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Inflammation and metabolic syndrome

Inflammation and metabolic syndrome

Mtabolic Smith, G. It is an Infkammation protein which increases Inflammation and metabolic syndrome macrophages and T cells in response to inflammation following IL-6 secretion. Article ADS CAS PubMed Google Scholar Aguirre, V. Cell 21— Cellular Immunosenescence. Inflammation and insulin resistance.

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INFLAMMATION Explained - Metabolic Health with Dr. Lauren Kelley-Chew

Inflammation and metabolic syndrome -

Such dysmetabolism results in chronic low-grade inflammation, an important hallmark of metabolic disorder. Many key players resulting in metabolic inflammation have been identified suggesting the need for nutritional intervention.

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The displayed data aggregates results from Frontiers and PubMed Central®. Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance. Cinti, S. Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans.

Lipid Res. Arkan, M. IKK-β links inflammation to obesity-induced insulin resistance. Nature Med. Baumgartl, J. Myeloid lineage cell-restricted insulin resistance protects apolipoproteinE-deficient mice against atherosclerosis. Cell Metab. Han, S. Macrophage insulin receptor deficiency increases ER stress-induced apoptosis and necrotic core formation in advanced atherosclerotic lesions.

Yu, C. Mechanism by which fatty acids inhibit insulin activation of insulin receptor substrate-1 IRS-1 -associated phosphatidylinositol 3-kinase activity in muscle. Chawla, A.

Nuclear receptors and lipid physiology: opening the X-files. Glass, C. Combinatorial roles of nuclear receptors in inflammation and immunity. Nature Rev. Article CAS Google Scholar. Lee, C. Minireview: lipid metabolism, metabolic diseases, and peroxisome proliferator-activated receptors.

Endocrinology , — Joseph, S. Reciprocal regulation of inflammation and lipid metabolism by liver X receptors. Castrillo, A. Crosstalk between LXR and Toll-like receptor signaling mediates bacterial and viral antagonism of cholesterol metabolism.

Cell 12 , — Lin, Y. The lipopolysaccharide-activated Toll-like receptor TLR -4 induces synthesis of the closely related receptor TLR-2 in adipocytes. Bookout, A. Anatomical profiling of nuclear receptor expression reveals a hierarchical transcriptional network. Cell , — Ogawa, S.

Molecular determinants of crosstalk between nuclear receptors and Toll-like receptors. Makowski, L. Lack of macrophage fatty-acid-binding protein aP2 protects mice deficient in apolipoprotein E against atherosclerosis.

Rosen, E. PPARγ: a nuclear regulator of metabolism, differentiation, and cell growth. Uncoupling of obesity from insulin resistance through a targeted mutation in aP2, the adipocyte fatty acid binding protein.

Maeda, K. Tuncman, G. A genetic variant at the fatty acid-binding protein aP2 locus reduces the risk for hypertriglyceridemia, type 2 diabetes, and cardiovascular disease. Natl Acad. USA , — Article ADS CAS PubMed PubMed Central Google Scholar. Shum, B. The adipocyte fatty acid-binding protein aP2 is required in allergic airway inflammation.

Fatty acid binding proteins — the evolutionary crossroads of inflammatory and metabolic responses. Taniguchi, C. Critical nodes in signalling pathways: insights into insulin action.

Cell Biol. White, M. IRS proteins and the common path to diabetes. IRSmediated inhibition of insulin receptor tyrosine kinase activity in TNF-α- and obesity-induced insulin resistance.

Aguirre, V. The c-Jun NH2-terminal kinase promotes insulin resistance during association with insulin receptor substrate-1 and phosphorylation of Ser Paz, K. Emanuelli, B. SOCS-3 inhibits insulin signaling and is up-regulated in response to tumor necrosis factor-α in the adipose tissue of obese mice.

Rui, L. SOCS-1 and SOCS-3 block insulin signaling by ubiquitin-mediated degradation of IRS1 and IRS2. Howard, J. Enhanced leptin sensitivity and attenuation of diet-induced obesity in mice with haploinsufficiency of Socs3.

Gao, Z. Serine phosphorylation of insulin receptor substrate 1 by inhibitor kappa B kinase complex. Griffin, M. Free fatty acid-induced insulin resistance is associated with activation of protein kinase C theta and alterations in the insulin signaling cascade.

Diabetes 48 , — Zick, Y. STKE pe4 Baud, V. Signal transduction by tumor necrosis factor and its relatives. Trends Cell Biol. Hirosumi, J. A central role for JNK in obesity and insulin resistance.

