代谢综合征患者血清色素上皮衍生因子水平变化的研究

目的 探讨代谢综合征(MS)患者血清色素上皮衍生因子(PEDF)水平的变化及其在MS发生、发展中的意义.方法 将93例门诊及住院MS患者按指标异常个数分为3个代谢指标异常组(Ⅲ组,n=30)、4个代谢指标异常组(Ⅳ组,n=42)、5个代谢指标异常组(Ⅴ组,n=20).35名门诊体检正常人群作为正常对照组(NC组).采用酶联免疫吸附试验测定血清PEDF浓度,同时测量身高、体重、腰围、血压,测定血脂、空腹血糖、空腹胰岛素、血清纤维蛋白原含量,计算稳态模型评估-胰岛素抵抗指数(HOMA-IR).采用多元逐步回归法分析PEDF的相关危险因素.结果 4组患者血清PEDF及纤维蛋白原水平逐渐升高(F=23.852、9.671,P均＜0.01).PEDF与体重指数、腰围、收缩压、舒张压、甘油三酯、纤维蛋白原、空腹血糖、空腹胰岛素、HOMA-IR呈正相关(r=0.253 ～0.440,P均＜0.01),与高密度脂蛋白-胆固醇(HDL-C)呈负相关(r=-0.334,P＜O.01).纤维蛋白原、HDL-C、空腹血糖、HOMA-IR是PEDF的相关危险因素(t=-2.977 ～3.793,P均＜0.05).结论 随着MS代谢异常指标个数的增多,PEDF水平升高,且与糖、脂代谢紊乱和胰岛素抵抗相关.PEDF可能是MS发病的预测因子.     

原发性高血压患者血清脂联素浓度的变化及肾素-血管紧张素系统对其影响

目的:探讨原发性高血压患者血清脂联素浓度的变化及肾素-血管紧张素系统对血清脂联素的影响.方法:本研究入选原发性高血压患者60例及健康人30例(正常对照组),以正常对照组人群胰岛素敏感性指数(ISI)的均数±标准差作为有无胰岛素抵抗的分界线,将原发性高血压患者分成两组,即胰岛素抵抗组23例及无胰岛素抵抗组37例.检测血清脂联素、空腹血糖、血清胰岛素、总胆固醇、高密度脂蛋白胆固醇、甘油三酯、胰岛素敏感性指数、收缩压、舒张压、平均压、身高、体重及体重指数等指标.另外,从60例原发性高血压患者中选出能够完成整个实验,积极配合随访的40例患者,并分成两部分,每部分20例,分别用血管紧张素转换酶抑制剂培哚普利及血管紧张素Ⅱ受体拮抗剂缬沙坦治疗两周,治疗前、后检测上述指标.结果:①胰岛素抵抗组的血清胰岛素和甘油三酯与正常对照组及无胰岛素抵抗组相比,胰岛素抵抗组明显升高(P＜0.01),胰岛素抵抗组的脂联素和胰岛素敏感性指数与正常对照组及无胰岛素抵抗组相比,胰岛素抵抗组明显降低(P＜0.01).②高血压患者用培哚普利及缬沙坦治疗两周后,平均压显著下降(P＜0.05),血清脂联素浓度和胰岛素敏感性指数明显升高(P＜0.05).③原发性高血压患者血清脂联素与收缩压和舒张压呈直线相关(r分别为0.35和0.28,P＜0.01和P＜0.05);血清脂联素与胰岛素敏感性指数和高密度脂蛋白胆固醇呈直线相关(r分别为0.45和0.53,P均＜0.01);血清脂联素与血清胰岛素、体重指数及甘油三酯负相关(r分别为-0.41,-0.61和-0.35,P＜0.01,P＜0.01和P＜0.05);血清脂联素与平均压无明显相关性.结论:原发性高血压患者低脂联素血症与脂代谢紊乱和胰岛素抵抗密切相关.肾素-血管紧张素系统,可提高原发性高血压患者胰岛素敏感性,从而使血清脂联素浓度升高.     

