Effects of Impaired Glucose Metabolism on Heart Rate Variability and Blood Pessure Variability in Essential Hpertensive Patients

To investigate the effects of impaired glucose metabolism （IGM） on cardiovascular autonomic nervous systems in essential hypertensive （EH） patients by comparing heart rate variability （HRV） and blood pressure variability （BPV） in EH patients with or without type 2 diabetes mellitus （T2DM）. Simultaneous 24-h recordings of ambulatory ECG and blood pressure monitoring were performed in 36 male old patients with simple EH and 33 male old patients with EH combined with T2DM. HRV analysis included time domain parameters such as SDNN, SDANN, SDNNi, rMSSD and pNN50, and total spectral power （TP） of HRV, which mainly consists of VLF, LF and HF component along with LF/HF ratio, was also obtained. The value of ambulatory blood pressure was represented as the mean blood pressure （mean systolic/mSBP, diastolic/mDBP and pulse pressure/mPP） during different periods （24 h/24 h, day time/d and night time/n）. Standard deviation （SD） as well as coefficient of variance （CV） of blood pressure during each above-mentioned period were obtained to reflect the long-term BPV. Our result showed that SDNN, SDNNi, SDANN, rMSSD, PNN50, TP and HF of HRV in cases of EH with T2DM were all significantly lower than those in simple EH subjects （P〈0.05）. No significant differences in VLF or LF was found between the two groups （P〉0.05）, while LF/HF ratio was significantly higher in EH with T2DM patients than in simple EH subjects （P〈0.01）. Moreover, dmSBP, 24 h-mPP and dmPP were all significantly higher in EH with T2DM patients than in simple EH subjects （P〈0.05）, while nmSBP, 24 h-mSBP, 24 h-mDBP, dmDBP, nmDBP or nmPP showed no significant difference between this two groups of patients （P〉0.05）. And dSBPSD, dSBPCV and 24 h-SBPSD were all significantly higher in EH with T2DM patients than in simple EH subjects （P〈0.05）, while the other BPV indexes showed no significant difference between this two groups （P〉0.05）. It is concluded that the cardiovascular autonomic nervous systems in EH patients was further impaired by T2DM, displaying lowering of HRV and enlargement of BPV, which in turn induced abnormal structural and functional changes of cardiovascular systems. Therefore, improving cardiovascular autonomic nervous systems might reduce the occurrence of cardiovascular complications in the EH patients with IGM.

Ethanol exposed maturing rat cerebellar granule cells show impaired energy metabolism and increased cell death after oxygen-glucose deprivation

Alcohol, a widely abused drug, has deleterious effects on the immature nervous system. This study investigates the effect of chronic in vitro ethanol exposure on the metabolism of immature rat cerebellar granular cells(CGCs) and on their response to oxygen-glucose deprivation(OGD). Primary CGC cultures were exposed to ethanol(100 mM in culture medium) or to control ethanol-free medium starting day one in vitro(DIV1). At DIV8, the expression of ATP synthase gene ATP5 g3 was quantified using real-time PCR, then cultures were exposed to 3 hours of OGD or normoxic conditions. Subsequently, cellular metabolism was assessed by a resazurin assay and by ATP level measurement. ATP5 g3 expression was reduced by 12-fold(P = 0.03) and resazurin metabolism and ATP level were decreased to 74.4 ± 4.6% and 55.5 ± 6.9%, respectively after chronic ethanol treatment compared to control values(P < 0.01). Additionally, after OGD exposure of ethanol-treated cultures, resazurin metabolism and ATP level were decreased to 12.7 ± 1.0% and 9.0 ± 2.0% from control values(P < 0.01). These results suggest that chronic ethanol exposure reduces the cellular ATP level, possibly through a gene expression down-regulation mechanism, and increases the vulnerability to oxygen-glucose deprivation. Thus, interventions which improve metabolic function and sustain ATP-levels could attenuate ethanol-induced neuronal dysfunction and should be addressed in future studies.

