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Model for cachexia in chronic disease: secretory products of endotoxin-stimulated macrophages induce a catabolic state in 3T3-L1 adipocytes.

作者信息

Pekala P H, Price S R, Horn C A, Hom B E, Moss J, Cerami A

出版信息

Trans Assoc Am Physicians. 1984;97:251-9.

PMID:6100150
Abstract
摘要

相似文献

1
Model for cachexia in chronic disease: secretory products of endotoxin-stimulated macrophages induce a catabolic state in 3T3-L1 adipocytes.慢性病恶病质模型：内毒素刺激的巨噬细胞分泌产物诱导3T3-L1脂肪细胞出现分解代谢状态。
Trans Assoc Am Physicians. 1984;97:251-9.
2
Fat loss in cachexia--is there a role for adipocyte lipolysis?恶病质中的脂肪减少——脂肪细胞脂解作用是否起作用？
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3
Lipolysis is stimulated by PEGylated conjugated linoleic acid through the cyclic adenosine monophosphate-independent signaling pathway in 3T3-L1 cells: activation of MEK/ERK MAPK signaling pathway and hyper-secretion of adipo-cytokines.聚乙二醇化共轭亚油酸通过3T3-L1细胞中不依赖环磷酸腺苷的信号通路刺激脂肪分解：激活MEK/ERK MAPK信号通路并导致脂肪细胞因子过度分泌。
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4
Cyclic AMP-dependent protein kinase activity and lipolysis in adipose tissue. Effect of fasting, oligomycin and iodoacetamide.环磷酸腺苷依赖性蛋白激酶活性与脂肪组织中的脂肪分解。禁食、寡霉素和碘乙酰胺的影响。
Rev Esp Fisiol. 1981 Dec;37(4):455-62.
5
Relationship among isoproterenol, cyclic AMP, cyclic AMP-dependent protein kinase and lipolysis in perfused fat cells.异丙肾上腺素、环磷酸腺苷、环磷酸腺苷依赖性蛋白激酶与灌注脂肪细胞中脂肪分解之间的关系。
J Pharmacol Exp Ther. 1981 Jul;218(1):128-33.
6
Inhibition of cyclic AMP accumulation in hamster adipocytes with phosphatidic acid: differences and similarities with alpha adrenergic effects.磷脂酸对仓鼠脂肪细胞中环磷酸腺苷积累的抑制作用：与α肾上腺素能效应的异同
J Cyclic Nucleotide Res. 1980;6(6):437-49.
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Regulation of adipose tissue metabolism in cancer cachexia.癌症恶病质中脂肪组织代谢的调节
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Effect of eicosapentaenoic acid (EPA) on expression of a lipid mobilizing factor in adipose tissue in cancer cachexia.二十碳五烯酸（EPA）对癌症恶病质中脂肪组织脂质动员因子表达的影响。
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Active spice-derived components can inhibit inflammatory responses of adipose tissue in obesity by suppressing inflammatory actions of macrophages and release of monocyte chemoattractant protein-1 from adipocytes.活性香料衍生成分可通过抑制巨噬细胞的炎症作用以及脂肪细胞中单核细胞趋化蛋白-1的释放，来抑制肥胖症中脂肪组织的炎症反应。
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Regulation of leptin release by insulin, glucocorticoids, G(i)-coupled receptor agonists, and pertussis toxin in adipocytes and adipose tissue explants from obese humans in primary culture.胰岛素、糖皮质激素、G(i) 偶联受体激动剂及百日咳毒素对原代培养的肥胖人类脂肪细胞和脂肪组织外植体中瘦素释放的调节作用。
Metabolism. 2003 Jan;52(1):60-6. doi: 10.1053/meta.2003.50005.

引用本文的文献

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Adipose tissue macrophages as potential targets for obesity and metabolic diseases.脂肪组织巨噬细胞作为肥胖和代谢性疾病的潜在靶点。
Front Immunol. 2023 Apr 19;14:1153915. doi: 10.3389/fimmu.2023.1153915. eCollection 2023.
2
A decade of progress in adipose tissue macrophage biology.脂肪组织巨噬细胞生物学十年进展
Immunol Rev. 2014 Nov;262(1):134-52. doi: 10.1111/imr.12216.
3
Cachexia in malaria and heart failure: therapeutic considerations in clinical practice.疟疾和心力衰竭中的恶病质：临床实践中的治疗考量
Postgrad Med J. 2004 Nov;80(949):642-9. doi: 10.1136/pgmj.2004.020891.
4
Cytokines and proteoglycans.细胞因子和蛋白聚糖。
Experientia. 1993 May 15;49(5):456-69. doi: 10.1007/BF01923589.
5
The expression of tumor necrosis factor in human adipose tissue. Regulation by obesity, weight loss, and relationship to lipoprotein lipase.肿瘤坏死因子在人体脂肪组织中的表达。受肥胖、体重减轻的调节及其与脂蛋白脂肪酶的关系。
J Clin Invest. 1995 May;95(5):2111-9. doi: 10.1172/JCI117899.
6
Perturbations of triglycerides but not of cholesterol metabolism are prevented by anti-tumour necrosis factor treatment in rats bearing an ascites hepatoma (Yoshida AH-130).在患有腹水型肝癌（吉田AH - 130）的大鼠中，抗肿瘤坏死因子治疗可预防甘油三酯的紊乱，但不能预防胆固醇代谢的紊乱。
Br J Cancer. 1995 Nov;72(5):1138-43. doi: 10.1038/bjc.1995.477.
7
Tumor necrosis factor-alpha stimulates hepatic lipogenesis in the rat in vivo.肿瘤坏死因子-α在体内刺激大鼠肝脏脂肪生成。
J Clin Invest. 1987 Jul;80(1):184-90. doi: 10.1172/JCI113046.
8
Tumor necrosis factor can induce fever in rats without activating protein breakdown in muscle or lipolysis in adipose tissue.肿瘤坏死因子可在不激活肌肉中蛋白质分解或脂肪组织中脂肪分解的情况下诱导大鼠发热。
J Clin Invest. 1988 May;81(5):1384-9. doi: 10.1172/JCI113467.
9
Cachectin/tumor necrosis factor exerts endocrine, paracrine, and autocrine control of inflammatory responses.恶病质素/肿瘤坏死因子对炎症反应发挥内分泌、旁分泌和自分泌调节作用。
J Cell Biol. 1988 Oct;107(4):1269-77. doi: 10.1083/jcb.107.4.1269.