多囊卵巢综合征及2型糖尿病患者血清Apelin水平及相关因素分析

目的测定多囊卵巢综合征(PCOS)及2型糖尿病(T2DM)患者的血清Apelin水平,探讨其与肥胖、性激素、代谢指标及胰岛素抵抗的相关性。方法 24例PCOS患者、26例T2DM和22例正常糖调节(NGR)者按体重指数(BMI)≥25kg/m2或<25kg/m2又各自分为超重(over weight,OW)与正常体重(normal weight,NW)亚组,采用放射免疫法检测空腹血清Apelin水平,空腹血糖(FPG)、空腹胰岛素(FINS)、性激素水平,计算BMI,并以稳态模型方法计算胰岛素抵抗指数(HOMA-IR)。结果 PCOS组患者血清Apelin水平高于NGR组[(247.8±47.5)ng/Lvs.(220.2±42.3)ng/L,P<0.05],T2DM组患者血清Apelin水平明显高于NGR组[(249.5±55.2)ng/Lvs.(220.2±42.3)ng/L,P<0.05],血清Apelin水平在PCOS组及T2DM组间比较,差异无统计学意义。在PCOS组、T2DM及NGR组中,OW亚组Apelin水平高于相应NW亚组。空腹血清Apelin水平与BMI、FPG、FINS、HOMA-IR、TG及TC呈正相关(r值分别为0.612、0.356、0.407、0.411、0.349、0.334,P<0.05)。结论血清Apelin水平变化与BMI、胰岛素抵抗及血脂有关,并可能在PCOS及T2DM的发生发展中起一定的作用。     

2型糖尿病患者血清视黄醇结合蛋白4水平的临床意义

目的 检测2型糖尿病(T2DM)患者正常体重组和肥胖组的血清视黄醇结合蛋白4(RBP4)水平,探讨与血脂和胰岛素敏感性等的相关性.方法 以体重指数(BMI)将63例糖尿病患者分成两组:T2DM超重/肥胖组和T2DM正常体重组,均采用HOMA-IR评价各组胰岛素敏感性,测定受试者的BMI、腰臀比(WHR),检测空腹状态下血清RBP4、血糖、糖化血红蛋白(HbAlc)、血浆葡萄糖(FBG)、总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)及低密度脂蛋白胆固醇(LDL-C)和胰岛素水平,并以55例健康体检者作对照.结果 T2DM超重/肥胖组血清RBP4浓度明显高于对照组和T2DM正常体重组,差异均有统计学意义(t分别=3.04、2.77,P均＜0.05);RBP4与HOMA-IR、BMI、WHR、TG明显正相关(r分别=0.33、O.28、0.24、0.32,P均＜0.05);多元线性逐步回归分析发现:HOMA-IR、BMI、TG、性别和年龄是血清RBP4的独立相关因素(r分别=0.33、0.56、0.55、-0.41、0.37,P均＜0.05).结论 血清RBP4与胰岛素抵抗呈正相关,可能与T2DM发病有一定关系.     

多囊卵巢综合征患者血清ANGPTL8、CTRP12水平及其与胰岛素抵抗、性激素指标的相关性分析

目的 探究多囊卵巢综合征(PCOS)患者血清血管生成素样蛋白8(ANGPTL8)、补体C1q/肿瘤坏死因子相关蛋白12(CTRP12)水平及其与性激素指标、胰岛素抵抗的相关性分析。方法 选取2021年1月至2023年1月在该院就诊的PCOS患者106例,按照体质量指数(BMI),将PCOS患者分为肥胖组(49例)和非肥胖组(57例);另选取60例同期体检健康女性为对照组。比较受试者一般资料及血清CTRP12、ANGPTL8水平。用Pearson法分析CTRP12、ANGPTL8水平与PCOS患者性激素指标及胰岛素抵抗的相关性。采用多元线性回归分析PCOS患者血清ANGPTL8、CTRP12水平的影响因素。结果 与对照组相比,肥胖组、非肥胖组舒张压(DBP)、空腹血糖(FPG)、收缩压(SBP)、空腹胰岛素(FINS)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、餐后2 h血糖(2hPG)、胰岛素抵抗指数(HOMA-IR)、黄体生成素(LH)、总胆固醇(TC)、促卵泡素(FSH)、睾酮(T)、雌二醇(E2)、ANGPTL8水平较高,差异有统计学意义(P<0.05),血清CT...     

