated fatty acids modulate the excitability of neurons by blocking voltage-gated sodium channels.81 Another possibility is that by reducing glucose metabolism, ketogenic diets may activate anticonvulsant mechanisms, as has been reported in a rat model.82 In addition, caloric restriction per se has been suggested to exert neuroprotective effects, including improved mitochondrial function, decreased oxidative stress and apoptosis, and inhibition of proinflammatory mediators, such as the cytokines tumour necrosis factor - α and interleukins.83 Although promising data have been collected (see below), at the present time the real clinical benefits of ketogenic diets in most neurological diseases remain largely speculative and uncertain, with the significant exception of its use in the treatment of convulsion diseases.

- steroid dehydrogenase gene expression in canine adipose tissue and adipocytes: stimulation by lipopolysaccharide and tumor necrosis factor?.