Regulation of lipoprotein lipase synthesis by recombinant tumor necrosis factor—The primary regulatory role of the hormone in 3T3-L1 adipocytes☆
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2017, Life SciencesCitation Excerpt :Several in vitro and in vivo studies have reported the involvement of TNF-α in lipolysis by decreasing LPL activities. The activity of LPL was decreased by TNF-α in 3T3-L1 cells [66]. Another study reported that the decrease in mRNA level of LPL is caused by TNF-α [67].
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2013, NutritionCitation Excerpt :RSV induced a significant reduction in three proinflammatory cytokines (TNF-α, MCP1, CRP). Taking into account that TNF-α activates lipolysis and inhibits LPL [43,44], the reduction in TNF-α concentration found in RSV-treated rats could be related to the changes induced by this polyphenol in triacylglycerol metabolism. For the analysis of gene and protein adipokine expressions in adipose tissue we chose the epididymal location because 1) it was the main adipose tissue reduced by resveratrol, 2) it has been reported that cytokine production is higher in internal depots than in subcutaneous fat pad [3,4] and 3) macrophage infiltration is higher in internal than in subcutaneous depots [45].
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2012, Clinica Chimica ActaCitation Excerpt :Chronic administration of these cytokines, either alone or in combination, is capable of reducing food intake and reproducing the different features of the cancer anorexia–cachexia syndrome [3,10–13]. Recent experimental studies indicate that tumor necrosis factor (TNF)-α can induce lipid depletion in White Adipose Tissue, either by stimulation of lipolysis [14] or through inhibition of Lipoprotein lipase (LPL), by suppressing transcription [15]. TNF-α has indeed been shown to selectively decrease LPL mRNA levels as well as activity in 3T3-L1 adipocytes [16], thus preventing adipocytes from extracting free fatty acids (FFA) from plasma lipoproteins for storage and resulting in a net flux of lipids into the circulation.
Adipokine gene transcription level in adipose tissue of runt piglets
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This work was supported in part by NIH Grant GM 32892, the North Carolina Board of Science and Technology, Biogen, Inc., and by grants from the Swedish Medical Research Council (B13X-727) and the Lions in Umea Research Fund (399/85).
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This work is submitted in partial fulfillment of the requirements for the Ph.D. degree from East Carolina University. Current address: Laboratory of Cellular Regulation, National Heart, Lung and Blood Institute, NIH, Bethesda, Md. 20205.