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首页> 外文期刊>The Journal of Nutritional Biochemistry >Acute and chronic saturated fatty acid treatment as a key instigator of the TLR-mediated inflammatory response in human adipose tissue, in vitro
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Acute and chronic saturated fatty acid treatment as a key instigator of the TLR-mediated inflammatory response in human adipose tissue, in vitro

机译：急性和慢性饱和脂肪酸治疗是体外TLR介导的人类脂肪组织炎症反应的关键因素

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A post-prandial increase in saturated fatty acids (SFAs) and glucose (Glc) activates an inflammatory response, which may be prolonged following restoration of physiological SFAs and Glc levels - a finding referred to as 'metabolic memory'. This study examined chronic and oscillating SFAs and Glc on the inflammatory signalling pathway in human adipose tissue (AT) and adipocytes (Ads) and determined whether Ads are subject to "metabolic memory." Abdominal (Abd) subcutaneous (Sc) explants and Ads were treated with chronic low glucose (L-Glc): 5.6 mM and high glucose (H-Glc): 17.5 mM, with low (0.2 mM) and high (2 mM) SFA for 43 h. Abd Sc explants and Ads were also exposed to the aforementioned treatment regimen for 12-h periods, with alternating rest periods of 12 h in L-Glc. Chronic treatment with L-Glc and high SFAs. H-Glc and high SFAs up-regulated key factors of the nuclear factor-kappa B (NF kappa B) pathway in Abd Sc AT and Ads (TLR4, NF kappa B; P<.05), whilst down-regulating MyD88. Oscillating Glc and SFA concentrations increased TLR4, NF kappa B. IKK beta (P<.05) in explants and Ads and up-regulated MyD88 expression (P<.05). Both tumor necrosis factor a and interleukin 6 (P<.05) secretion were markedly increased in chronically treated Abd Sc explants and Ads whilst, with oscillating treatments, a sustained inflammatory effect was noted in absence of treatment. Therefore, SFAs may act as key instigators of the inflammatory response in human AT via NF kappa B activation, which suggests that short-term exposure of cells to uncontrolled levels of SFAs and Glc leads to a longer-term inflammatory insult within the Ad, which may have important implications for patients with obesity and Type 2 diabetes
机译：餐后饱和脂肪酸（SFA）和葡萄糖（Glc）的增加会激活炎症反应，在恢复生理SFA和Glc水平后可能会延长炎症反应-这一发现称为“代谢记忆”。这项研究检查了人类脂肪组织（AT）和脂肪细胞（Ads）的炎症信号通路中的慢性SFA和振荡性SFA和Glc，并确定Ads是否受“代谢记忆”的影响。腹部（Abd）皮下（Sc）外植体和Ads用慢性低血糖（L-Glc）：5.6 mM和高血糖（H-Glc）：17.5 mM，低（0.2 mM）和高（2 mM）SFA处理持续43小时。 Abd Sc外植体和Ads也暴露于上述治疗方案12 h，在L-Glc中交替休息12 h。 L-Glc和高SFA的慢性治疗。 H-Glc和高SFA上调了Abd Sc AT和Ads中的核因子-κB（NF kappa B）通路的关键因子（TLR4，NFκB; P <.05），同时下调了MyD88。振荡的Glc和SFA浓度增加了外植体和Ads中的TLR4，NFκB.IKK beta（P <.05）和MyD88表达上调（P <.05）。在长期治疗的Abd Sc外植体和Ads中，肿瘤坏死因子a和白细胞介素6（P <.05）的分泌均显着增加，而在进行振荡治疗时，如果不进行治疗，则可观察到持续的炎症作用。因此，SFA可能是通过NFκB活化导致人类AT炎症反应的关键诱因，这表明短期将细胞暴露于不受控制的SFA和Glc水平会导致Ad内发生长期炎症。可能对肥胖和2型糖尿病患者有重要影响

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