Prada, P. Western diet modulates insulin signaling, c-Jun N-terminal kinase activity, and insulin receptor substrate-1 ser phosphorylation in a tissue-specific fashion. Ozcan, U. Endoplasmic reticulum stress links obesity, insulin action, and type 2 diabetes.

Article ADS PubMed CAS Google Scholar. Functional in vivo interactions between JNK1 and JNK2 isoforms in obesity and insulin resistance. Ricci, R. Requirement of JNK2 for scavenger receptor A-mediated foam cell formation in atherogenesis.

Kaneto, H. Possible novel therapy for diabetes with cell-permeable JNK-inhibitory peptide. Liu, G. JNK: bridging the insulin signaling and inflammatory pathway. Drugs 6 , — Yuan, M.

Reversal of obesity- and diet-induced insulin resistance with salicylates or targeted distruption of Ikkβ. Hundal, R. Mechanism by which high-dose aspirin improves glucose metabolism in type 2 diabetes. Cai, D. Local and systemic insulin resistance resulting from hepatic activation of IKK-β and NF-κB.

Kim, J. PKC-theta knockout mice are protected from fat-induced insulin resistance. Boden, G. Free fatty acids produce insulin resistance and activate the proinflammatory nuclear factor-kappaB pathway in rat liver.

Diabetes 54 , — Liu, J. NF-κB is required for UV-induced JNK activation via induction of PKCδ. Cell 21 , — Marciniak, S. Endoplasmic reticulum stress signaling in disease. Schroder, M. The mammalian unfolded protein response. Article PubMed CAS Google Scholar. Harding, H.

Perk is essential for translational regulation and cell survival during the unfolded protein response. Cell 5 , — Protein translation and folding are coupled by an endoplasmic-reticulum-resident kinase.

Urano, F. Coupling of stress in the ER to activation of JNK protein kinases by transmembrane protein kinase IRE1. Deng, J. Translational repression mediates activation of nuclear factor κ B by phosphorylated translation initiation factor 2. Hu, P. Autocrine tumor necrosis factor α links endoplasmic reticulum stress to the membrane death receptor pathway through IRE1α-mediated NF-κB activation and down-regulation of TRAF2 expression.

Ozawa, K. The endoplasmic reticulum chaperone improves insulin resistance in type 2 diabetes. Nakatani, Y. Involvement of endoplasmic reticulum stress in insulin resistance and diabetes.

Chemical chaperones reduce ER stress and restore glucose homeostasis in a mouse model of type 2 diabetes. Article ADS PubMed PubMed Central CAS Google Scholar. Zhang, K. Endoplasmic reticulum stress activates cleavage of CREBH to induce a systemic inflammatory response.

Cullinan, S. Xue, X. Tumor necrosis factor α TNFα induces the unfolded protein response UPR in a reactive oxygen species ROS -dependent fashion, and the UPR counteracts ROS accumulation by TNFα.

Alternatively, resistance to the anti-inflammatory actions of insulin would result in enhanced circulating levels of proinflammatory cytokines resulting in persistent low-grade inflammation. The role of adipose tissue as an endocrine organ capable of secreting a number of adipose tissue-specific or enriched hormones, known as adipokines, is gaining appreciation.

Although the precise role of adipokines in the metabolic syndrome is still debated, an imbalance between increased inflammatory stimuli and decreased anti-inflammatory mechanisms may be an intriguing working hypothesis.

The proinflammatory state that accompanies the metabolic syndrome associates with both insulin resistance and endothelial dysfunction, providing a connection between inflammation and metabolic processes which is highly deleterious for vascular functions.

Author Inflammaation Departments of Syndrone Nutrition, Syndroe Medicine, and the Center for Human Nutrition, Synddome of Inflammation and metabolic syndrome Southwestern Medical Center, Syndtome. In this syndromw of THE Inflammation and metabolic syndrome, Sesso and Inflammation and metabolic syndrome Heart health research report a positive relationship Increase calorie burn naturally increased serum levels of C-reactive syndrlme and the risk for development of incident hypertension in participants of the Women's Health Study. A total of 20 women were followed up prospectively for a median of 7. C-reactive protein levels in the upper ranges of the normal distribution high-normal levels of C-reactive protein are widely believed to reflect a state of low-grade chronic inflammation; therefore, the association between higher C-reactive protein levels and new-onset hypertension led Sesso et al 1 to suggest that hypertension may be an inflammatory disease. Grundy SM. Inflammation, Hypertension, and the Metabolic Syndrome. Artificial Intelligence Resource Center. Inflammation and metabolic syndrome

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5 thoughts on “Inflammation and metabolic syndrome

  1. Ich tue Abbitte, dass sich eingemischt hat... Ich finde mich dieser Frage zurecht. Geben Sie wir werden besprechen.

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