代谢综合征患者血清Apelin水平的变化

目的:探讨代谢综合征(MS)患者血清Apelin水平的变化。方法:69例MS患者和63例正常糖调节(NGR)者,采用酶联免疫吸附法测定空腹血清Apelin含量,同时检测空腹血糖和胰岛素水平,以稳态模型评价胰岛素抵抗指数(HOMA-IR)。结果:MS组血清Apelin水平明显升高,确诊2型糖尿病MS组明显高于糖调节受损的MS组(475.8±37.3vs451.5±54.7)ng/L(P<0.05)和超重/肥胖者(475.8±37.3vs430.3±52.1)ng/L(P<0.01),且均高于NC组。多元逐步回归分析结果示:ln(HOMA-IR)、BMI和TC是血清Apelin独立相关因素(r2分别为0.459、0.494、0.293,均P<0.05)。结论:MS中多种代谢成分异常与血清Apelin升高密切相关,其可能是由于胰岛素抵抗加重所致。     

2型糖尿病患者血清补体因子H与胰岛素抵抗相关性研究

目的探讨2型糖尿病(T2DM)患者糖脂代谢和胰岛素抵抗的变化情况,分析其与患者血清补体因子H表达之间的相关性。方法选择2015年1月至2016年2月期间T2DM的患者120例为研究对象,根据亚太地区2000年的肥胖标准分为肥胖组(64例)和非肥胖组(56例),另选择同期体检的健康人群60例为对照组。比较各组患者的血清补体因子H表达情况及空腹胰岛素、空腹血糖、血脂水平,计算胰岛素抵抗指数(HOMA-IR),分析各指标与补体因子H表达的相关性。结果肥胖组、非肥胖组、对照组血清补体因子水平分别为(196.38±23.49)mg/L、(184.34±21.48)mg/L和(173.26±18.37)mg/L,肥胖组非肥胖组对照组,组间比较差异有显著的统计学意义(P0.01);T2DM患者血清补体因子H与体质指数(BMI)、空腹胰岛素(FINS)、胰岛素抵抗指数(HOMA-IR)、甘油三酯(TG)、空腹血糖(FBG)水平均呈正相关(r=0.397、0.601、0.333、0.312、0.524,P均0.01),与高密度脂蛋白胆固醇(HDL-C)呈负相关(r=-0.588,P0.01)。结论补体因子H可能参与了肥胖及T2DM的发病过程,临床上有望将补体系统作为T2DM的治疗靶点。     

2型糖尿病患者血清抵抗素与血糖、血脂及胰岛素抵抗的关系

目的:探讨2型糖尿病患者血清抵抗素与血糖、血脂及胰岛素抵抗的关系。方法:52例2型糖尿病(T2DM)患者按体质指数(BMI)分为肥胖(BMI≥25kg/m2)(26例)与非肥胖(BMI<25kg/m2)(26例)2组,及17例糖耐量正常的同期健康体检者作为对照组,采用酶联免疫分析法检测空腹血清抵抗素水平;同时行口服葡萄糖耐量(OGTT)和胰岛素释放试验,检测血脂,测量血压、身高、体重、腰围、臀围,计算BMI和腰臀比值(WHR),并以稳态模型(HOMA)计算胰岛素抵抗指数(HOMA-IR)。结果:肥胖T2DM患者血清抵抗素水平(ng/mL)明显高于非肥胖T2DM患者(P<0.01);肥胖T2DM组高于对照组、对照组略高于T2DM非肥胖者,但差异无显著性(P>0.05);女性血清抵抗素水平明显高于男性(P<0.05)。空腹血清抵抗素与BMI、HOMA-IR呈正相关(r=0.403、r=0.337、P<0.001);与FINS及餐后2hINS呈正相关(r=0.652、r=0.428、P<0.001);与甘油三酯呈正相关(r=0.320、P<0.01);与空腹血糖无关而与餐后2h血糖呈负相关(r=-0.303,P<0...     

