The Inflammatory Profile of Obesity and the Role on Pulmonary Bacterial and Viral Infections

Obesity is a globally increasing health problem, entailing diverse comorbidities such as infectious diseases. An obese weight status has marked effects on lung function that can be attributed to mechanical dysfunctions. Moreover, the alterations of adipocyte-derived signal mediators strongly influence the regulation of inflammation, resulting in chronic low-grade inflammation. Our review summarizes the known effects regarding pulmonary bacterial and viral infections. For this, we discuss model systems that allow mechanistic investigation of the interplay between obesity and lung infections. Overall, obesity gives rise to a higher susceptibility to infectious pathogens, but the pathogenetic process is not clearly defined. Whereas, viral infections often show a more severe course in obese patients, the same patients seem to have a survival benefit during bacterial infections. In particular, we summarize the main mechanical impairments in the pulmonary tract caused by obesity. Moreover, we outline the main secretory changes within the expanded adipose tissue mass, resulting in chronic low-grade inflammation. Finally, we connect these altered host factors to the influence of obesity on the development of lung infection by summarizing observations from clinical and experimental data.     

Oxidative Stress in Obesity: A Critical Component in Human Diseases

Obesity, a social problem worldwide, is characterized by an increase in body weight that results in excessive fat accumulation. Obesity is a major cause of morbidity and mortality and leads to several diseases, including metabolic syndrome, diabetes mellitus, cardiovascular, fatty liver diseases, and cancer. Growing evidence allows us to understand the critical role of adipose tissue in controlling the physic-pathological mechanisms of obesity and related comorbidities. Recently, adipose tissue, especially in the visceral compartment, has been considered not only as a simple energy depository tissue, but also as an active endocrine organ releasing a variety of biologically active molecules known as adipocytokines or adipokines. Based on the complex interplay between adipokines, obesity is also characterized by chronic low grade inflammation with permanently increased oxidative stress (OS). Over-expression of oxidative stress damages cellular structures together with under-production of anti-oxidant mechanisms, leading to the development of obesity-related complications. The aim of this review is to summarize what is known in the relationship between OS in obesity and obesity-related diseases.     

1-脱氧野尻霉素对肥胖小鼠脂代谢的影响及机理

探究1-脱氧野尻霉素（1-deoxynojirimycin,DNJ）对营养性肥胖的脂代谢调控作用及其途径,旨在为开发 DNJ降糖、降脂减肥产品提供依据。通过饲喂高脂饲料建立肥胖小鼠模型,之后喂食普通饲料40 d,同时实验组灌 胃不同剂量（8.0、4.0、2.0 mg/（kg·d）,以体质量计）DNJ,用酶联免疫吸附测定（enzyme linked immunosorbent assay,ELISA）法测定小鼠的血脂水平、脂肪细胞因子、脂肪酸合成及氧化过程中相关酶活力。结果显示,与阴 性对照组比较,在8.0 mg/（kg·d）剂量组中DNJ可使雌、雄鼠体质量分别下降9.06%、14.07%,肝脂含量分别下降 4.13%、27.82%,腹腔脂肪系数分别下降9.00%、34.30%,血清总胆固醇含量分别下降11.57%、35.13%,总甘油三 酯含量分别下降46.89%、30.65%,高密度脂蛋白含量分别增加28.86%、7.00%,游离脂肪酸含量分别下降10.60%、 10.20%,内脂素含量分别下降38.44%、26.76%,脂联素含量分别上升29.66%、26.96%,肝脏中乙酰辅酶A羧化酶 活力分别下降17.03%、15.52%,脂肪酸合成酶活力分别下降23.53%、21.13%,肉毒碱脂酰转移酶Ⅰ活力分别上升 20.38%、17.20%,酰基辅酶A氧化酶活力分别上升11.00%、16.29%。上述结果表明,肥胖小鼠在控制饮食的同时摄 入适量DNJ可以有效控制脂肪的合成、促进脂肪的氧化分解,达到调控血脂、减少脂肪积累、控制体质量的目的。 DNJ对雌、雄鼠脂代谢调控的作用途径不同,其对雄鼠的降脂效果更显著。     

1-脱氧野尻霉素对高脂饮食肥胖小鼠脂代谢的改善作用

探讨1-脱氧野尻霉素(DNJ)对高脂饮食肥胖小鼠脂代谢的影响及作用机理,为DNJ降脂机理研究提供理论依据。通过喂饲高脂饲料建立小鼠肥胖模型,在持续饲喂高脂饲料的同时灌胃不同剂量的DNJ,40 d后测定实验小鼠一般生理指标,血清及肝脏的相关指标。结果表明,与高脂对照组相比,灌胃8.0 mg/kg bw/d DNJ可显著降低高脂饮食肥胖小鼠的体重、腹腔脂肪系数及肝脂肪含量(P<0.05);显著降低血清中总胆固醇(TC)、甘油三脂(TG)、低密度脂蛋白胆固醇(LDL-C)、游离脂肪酸(FFA)、内脂素水平,显著增加高密度脂蛋白胆固醇(HDL-C)、脂联素(ADP)含量(P<0.05);8.0 mg/kg bw/d DNJ可显著降低肝脏组织中促进脂肪合成的相关酶脂肪合成酶(FAS)、乙酰辅酶A羧化酶(ACC),显著增加分解相关酶酰基辅酶A氧化酶(ACO)、肉毒碱脂酰转移酶Ⅰ(CPT-1)的酶活(P<0.05)。结论:DNJ可能通过控制脂肪因子分泌及脂代谢相关酶活性来抑制脂肪合成,促进脂肪分解,达到调控高脂饮食肥胖小鼠脂代谢的目的。     

黄芪多糖对胰岛素抵抗大鼠脂肪因子的影响

目的:探讨黄芪多糖(astragalus polysaccharide,APS)对2型糖尿病(2-DM)胰岛素抵抗(IR)大鼠血清肿瘤坏死因子(TNF-α)、瘦素(Leptin)和胰岛素敏感指标的影响。方法:将Wistar大鼠随机分为正常对照组、模型组、APS高、中、低剂量治疗组。用药12 w后,测定FBG、空腹胰岛素水平(FINS)、Leptin、TNF-α,计算胰岛素敏感指数(ISI)和抵抗指数(HOMA-IR)。结果:APS能提高模型大鼠ISI,降低HOMA-IR指数,降低Leptin和TNF-α水平。结论:APS对大鼠IR具有显著的改善作用,其机制可能与降低血浆Leptin、TNF-α水平有关。