Relationship between serum testosterone and metabolic syndrome in overweight and obese young

目的 探讨肥胖青少年血清睾酮与代谢综合征(MS)的关系.方法 选取14～30岁的肥胖青少年574例为研究对象,分为MS组(n=305例,其中男87例,女218例)和非MS组(n=269例,其中男60例,女209例).应用化学发光法测定血清睾酮水平.结果 男性中,MS组的睾酮水平低于非MS组[(3.0±1.1) ng/ml和(3.5±1.4) ng/ml,P＜0.01];睾酮与体质量指数(BMI)、腰围、空腹血糖(FPG)、空腹胰岛素(FINS)、胰岛素抵抗指数(HOMA-IR)、三酰甘油(TG)呈负相关.女性中,MS组与非MS组睾酮水平比较差异无统计学意义[(0.8±0.3)ng/ml和(0.8±0.4)ng/ml,P＞0.05].睾酮与收缩压(SBP)、FINS、HOMA-IR呈正相关.无论男性还是女性,睾酮与MS各组分的多重回归分析显示只有HOMA-IR与睾酮水平独立相关.结论 肥胖青少年男性血清睾酮水平与代谢综合征密切相关.肥胖青少年女性睾酮与代谢综合征之间的关系仍需进一步研究.胰岛素抵抗可能是代谢综合征与睾酮之间相互作用的关键因素.     

血清Apelin水平与代谢综合征患者代谢指标的相关性观察

目的 探讨MS患者血清Apelin与血糖、血压的关系.方法 将132例研究对象分为MS组69例和糖耐量正常(NGT)组63名;MS组再分为T2DM组35例和IGR组34例,NGT组按BMI分为超重/肥胖(Ob)组33例与正常对照(NC)组30名.计算BMI,测定空腹Apelin、血糖、血压、血脂、FIns.结果 MS组Apelin、FIns、ln(HOMA-IR)、SBP均高于NGT组(P＜0.05).FPG、SBP和BMI是Apelin的独立相关因素(r2分别为0.429、0.315、0.253,P均＜0.01).结论 MS患者血清Apelin 水平升高,与SBP、FPG、2hPG、FIns和HOMA-IR独立相关.     

代谢综合征患者餐后三酰甘油水平

目的 探讨代谢综合征(MS)患者口服脂肪餐试验后三酰甘油(TG)浓度的变化.方法 住院MS患者42例年龄(56.4±10.2)岁作为实验组,另有正常者21例年龄(58.9±10.0)岁作为对照组.两组均口服脂肪餐(脂肪含量62%,53.4g/m2体表面积)并分别测定空腹,餐后2 h、4 h、6 h、8 h、10 h的TG浓度,用餐后TG浓度的曲线下面积(AUC)反映餐后TG的反应及代谢能力.结果 空腹胰岛素水平、胰岛素抵抗指数及体质量指数(BMI)实验组均显著高于对照组(P＜0.05,P＜0.01,P＜0.01).实验组患者餐后TG的AUC值与高峰浓度均显著高于对照组[实验组:(22.4±14.2)比对照组:(10.3±6.1)mmol/(L·h),实验组:(6.0±2.0)比对照组:(3.1±1.3)mmol/(L·h),P均＜0.01].餐后TG平均高峰浓度实验组出现在餐后6 h,与对照组出现在餐后4 h相比明显后延.多元线性回归分析以空腹TG、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)水平、年龄、BMI及胰岛素抵抗指数作为自变量.发现只有空腹TG水平是AUC水平的独立预测因子(B=10.3,P＜0.01).结论 MS患者餐后TG的反应水平比正常人显著升高,且清除延缓;餐后TG代谢失衡应是MS的重要特征之一.空腹TG水平是MS患者餐后TG代谢失衡的最主要的影响.     

代谢综合征组分与尿微量白蛋白发生率的关系

目的 探讨尿微量白蛋白(MAU)发生率与代谢综合征(MS)组分的关系.方法 选择3018例广西社区人群,测定其上午8:00-10:00随机尿白蛋白、体质量指数、血压、腰围、空腹血糖(FBS)、糖负荷后2 h血糖、血脂谱、空腹胰岛素.尿白蛋白≥30 mg/L判定为MAU.结果 (1)MAU发生率为11.1%,无论男、女性,MAU发生率均随年龄的增长而增加(P＜0.01).MAU组比非MAU组的体质量指数、腰围、舒张压、三酰甘油(TG)、空腹血糖及胰岛素抵抗指数等指标均有明显升高(P＜0.05).(2)无代谢异常、任意一种代谢异常、任意两种代谢异常及任意3种代谢异常者(MS)MAU发生率分别为7.4%、9.6%、13.3%和22.7%.MAU发生率随代谢紊乱加重呈升高趋势(趋势分析P＜0.01).(3)高血压、高血糖、中心性肥胖和胰岛素抵抗分别是MAU的独立风险因素(高血压OR值为2.135,P＜0.01;高血糖OR值为1.903,P＜0.01;中心性肥胖OR值为1.388,P＜0.05;胰岛素抵抗β为0.175,P＜0.01).与无代谢异常相比,两种代谢异常者发生MAU的风险增加1.446倍,MS者增加1.915倍(P均＜0.05).结论 高血糖、高血压、中心性肥胖和胰岛素抵抗是发生MAU的独立危险因素.多种代谢异常集聚的个体发生MAU的风险显著增加,尤以MS为甚.     