脂肪因子Omentin-1与妊娠期糖尿病相关性研究

目的观察妊娠期糖尿病(GDM)患者血清脂肪因子Omentin-1水平变化,并探讨其临床意义。方法采用酶联免疫吸附测定(ELISA)法定量85例GDM及匹配设置的85例糖耐量正常孕妇(NGT)血清Omentin-1水平,同时检测两组糖脂生化指标、炎性指标、空腹胰岛素(FINS)水平,计算胰岛素抵抗指数(HOMA-IR)。结果 GDM组孕前体质量指数(BMI)、超敏-C反应蛋白(hs-CRP)、血脂、血糖、FINS及HOMA-IR均明显高于NGT组,血清Omentin-1明显低于NGT组,差异有统计学意义(P0.05)。产前肥胖和/或HOMA-IR≥2时,血清Omentin-1水平明显降低。血清Omentin-1与高密度脂蛋白(HDL)呈正相关,而与孕前BMI、产前BMI、FPG、FINS及HOMA-IR呈负相关。多元逐步回归分析孕前BMI、三酰甘油(TG)、空腹血糖(FPG)、FINS是GDM血清Omentin-1的独立影响因素。结论血清Omentin-1与GDM关系密切,反映孕妇糖、脂代谢紊乱和胰岛素抵抗程度,可能直接参与了GDM疾病的发生和发展。     

T2MD患者空腹血糖水平与新发缺血脑卒中的关系研究

目的探讨2型糖尿病(T2MD)患者空腹血糖水平对新发缺血脑卒中的影响。方法以2012年6月至2014年6月收治的168例T2MD患者为研究对象,根据患者头部CT诊断结果将患者分为T2MD无缺血脑卒组(T2MD组)82例以及T2MD合并缺血脑卒中组(合并脑卒中组)86例,另选取80例正常体检者为对照组。分别测定三组体重指数(BMI)、空腹血糖值(FBG)、糖化血红蛋白(Hb A1C)、空腹胰岛素(FINS)、收缩压(SBP)、舒张压(DBP)、同型半胱氨酸(Hcy)、总胆固醇(TC)、甘油三脂(TG)、低密度脂胆固醇(LDL-C)、高密度脂胆固醇(HDL-C),并计算胰岛素抵抗指数(HOMA-IR)。空腹血糖与各指标的关系应用Pearson单因素分析,FBG与脑卒中的关系应用Logistic多因素进行分析。结果 T2MD组及合并脑卒中组BMI、FBG、Hb A1C、Hcy、FINS、HOMA-IR、TC、TG、LDL-C水平显著高于对照组(P0.05),而HDL-C水平则低于对照组(P0.05),其中合并脑卒中组FBG、Hb A1C、FINS、HOMA-IR、Hcy、LDL-C水平显著高于T2MD组(P0.05)。经Pearson单因素分析可知,FBG与FINS、HOMA-IR、LDL-C呈正相关(P0.05)。经Logistic多因素分析显示,FBG、FINS、HOMA-IR、Hcy是T2MD合并脑卒中发生的独立危险因素。结论T2MD患者空腹血糖水平与新发缺血性脑卒中关系密切,且是脑卒中存在的独立危险因子。通过控制T2MD患者空腹血糖水平可有效预防缺血性脑卒中的发生。     

多囊卵巢综合征患者血清脂联素、瘦素水平与胰岛素抵抗关系的探讨

目的 研究多囊卵巢综合征(PCOS)患者血清脂联素(APN)、瘦素(LEP)改变与胰岛素抵抗(IR)的关系.方法 按体重指数(BMI)将PCOS患者104例分为肥胖组(67例)和非肥胖组(37例),随机选择健康体检的护士作为正常对照组(28例),检测性激素[包括促卵泡生成素(FSH),黄体生成素(LH),睾酮(T)]、血糖(FBG)、胰岛素(FINS)、LEP和APN等指标,并计算体重指数(BMI)、胰岛素抵抗指数(HOMA-IR),采用软件SPSS13.0行组间比较的方差分析,组间两两比较的q检验(SNK法),APN,LEP与各指标的Pearson相关性分析,形成HOMA-IR主要因素的多元逐步回归分析.结果 ①方差分析显示PCOS伴肥胖组BMI,LH/FSH,T,FINS,LEP,HOMA-IR均高于对照组(P<0.01),APN低于对照组(P<0.01);PCOS非肥胖组LH/FSH,T高于对照组(P<0.01),LEP,HOMA-IR高于对照组(P<0.05),BMI,APN低于对照组(P<0.05);两组FINS,差异无统计学意义(P>0.05);两病理组中肥胖组BMI,FINS,LEP,HOMA-IR均高于非肥胖组(P<0.01),APN低于非肥胖组(P<0.05),两组LH/FSH,T差异无统计学意义(P>0.05).②Pearson相关性分析PCOS患者血清APN与BMI,FINS,HOMA-IR呈负相关(r=-0.52,-0.44,-0.49,P<0.01),血清LEP与BMI,FINS,HOMA-IR呈正相关(r=0.41,0.32,0.35,P<0.01),血清APN,LEP与LH/FSH比值及T无显著相关性(P>0.05);血清APN与LEP呈显著负相关(r=-0.62,P<0.01).多元逐步回归分析显示BMI,APN,LEP是形成HOMA-IR的主要因素.结论 PCOS患者存在低APN,高LEP血症和胰岛素抵抗,且相互之间密切相关;血清APN,LEP含量可作为PCOS患者的辅助诊断指标.     