Impaired fasting glucose:Pro-diabetic,“atheroprotective”and modified by metabolic syndrome

AIM:To investigate whether impaired fasting glucose(IFG)confers cardiovascular risk.METHODS:A non-diabetic population-based sample representative of middle-aged and elderly Turks was studied at 8.5 years’follow-up for incident diabetes and coronary heart disease(CHD).Metabolic syndrome(MetS)was defined by ATP-Ⅲcriteria modifiedfor male abdominal obesity,and IFG and type 2 diabetes were identified by criteria of the American Diabetes Association.Stratification by presence of MetS was used.Outcomes were predicted providing estimates for hazard ratio(HR)obtained by use of Cox proportional hazards regression analysis in models that controlled for potential confounders.RESULTS:In 3181 adults(aged 52±11.5 years at baseline),analysis stratified by MetS,gender and IFG status distinguished normoglycemic subjects by a"hypertriglyceridemic waist"phenotype consisting of significantly higher waist circumference,fasting triglyceride and lower high-density lipoprotein-cholesterol,regardless of gender and MetS.Additionally,lipoprotein(Lp)(a)tended to be lower in(especially female)participants with MetS.Multivariable linear regression in a subset of the sample demonstrated decreased Lp(a)levels to be associated with increased fasting glucose and insulin concentrations,again particularly in women.In Cox regression analysis,compared with normoglycemia,baseline IFG adjusted for major confounders significantly predicted incident diabetes at a 3-fold HR in men and only women with MetS.Cox models for developing CHD in 339 individuals,adjusted for conventional risk factors,revealed that IFG status protected against CHD risk[HR=0.37(95%CI:0.14-0.998)]in subjects free of MetS,a protection that attenuated partly in male and fully in female participants with MetS.CONCLUSION:IFG status in non-diabetic people without MetS displays reduced future CHD risk,yet is modulated by MetS,likely due to autoimmune activation linked to serum Lp(a).

Evaluation of glucose metabolism in women with multiple ovarian follicles

Objective ：To investigate glucose metabolism in women with multiple ovarian follicles （MOF） and explore the relationship between glucose metabolism, insulin resistance and body weight. Methods：We evaluated 46 women with MFO and 30 normal women as controls. All the subjects were given 75g of glucose orally in order to perform the oral glucose tolerance test （OGTT） and insulin releasing test （IRT）, and they were also evaluated for insulin resistance using the insulin resistance index with homeostatic model assessment （HOMA）. Results：The occurrence of impaired glucose tolerance in women with MOF was 10.87%, which was significantly higher than that in the control group （3.33% ,P 〈 0.05）. The rate of insulin resistance was 30.43% in the study group as compared to 10.00% in the control group. The results showed that there was significant difference between the two groups（P 〈 0.05）. The levels of FSH,LH,PRL,E2,T and P between the two groups had no significant difference （P 〉 0.05）. BMI in women with impaired glucose tolerance was correlated positively to insulin resistance （r = 0.567, P 〈 0.05）. Conclusion：Abnormal glucose metabolism was observed in women with unitary multiple ovarian follicles, and this could be attributed to obesity and insulin resistance. Women with MOF and associated obesity should be subjected to OGTT so that their glucose levels can be monitored as a preventive measure.

Overexpression of Sirt6 ameliorates sleep deprivation induced-cognitive impairment by modulating glutamatergic neuron function

Sleep benefits the restoration of energy metabolism and thereby suppo rts neuronal plasticity and cognitive behaviors.Sirt6 is a NAD+-dependent protein deacetylase that has been recognized as an essential regulator of energy metabolism because it modulates various transcriptional regulators and metabolic enzymes.The aim of this study was to investigate the influence of Sirt6 on cerebral function after chronic sleep deprivation(CSD).We assigned C57BL/6J mice to control or two CSD groups and subjected them to AAV2/9-CMV-EGFP or AAV2/9-CMV-Sirt6-EGFP infection in the prelimbic cortex(PrL).We then assessed cerebral functional connectivity(FC) using resting-state functional MRI,neuron/astrocyte metabolism using a metabolic kinetics analysis;dendritic spine densities using sparse-labeling;and miniature excitato ry postsynaptic currents(mEPSCs) and action potential(AP) firing rates using whole-cell patchclamp recordings.In addition,we evaluated cognition via a comprehensive set of behavioral tests.Compared with controls,Sirt6 was significantly decreased(P<0.05) in the PrL after CSD,accompanied by cognitive deficits and decreased FC between the PrL and accumbens nucleus,piriform cortex,motor co rtex,somatosensory co rtex,olfactory tubercle,insular cortex,and cerebellum.Sirt6 ove rexpression reve rsed CSD-induced cognitive impairment and reduced FC.Our analysis of metabolic kinetics using [1-13C] glucose and [2-13C] acetate showed that CSD reduced neuronal Glu4and GABA2synthesis,which could be fully restored via forced Sirt6 expression.Furthermore,Sirt6 ove rexpression reversed CSD-induced decreases in AP firing rates as well as the frequency and amplitude of mEPSCs in PrL pyramidal neurons.These data indicate that Sirt6 can improve cognitive impairment after CSD by regulating the PrL-associated FC network,neuronal glucose metabolism,and glutamatergic neurotransmission.Thus,Sirt6 activation may have potential as a novel strategy for treating sleep disorder-related diseases.