血清心血管活性多肽Apelin与原发性高血压伴代谢异常的关系

背景 心血管活性多肽Apelin是近年来发现的心血管活性多肽,也是重要的脂肪细胞因子,参与糖脂代谢异常的调节.目的 探讨血清Apelin水平与原发性高血压伴糖脂代谢异常的关系.方法 选取原发性高血压患者100例及正常血压对照者121例,进行血清Apelin水平测定.结果 在所有研究对象中,血清Apelin水平与低密度脂蛋白(LDL)呈正相关(r=0.26,P<0.01).原发性高血压组和正常血压组血清Apelin水平无显著差异[(1.04±0.6)比正常血压组(0.9±0.9)μg/L,P0.05].在原发性高血压患者中,血清Apelin水平与体质量指数(BMI,r-0.22,P<0.05)、腰围(r-0.26,P<0.05)、空腹血糖(r=0.25,P<0.05)及胰岛素抵抗指数(HOMA-IR,r=0.34,P<0.01)呈正相关.结论 血清Apelin浓度与原发性高血压伴代谢异常可能有轻度相关.     

代谢综合征大鼠中血清瘦素和肿瘤坏死因子α与胰岛素抵抗的关系

目的探讨瘦素与肿瘤坏死因子-α(TNF-α)在代谢综合征的发生发展过程中扮演的角色.方法高糖高脂饮食喂养SD大鼠12周后分别测血糖、血脂、血清胰岛素的水平,胰岛素抵抗(IR)的程度用稳态模型(Homa-IR)的IR指数(IAI)评估,血清中瘦素的水平用放免法测定TNF-α用ELISA方法检测,另取大鼠腹内脂肪组织,用免疫组化的方法观测脂肪细胞中瘦素表达的情况.结果高糖高脂饮食喂养12周的大鼠体重、空腹血糖、血脂以及空腹血清胰岛素的水平均高于正常对照组(P＜0.01),IAI与正常对照组相比有显著性升高[(4.44±0.27)∶(5.45±0.51),P＜0.05],血清瘦素和TNF-α与正常对照组相比也有明显升高[(0.15±0.05)∶(0.41±0.23),P＜0.01].结论高糖高脂饮食可诱导大鼠代谢综合征模型的建立,IR与血清瘦素和TNF-α的关系密切,瘦素和TNF-α的水平升高可作为代谢综合征的临床特征之一,以此通过代谢综合征的发展情况预测心血管疾病的发生和发展.     

中心性肥胖正常糖调节人群中不同胰岛素敏感性者的代谢特征及脂联素水平

腰围匹配的中心性肥胖正常糖调节人群,不同胰岛素敏感性组间随着胰岛素抵抗的加重,收缩压、血清甘油三酯、空腹及餐后血糖逐渐升高,代谢综合征(MS)的构成比也随之升高;血清脂联素水平随胰岛素抵抗的加重而降低;此外,MS与非MS者间血清脂联索差异也有统计学意义(P<0.01)。     

Ghrelin改善果糖诱导大鼠胰岛素抵抗的机制研究

32只雄性SD大鼠分为正常对照组(n=16)和果糖组(n=16),分别予以正常饮水和10％果糖4周,2组再分别以生理盐水和50 nmol/kg胃促生长素(Ghrelin)干预6周(每组n=8),测定空腹血糖、血脂和胰岛素等生化指标,RT-PCR检测大鼠骨骼肌胰岛素受体(Ins-R) mRNA表达水平,Western印迹法检测胰岛素受体底物1(IRS-1)的磷酸化水平.结果显示,高果糖组大鼠血浆胰岛素浓度和稳态模型评估的胰岛素抵抗指数(HOMA-IR)均较正常对照组明显升高[(13.1±3.6对9.0±1.5)μU/ml,P＜O.05;2.78±0.14对1.81 ±0.13,P＜0.01)],而高果糖喂养的大鼠经Ghrelin干预后胰岛素水平[(9.6±2.5) μU/ml,P＜0.05]和HOMA-IR(1.96±0.12,P＜0.01)明显降低,骨骼肌Ins-R mRNA表达和IRS-1磷酸化水平明显升高(P＜0.01),提示Ghrelin可能通过恢复骨骼肌Ins-R和受体后功能,改善胰岛素抵抗.     