单纯性肥胖成人血清高敏C反应蛋白、血脂水平与胰岛素抵抗的相关性研究

目的 探讨单纯性肥胖成人血清高敏C反应蛋白(hs-CRP)、血脂水平与胰岛素抵抗(IR)的关系.方法 选择单纯性肥胖成人99例[按体质量指数(BMI)分为i度肥胖组46例,ii度肥胖组38例,iii度肥胖组15例],单纯性超重成人56例及健康成人80例.测定所有入选对象的身高、体质量、腰围、臀围、空腹血糖(FBG)、空腹胰岛素(FIN)、血脂、hs-CRP水平,并计算胰岛素抵抗指数(HOMA-IR)、BMI及腰臀比(WHR).结果 hs-CRP、HOMA-IR、FBG、FIN、TG、TC、LDL-C、脂肪肝发生率随着BMI的升高呈逐渐升高趋势,HDL-C则呈现逐渐降低趋势.血清hs-CRP与BMI、WHR、FIN、HOMA-IR、TG呈显著正相关(P＜0.05～P<0.01),与HDL-C呈显著负相关(P<0.01),多元逐步回归分析提示,BMI、HOMA-IR、HDL-C是影响hs-CRP的独立危险因素.结论 单纯性肥胖成人存在IR,炎性因子hs-CRP的过量表达参与并加重单纯性肥胖成人IR、血脂紊乱的发生和发展.     

NO and HNO donors,nitrones, and nitroxides: Past,present, and future

The biological effects attributed to nitric oxide (^?NO) and nitroxyl (HNO) have been extensively studied, propelling their array of putative clinical applications beyond cardiovascular disorders toward other age‐related diseases, like cancer and neurodegenerative diseases. In this context, the unique properties and reactivity of the N‐O bond enabled the development of several classes of compounds with potential clinical interest, among which ^?NO and HNO donors, nitrones, and nitroxides are of particular importance. Although primarily studied for their application as cardioprotective agents and/or molecular probes for radical detection, continuous efforts have unveiled a wide range of pharmacological activities and, ultimately, therapeutic applications. These efforts are of particular significance for diseases in which oxidative stress plays a key pathogenic role, as shown by a growing volume of in vitro and in vivo preclinical data. Although in its early stages, these efforts may provide valuable guidelines for the development of new and effective N‐O‐based drugs for age‐related disorders. In this report, we review recent advances in the chemistry of NO and HNO donors, nitrones, and nitroxides and discuss its pharmacological significance and potential therapeutic application.     

Genomics, Nutrition, Obesity, and Diabetes

PURPOSE: To present evidence of genetic and environmental interactions as they relate to nutrition, diabetes, and obesity. METHODS: A review of seminal literature related to genetics, obesity, and diabetes. FINDINGS: Multifactorial interactions are important in the development of nutrition-related disorders, but the challenge remains to explain how these interactions are expressed. Treating subpopulations of people might be important and useful to some extent at present, but in the future treating people of given genetic predispositions and other personal and environmental factors will have greater effects on quality-of-life indicators and life expectancies. CONCLUSIONS: Individualization coupled with multifactorial interactions will lead to new and more effective preventive and treatment modalities of nutrition-related disorders. With obesity and diabetes, genomics will bridge the traditional use of diet, exercise, and weight reduction with other environmental factors, ultimately leading to healthier lives.     

Platelets,thrombosis, coagulation,and atherosclerosis

When I first got the invitation to join a medical delegation going to Moldova, I thought for a moment that our destination was the fictional country in the old Marx Brothers movie Duck Soup. On further checking, it turns out that entertaining place was called Freedonia. I now know that Moldova is indeed a real country, bordered on the west by Romania and on the other three sides by the Ukraine. It is a proud country, rich with traditions, and its people are warm, giving, eager to learn ways to improve their healthcare system, and deeply appreciative of our attempts to help them in the task.     

