Effect of supramaximal exercise training on metabolic outcomes in obese adults

The purpose of this study was to evaluate the effects of 6 weeks of supramaximal exercise training (SET) on performance variables and metabolic changes in sedentary obese adults.

Twenty-four obese adults were randomly allocated into a non-trained (NT) [n = 12; body mass index (BMI) = 33(3)] and SET group [n = 12; BMI = (33(2)]. After baseline metabolic and fitness measurements, the participants completed a 6-week SET intervention. Metabolic, anthropometric, and fitness assessments were repeated post-intervention.

For SET, fasting glucose (4.64(0.15) vs. 4.32(0.22) mmol · l^–1; P < 0.01), insulin (23.2(4.6) vs. 13.8(3.3) µmol · ml^–1; P < 0.01), homoeostasis model assessment-insulin resistance index (4.78(1.2) vs. 2.65(1.5); P < 0.01) and systolic blood pressure (127(3) vs. 120(3) mmHg; P < 0.01) were significantly lower 24-h post-intervention than at baseline and for the NT group, and these changes remained significant at 72-h and 2-weeks post-intervention (P < 0.01, respectively). Interestingly, nonesterified fatty acids (0.62(0.09) vs. 0.71(0.11) mmol · l^–1; P < 0.01) and resting fat oxidation rate (57(11) vs. 63(4)%; P < 0.01) increased significantly from baseline 24-h post-intervention in the SET group and from baseline at 72-h (P < 0.01, respectively) and 2-weeks post-intervention (P < 0.01, respectively). Six weeks of SET improved a number of metabolic and vascular risk factors in obese, sedentary adults, highlighting the potential of SET to provide an alternative exercise model for the improvement of metabolic health in this population.     

太极拳锻炼对肥胖老年人肠道益生菌和血脂代谢影响的相关性研究

为探讨太极拳练习对肥胖老年人肠道益生菌和血脂影响的相关性,本研究对为期一年太极拳练习的肥胖老年人肠道益生菌中的肠嗜酸杆菌、乳酸杆菌和双歧杆菌和血清甘油三脂(TG)、总胆固醇(TC)、低密度脂蛋白(LDL-C)和高密度脂蛋白(HDL-C)进行定期检测。结果表明:与3个月时相比,6个月、9个月和12个月时的肠嗜酸杆菌、乳酸杆菌和双歧杆菌数量均明显增加,血清TC、TG和LDL-C浓度明显降低,HDL-C浓度明显升高,且均呈现明显的练习时间依赖性,即太极拳练习时间越长,肠道益生菌和血脂改善越明显。肠道益生菌可以通过多种途径明显加强胆固醇的转化利用,改善血脂代谢,提示肠道益生菌数量增加可能是太极拳练习改善肥胖老年人脂代谢的生物学机制之一。     

Lipoproteins and cholesterol homeostasis in paediatric nephrotic syndrome patients

IntroductionThe aim of this study was to investigate lipoprotein particle distributions and the likelihood of achieving cholesterol homeostasis in the remission phase of nephrotic syndrome (NS) in paediatric patients. We hypothesized that lipoprotein particle distributions moved toward less atherogenic profile and that cholesterol homeostasis was achieved.Materials and methodsThirty-three children, 2 to 9 years old with NS were recruited. Blood sampling took place both in the acute phase and during remission. Serum low-density lipoprotein particles (LDL) and high-density lipoprotein particles (HDL) were separated using non-denaturing polyacrylamide gradient gel (3-31%) electrophoresis. Serum non-cholesterols sterols (NCSs), desmosterol, lathosterol, 7-dehydrocholesterol (7-DHC), campesterol and β-sitosterol were measured by high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS).ResultsAll patients had desirable serum HDL cholesterol concentrations during remission. The dominant lipoprotein diameters and LDL subclass distribution did not change significantly during follow-up. In contrast, HDL lipoprotein particle distribution shifted towards larger particles. The absolute concentration of desmosterol was significantly lower during remission (P = 0.023). β-sitosterol concentration markedly increased during remission (P = 0.005). Desmosterol/β-sitosterol (P < 0.001) and 7-DHC/β-sitosterol (P = 0.005) ratios significantly declined during disease remission.ConclusionsFavourable changes in the serum lipid profiles, HDL particle subclass distribution and cholesterol metabolism in paediatric patients with NS during remission took place. For the first time, we found that cholesterol homeostasis changed in favour of increased cholesterol absorption during disease remission. Nevertheless, complete cholesterol homeostasis was not achieved during disease remission.     

Erythrocytic adenosine deaminase in post myocardial infarction angina patients

A comparative study on the levels of erythrocyte adenosine deaminase and lipid peroxidation has been undertaken in post myocardial infarction angina patients along with age and sex matched healthy individuals serving as control. Present findings show that levels of adenosine deaminase is highly elevated in post myocardial infarction angina patients compared to healthy persons. Malondialdehyde levels are also significantly increased in post myocardial infarction angina patients. The study shows that adenosine deaminase has an important implication in ischemic myocardial syndrome.     