Three layer functional model and energy exchange concept of aging process

Relying on a certain degree of abstraction, we can propose that no particular distinction exists between animate or living matter and inanimate matter. While focusing attention on some specifics, the dividing line between the two can be drawn. The most apparent distinction is in the level of structural and functional organization with the dissimilar streams of ‘energy flow’ between the observed entity and the surrounding environment. In essence, living matter is created from inanimate matter which is organized to contain internal intense energy processes and maintain lower intensity energy exchange processes with the environment. Taking internal and external energy processes into account, we contend in this paper that living matter can be referred to as matter of dissipative structure, with this structure assumed to be a common quality of all living creatures and living matter in general. Interruption of internal energy conversion processes and terminating the controlled energy exchange with the environment leads to degeneration of dissipative structure and reduction of the same to inanimate matter, (gas, liquid and/or solid inanimate substances), and ultimately what can be called ‘death.’ This concept of what we call dissipative nature can be extended from living organisms to social groups of animals, to mankind. An analogy based on the organization of matter provides a basis for a functional model of living entities. The models relies on the parallels among the three central structures of any cell (nucleus, cytoplasm and outer membrane) and the human body (central organs, body fluids along with the connective tissues, and external skin integument). This three-part structural organization may be observed almost universally in nature. It can be observed from the atomic structure to the planetary and intergalactic organizations. This similarity is corroborated by the membrane theory applied to living organisms. According to the energy nature of living matter and the proposed functional model, the decreased integrity of a human body's external envelope membrane is a first cause of the structural degradation and aging of the entire organism. The aging process than progresses externally to internally, as in single cell organisms, suggesting that much of the efforts towards the restoration and maintenance of the mechanisms responsible for structural development should be focused accordingly, on the membrane, i.e., the skin. Numerous reports indicate that all parts of the human body, like: bones, blood with blood vessels, muscles, skin, and so on, have some ability for restoration. Therefore, actual revival of not only aging tissue of the human body's membrane, but the entire human body enclosed within, with all internal organs, might be expected. We assess several aging theories within the context of our model and provide suggestions on how to activate the body's own anti-aging mechanisms and increase longevity. This paper presents some analogies and some distinctions that exist between the living dissipative structure matter and inanimate matter, discusses the aging process and proposes certain aging reversal solutions.     

Unusual responses of nocturnal pineal melatonin synthesis and secretion to swimming: Attempts to define mechanisms

Abstract: The effect of swimming at night on rat pineal melatonin synthesis was compared with that of light exposure at night. Rats were forced to swim at 0030 hr (lights out at 2000 hr) and sacrificed by decapitation 15 and 30 min later, immediately after swimming. Other groups of animals were exposed to white light (650μW/cm²) for 15 and 30 min at same time. Swimming caused a rapid and highly significant drop in the melatonin content in the pineal gland; however, the activity of N-acetyltransferase (NAT), the supposed rate limiting enzyme in the melatonin production, was not changed. Despite the drop in pineal melatonin levels, serum concentrations of the indole remained elevated in the rats that swam. In contrast, melatonin levels in the pineal and serum of light exposed rats fell precipitously, accompanied by a significant suppression of NAT activity. Since we anticipated that the strenuous exercise associated with swimming may induce release of artrial natriuretic peptide (ANP) from the heart, which in turn could cause the release of pineal melatonin, in a second study we injected physiological saline intravenously to stretch the cardiac muscle and release ANP. Three milliliters of normal saline was injected during the day into the jugular vein of anesthetized rats that were pretreated with isoproterenol to stimulate pineal melatonin production. Animals were killed 15 min after the saline injection, and pineal NAT activity and pineal melatonin levels were measured. The saline injections caused no alteration in the elevated levels of either NAT or melatonin. These data suggest that the disparity in pineal NAT activity (which was high) and pineal melatonin (which was low), in animals swum at night, may not be caused by ANP which is released during strenuous exercise such as swimming.     