Analysis of Patients With Coronary Heart Disease Combined With Impaired Glucose Metabolism

Objectives To study the morbidity of patients with coronary artery disease （CAD） combined with impaired glucose metabolism. Methods Retrospective analysis of clinical data about patients with CAD in 1997, 2002 and 2007, separately. A total of 2951 patients were enrolled, among whom had coexistence of 457 abnormal glycometabolism, including impaired fasting glucose, impaired glucose tolerance and type 2 diabetes mellitus. Results The prevalence of abnormal glycometabolism in patients with CAD was increasing year by year. The morbidity raised from 3.8% and 16.5% to 10. 8% in these three years. Conclusion It is more and more common to detect CAD with impaired glucose metabolism, and it should be emphasized in the secondary prevention of CAD.

家庭医生模式干预对糖耐量减低患者骨代谢的影响

目的:探讨家庭医生模式干预对糖耐量减低患者骨代谢的影响。方法:以2022年1-12月在上海宜川社区卫生服务中心体检的,符合纳入和排除标准的120例糖耐量减低患者作为研究对象,将60例采用家医模式干预的患者设为干预组,将仅进行电话随访的60例患者设为对照组。观察两组患者干预前和干预后6个月的糖代谢、骨代谢相关指标的变化。结果:干预组干预前空腹血糖、糖化血红蛋白、自我效能评分、骨钙素、25羟维生素D、甲状旁腺激素、血清1型骨胶原N端肽、血清1型胶原交联C末端肽水平与对照组相比差异均无统计学意义(均P>0.05);干预后6个月后,干预组空腹血糖、糖化血红蛋白、自我效能评分、骨钙素、25羟维生素D、甲状旁腺激素、血清1型骨胶原N端肽、血清1型胶原交联C末端肽水平均优于治疗前和对照组,差异均有统计学意义(均P<0.05)。结论:家庭医生模式干预可改善糖耐量减低患者的糖代谢和骨代谢水平,值得在临床中推广应用。

兰术化浊汤对糖调节受损脂代谢及氧化应激的影响

目的探讨兰术化浊汤对糖调节受损脂代谢及氧化应激的影响。方法36只SD雄性大鼠,将其中30只构建糖调节受损大鼠模型,造模成功后,30只大鼠随机分为模型组、二甲双胍组(200 mg/kg)、兰术化浊汤低剂量组(5 g/kg)、兰术化浊汤中剂量组(10 g/kg)、兰术化浊汤高剂量组(20 g/kg),每组各6只,另6只设为空白组。治疗组分别按不同剂量灌胃给药,模型组与空白组按1 ml/100 g生理盐水灌胃,1次/d,连续4周。通过尾尖采血的方式检测空腹血糖(FBG)、糖耐量试验2 h血糖(OGTT2hPG),测量各组大鼠体重,生化分析血清总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)水平,试剂盒检测血清丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)水平。结果与空白组比较,模型组大鼠体重、HDL-C、SOD、GSH-PX水平降低,FBG、OGTT2hPG、TC、TG、LDL-C、MDA水平升高,差异有统计学意义(P<0.05);与模型组比较,兰术化浊汤中、高剂量组大鼠体重、HDL-C、SOD、GSH-PX水平升高,FBG、OGTT2hPG、TC、TG、LDL-C、MDA水平降低,差异有统计学意义(P<0.05)。结论兰术化浊汤可有效调节脂质代谢和氧化应激,从而改善糖调节受损。

医学营养干预在交界性糖耐量受损孕妇中的应用效果

目的:观察医学营养干预在交界性糖耐量受损(BGGI)孕妇中的应用效果。方法:回顾性分析2020年3月至2021年3月该院收治的96例BGGI孕妇的临床资料,根据干预方法不同将其分为对照组和观察组各48例。对照组采用常规营养干预,观察组在对照组基础上给予医学营养干预。比较两组孕妇体质量增长水平、不良妊娠结局、新生儿结局,干预前后糖代谢指标[空腹血糖(FPG)、餐后2 h血糖(2hPG)、糖化血红蛋白(HbAlc)]水平。结果:两组妊娠期高血压发生率比较,差异无统计学意义(P>0.05),观察组孕妇体质量增长水平、剖宫产发生率、产后出血发生率、妊娠期糖尿病发生率均低于对照组,差异有统计学意义(P<0.05);两组新生儿低血糖、新生儿黄疸、胎儿生长受限、进入新生儿监护室发生率比较,差异均无统计学意义(P>0.05),观察组新生儿体质量、巨大儿发生率均低于对照组,Apgar评分高于对照组,差异有统计学意义(P<0.05);临产前、产后12周,观察组FPG、2hPG、HbAlc水平均低于干预前与对照组,差异有统计学意义(P<0.05)。结论:在常规营养干预基础上采用医学营养干预可降低BGGI孕妇体质量增长和糖代谢指标水平,改善不良妊娠结局和新生儿结局,其效果优于常规营养干预。