刺五加皂甙对运动大鼠脂代谢影响的研究

本实验以SD大鼠为研究对象,给大鼠补充大剂量的刺五加皂甙（500mg／kg／d）,观察有训练大鼠在一次性消耗糖原游泳运动前后的血FFA水平、血TG值、血LPL活性的变化。结论：刺五加皂甙对运动大鼠影响的总趋势是,升高大鼠运动后血FFA水平。并减缓大鼠运动后血FFA的下降,使运动后即刻血LPL活性提高,降低了运动后即刻血TG浓度,降低了静息状态的TG值;同时刺五加皂甙具有一定的减控体重、降血脂和抗冠心病的功效。     

Plant latent defense response to microbial non-pathogenic factors antagonizes compatibility

Unlike microbe-associated molecular patterns (MAMPs) that are readily targeted by host immunity, microbial non-pathogenic factors (NPFs) appear negligible as they do not elicit defense. Little is known about whether and how NPFs may be monitored by hosts to control compatibility. Herein, a forward genetic screening isolated an Arabidopsis mutant with a loss of plant-rhizobacteria mutualism, leading to the disclosure of a plant latent defense response (LDR) to NPFs. The activation of LDR in the mutant, named rol1 for regulator of LDR 1, is triggered by several non-pathogenic volatile organic compounds and antagonizes plant compatibility with the beneficial bacterium Bacillus amyloliquefaciens GB03. The activation of LDR in rol1 is mediated through the prokaryotic pathway of chloroplastic lipid biosynthesis. The rol1 root microbiome showed a reduced proportion of the Bacillaceae family. We propose that, parallel to the forefront immunity to MAMPs, LDR to certain NPFs provides a hidden layer of defense for controlling compatibility with commensal or beneficial microbes.     

有氧运动对高胆固醇饮食小鼠血浆脂质水平的影响

以AS易感型小鼠为对象进行了有氧耐力运动对抗动脉粥样硬化(AS)的研究。结果显示:跑台组血清TG 水平显著低于AS组(P< 0.05),而与正常组无显著差异(P> 0.05);与AS组相比,跑台组可显著降低小鼠血清胆固醇(Ch)、LDL-C 水平,升高HDL-C 水平。实验表明,长时间有规律的有氧耐力运动可通过改善血脂水平预防AS发生。     

Early oxidative change in low density lipoproteins during progressive chronic renal failure

Modified low density lipoproteins (LDL), including their oxidized forms, have been widely implicated in the etiology of atherosclerosis and concomitant cardiovascular disease (CVD) in chronic renal failure (CRF). The nature of events that lead to oxidative changes in LDL proteins are not clearly understood. Thus, patients suffering from CRF were grouped into mild, moderate and severe categories based on their blood urea and serum creatinine levels. Progression of CRF was accompanied not only with gradual increase in serum malondialdehyde (MDA) but also parallel increase in conjugated diene and MDA levels in LDL fractions separated from serum. Serum superoxide dismutase (SOD) activity was concurrently found to decrease, along with a decrease in high-density lipoprotein (HDL) cholesterol, during the progression of CRF. Gradual increase in the appearance of LDL oxidation products seems to accompany progressive manifestation of CRF. The results presented suggest that determination of serum MDA and SOD levels may enhance the diagnostic significance of the study of lipid profile in determining the risk for cardio vascular disease in CRF.     

固醇调节元件结合蛋白活性增加在二噁英染毒大鼠肝脏脂质沉积中的作用及运动干预研究

目的：研究固醇调节元件结合蛋白（SREBP）在二噁英染毒大鼠肝脏中的表达及在脂质代谢紊乱中的作用,探讨运动干预能否改变二噁英染毒大鼠的脂质代谢,为通过运动防治二噁英引起的代谢性疾病提供相应的理论依据。方法：24只雄性SD大鼠进行随机分组,对照组、染毒组、运动染毒组,每组8只。染毒组、运动染毒组大鼠腹腔注射二噁英（2,3,7,8-TCDD）,首次剂量为每公斤体重6.4微克,之后7周内,每隔1周按首次剂量的21%进行持续染毒。运动染毒组大鼠尾部以5%体重的负重量进行游泳运动,每天30分钟。8周后处死动物,计算肝脏指数,测定肝脏甘油三酯含量,肝脏组织HE和油红O染色检测病理性改变和脂肪沉积情况,Western Blot检测SREBP1-c蛋白表达含量,实时荧光定量PCR检测FASmRNA表达。结果：二噁英持续染毒大鼠肝脏中有明显脂质沉积现象。SREBP1-c活性及其靶基因FASmRNA表达显著增高,长期规律游泳运动能够显著降低这些蛋白和基因的表达。结论：二噁英染毒大鼠肝脏SREBP1-c活性显著增加,激活了脂质合成代谢FASmRNA的表达,从而促进脂质沉积。SREBP1-c可能是环境污染物二噁英导致代谢性疾病的重要转录因子。规律游泳运动可以逆转这种脂质沉积现象,提示游泳运动有助于降低二噁英染毒对大鼠的脂毒性作用,改善脂质代谢的紊乱。     

肝脏脂质代谢与自噬

肥胖患者肝脏中过量的脂质堆积可引起肝细胞内质网应激、线粒体功能紊乱和脂毒性,该作用与胰岛素抵抗（IR）和非酒精性脂肪肝病（NALFLD）等代谢紊乱疾病的发生密切相关。自噬是细胞对内外持续性刺激的非损伤性应答反应,具有维持细胞结构和代谢平衡的功能。研究发现,自噬参与降解肝细胞内过多的脂质堆积,维持肝脏脂质代谢稳态。本文介绍了自噬调节肝脏脂质代谢的分子作用机制。