The immunoneuroendocrine role of melatonin

Abstract: A tight, physiological link between the pineal gland and the immune system is emerging from a series of experimental studies. This link might reflect the evolutionary connection between self-recognition and reproduction. Pinealectomy or other experimental methods which inhibit melatonin synthesis and secretion induce a state of immunodepression which is counteracted by melatonin. In general, melatonin seems to have an immunoenhancing effect that is particularly apparent in immunodepressive states. The negative effect of acute stress or immunosuppressive pharmacological treatments on various immune parameters are counteracted by melatonin. It seems important to note that one of the main targets of melatonin is the thymus, i.e., the central organ of the immune system. The clinical use of melatonin as an immunotherapeutic agent seems promising in primary and secondary immunodeficiencies as well as in cancer immunotherapy. The immunoenhancing action of melatonin seems to be mediated by T-helper cell-derived opioid peptides as well as by lymphokines and, perhaps, by pituitary hormones. Melatonin-induced-immuno-opioids (MHO) and lymphokines imply the presence of specific binding sites or melatonin receptors on cells of the immune system. On the other hand, lymphokines such as -γ-interferon and interleukin-2 as well as thymic hormones can modulate the synthesis of melatonin in the pineal gland. The pineal gland might thus be viewed as the crux of a sophisticated immunoneuroendocrine network which functions as an unconscious, diffuse sensory organ.     

Melatonin and photoperiodic time measurement: Seasonal breeding in the sheep

Abstract: Well-established circadian physiology supports the view that photoperiodic time measurement utilizes the coincidence between the presence of light and a photosensitive phase of a 'biological clock' to alter reproductive status—the so-called external coincidence model of seasonal breeding. In this review, we examine the mechanism whereby photoperiod interacts with presumed suprachiasmatic nuclei activity to allow endogenous melatonin to normally synchronize reproductive activity to the optimal time of year. The Romney Marsh sheep is particularly explored as an experimental model. It is suggested that the on/off activity of seasonal reproduction may be a robust mechanism able to be predictably manipulated by the judicious use of the light/dark cycle and exogenous melatonin, but firmly based on circadian principles.     

Response of rat pineal melatonin to calcium, magnesium, and lithium is circadian stage dependent

Abstract: Herein we documented the response of pineal melatonin production to electrolytes known to be effective on pineal function in view of a possible circadian stage dependence. We studied the release of melatonin by perifused rat pineal glands at 2 different circadian stages corresponding to the middle of the light and dark periods, i.e., respectively, 7 and 19 HALO (Hours After Light Onset, L:D = 12:12). The initial efflux rates were, as expected, much higher in the perifusates of glands removed from rats sacrificed during the dark phase than of those removed during the light phase. After 3 hr of perifusion, melatonin release reached similar levels which were found constant up to the 8th hr of perifusion, whatever the circadian stage. Perifusion of the glands with physiological concentrations for the rat of calcium (5.2 mmol/1) and magnesium (1.34 mmol/1) resulted in a stimulatory effect on the pineal glands removed from rats sacrificed in the middle of the dark period (19 HALO), whereas no effects were observed on the pineal glands removed from rats sacrificed during the light (7 HALO). Lithium (0.28 and 0.55 mmol/1) was ineffective on melatonin release in pineal glands removed 7 and 19 HALO. Our results show differences in the initial efflux rates of melatonin and in the response of perifused pineal glands to calcium and magnesium according to the circadian stage.     

Changes in connexin43, the gap junction protein of astrocytes, during development of the rat pineal gland

Abstract: The abundance of gap junctions between rat pineal astrocytes formed by connexin43 (Cx43) was studied during development. Levels and distribution of Cx43 were measured by immunoblotting and indirect immunofluorescence, respectively. The amount of Cx43 in cells located within the gland was low until about the 7th postnatal day and increased to adult values between the 14th and 21st days postpartum. Although astrocytes, recognized by their vimentin immunoreactivity, were scarce before birth, they were abundant by the 7th postnatal day suggesting that the low levels of Cx43 found at this age corresponded to a low expression of this protein. Localization of the immunoreactivity to Cx43 and vimentin showed a close correlation, indicating that mature or immature pineal astrocytes form gap junctions made of Cx43. Since Cx43 levels attained their adult values at about the time the innervation and the functional state of the gland reached maturity (2–3 weeks after birth), it is proposed that astrocyte gap junctions are involved in the function of the adult rat pineal gland.     

Conservative management of perforated duodenal diverticulum： A case report and review of the literature

Duodenal diverticula are a relatively common condition. They are asymptomatic, unless they become complicated, with perforation being the rarest but most severe complication. Surgical treatment is the most frequently performed approach. We report the case of a patient with a perforated duodenal diverticulum, which was diagnosed early and treated conservatively with antibiotics and percutaneous drainage of secondary retroperitoneal abscesses. We suggest this method could be an acceptable option for the management of similar cases, provided that the patient is in good general condition and without septic signs.