Thoughts,images, worry,and anxiety

Recent models suggest that worry is primarily a verbal-linguistic process that enables images to be avoided and reduces somatic activation. Five-hundred and two subjects completed a questionnaire that assessed variables related to generalized anxiety disorder (GAD) criteria and also asked subjects to indicate the percentage of thoughts and images while worrying. Subjects were divided into excessive worriers (worry excessively about two or more topics more days than not for at least the last 6 months) and ordinary worriers (those who did not meet the previous criteria). As predicted, worry was reported as being composed predominantly of thoughts rather than images, and excessive worriers reported a significantly higher percentage of thoughts compared to ordinary worriers. The number of somatic symptoms was positively correlated with the percentage of images. This relationship was stronger among excessive worriers than ordinary worriers, specifically for autonomic hyperactivity symptoms. Further, in the excessive worry group only there was a significant negative correlation between the number of autonomic hyperactivity symptoms and the percentage of thoughts.This research was partially supported by grants from les Fonds de Recherche en Santé de Québec and the Medical Research Council of Canada. The study was completed while the first author was supported by the Medical Research Council of Canada.The authors gratefully acknowledge the assistance of France Blais for recruiting subjects, administering questionnaires, and entering data.     

Vomiting, diarrhea, constipation, and gastroenteritis

Diseases that cause vomiting, diarrhea, constipation, and gastroenteritis are major problems for populations worldwide. Patients, particularly infants, elderly, and immunocompromised individuals, may present at any point in a wide spectrum of disease states, underscoring the need for the clinician to treat these ailments aggressively. Several promising new treatment modalities, from oral rehydration solutions to antiemetic therapies, have been introduced over the past decade. Future directions include the use of probiotic agents and better tolerated rehydration solutions. Gastrointestinal disease will continue to be a focus worldwide in the search for better ways to cure illnesses associated with vomiting and diarrhea.     

Lipid messenger, diacylglycerol, and its regulator, diacylglycerol kinase, in cells, organs, and animals: history and perspective

Diacylglycerol kinase (DGK) metabolizes diacylglycerol (DG), a glycerolipid containing two acyl chains, to convert phosphatidic acid. DG is produced through phosphoinositide turnover within the membrane and is well known to act as a second messenger that modulates the activity of protein kinase C in the cellular signal transduction. Recent studies have revealed that DG also activates several proteins, including Ras guanine-nucleotide releasing protein and ion channels such as transient receptor potential proteins. Therefore, DGK is thought to participate in a number of signaling cascades by modulating levels of DG. Previous studies have disclosed that DGK is composed of a family of the isozymes, which differ in the structure, enzymological property, gene expression and localization, subcellular localization, and binding molecules. The present review focuses on the stories of phosphoinositide turnover and DG, including historical views, structural features, metabolism, and relevant cellular phenomena, together with the characteristics of DGK isozymes and the pathophysiological findings on animal studies using knockout mice and models for human diseases. Now it is being revealed that the structural and functional diversity and heterogeneity of and around DGK support the proper arrangement of the complex signal transduction machinery.     

Allergy,Anaphylaxis, and Nonallergic Hypersensitivity: IgE,Mast Cells,and Beyond

IgE-mediated type I hypersensitivity reactions have many reported beneficial functions in immune defense against parasites, venoms, toxins, etc. However, they are best known for their role in allergies, currently affecting almost one third of the population worldwide. IgE-mediated allergic diseases result from a maladaptive type 2 immune response that promotes the synthesis of IgE antibodies directed at a special class of antigens called allergens. IgE antibodies bind to type I high-affinity IgE receptors (FcεRI) on mast cells and basophils, sensitizing them to get triggered in a subsequent encounter with the cognate allergen. This promotes the release of a large variety of inflammatory mediators including histamine responsible for the symptoms of immediate hypersensitivity. The development of type 2-driven allergies is dependent on a complex interplay of genetic and environmental factors at barrier surfaces including the host microbiome that builds up during early life. While IgE-mediated immediate hypersensitivity reactions are undoubtedly at the origin of the majority of allergies, it has become clear that similar responses and symptoms can be triggered by other types of adaptive immune responses mediated via IgG or complement involving other immune cells and mediators. Likewise, various nonadaptive innate triggers via receptors expressed on mast cells have been found to either directly launch a hypersensitivity reaction and/or to amplify existing IgE-mediated responses. This review summarizes recent findings on both IgE-dependent and IgE-independent mechanisms in the development of allergic hypersensitivities and provides an update on the diagnosis of allergy.