高膳食纤维限能干预对肥胖合并糖耐量异常患者体重和代谢指标的影响

目的探究高膳食纤维限能干预对肥胖合并糖耐量异常患者体重和代谢指标的影响。方法前瞻性选取陕西省中医医院营养科门诊收治的60例肥胖合并糖耐量异常患者为研究对象,采用随机数字表法将其分为高膳食纤维限能组(30例,高膳食纤维限能干预)和常规饮食限能组(30例,常规饮食限能)。比较两组的干预效果。结果干预后,高膳食纤维限能组的甘油三酯(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)、空腹血糖(FBG)、餐后2 h血糖(2 h PG)水平及稳态模型胰岛素抵抗指数(HOMA-IR)优于常规饮食限能组(P<0.05)。干预后,高膳食纤维限能组的腰围、体质量指数(BMI)、体脂率、内脏脂肪指数小于常规饮食限能组(P<0.05)。高膳食纤维限能组的治疗有效率高于常规饮食限能组,差异具有统计学意义(P<0.05)。结论高膳食纤维限能干预在肥胖合并糖耐量异常患者中的效果较好,可改善体重和代谢指标。

Effect of impaired glucose tolerance on cardiac dysfunction in a rat model of prediabetes

Background The effect of impaired glucose tolerance （IGT） on cardiac function during the chronic prediabetes state is complicated and plays an important role in clinical outcome. However, the molecular mechanisms are not fully understood. This study was designed to observe cardiac dysfunction in prediabetic rats with IGT and to determine whether glucose metabolic abnormalities, inflammation and apoptosis are linked to it.Methods The IGT rat models were induced by streptozocin, and the heart functions were assessed by echocardiography. Myocardial glucose metabolism was analyzed by glycogen periodic acid-Schiff staining, and the pro-apoptotic effect of IGT was evaluated by TUNEL staining. Additionally, caspase-3 activation, macrophage migration inhibitory factor （MIF） and G-protein coupled receptor kinase 2 （GRK2） were detected by Western blotting in cardiac tissue lysates.Results Area-under-the-curve of blood glucose in rats injected with streptozotocin was higher than that in controls, increased by 16.28%, 38.60% and 38.61% at 2, 4 and 6 weeks respectively （F=15.370, P=0.003）. Abnormal cardiac functions and apoptotic cardiomyocytes were observed in the IGT rats, the ejection fraction （EF） being （68.594-6.62）% in IGT rats vs. （81.07±4.59）% in controls （t=4.020, P=0.002）. There was more glucose which was converted to glycogen in the myocardial tissues of IGT rats, especially in cardiac perivascular tissues. Compared to controls, the cleaved caspase-3, MIF and GRK2 were expressed at higher levels in the myocardial tissues of IGT rats.Conclusions IGT in the prediabetes period resulted in cardiac dysfunction linked to abnormal glycogen storage and apoptosis. Additionally, MIF and GRK2 may be involved in the pathogenesis of cardiac dysfunction in prediabetes and their regulation may contribute to the design of novel diagnostic and therapeutic strategies for those who have potential risks for diabetic cardiovascular complications.

降糖方对糖耐量异常大鼠糖脂代谢及骨骼肌组织IκB-α和NF-κBp65的影响

目的:探讨降糖方对糖耐量异常大鼠糖脂代谢及骨骼肌组织κB抑制蛋白α(IκB-α)、核转录因子肽p65(NF-κBp65)的影响。方法:SD大鼠随机分为正常组、模型组、盐酸二甲双胍组、降糖方低、高剂量组,采用高脂饮食喂养4周,链脲佐菌素(STZ)腹膜内注射建立糖耐量异常大鼠模型,治疗8周后,观察骨骼肌组织病理变化,测定空腹血糖(FPG)、血清胰岛素(FINS)、胰岛素抵抗指数(HOMA-IR)、甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白(LDL-C)、骨骼肌组织IκB-α mRNA、NF-κBp65 mRNA水平、骨骼肌组织白细胞介素-4(IL-4)、白细胞介素-12(IL-12)、肿瘤坏死因子-α(TNF-α)蛋白水平。结果:正常组大鼠骨骼肌组织结构正常,模型组骨骼肌排列紊乱、肌纤维断裂、可见明显炎症细胞浸润;盐酸二甲双胍及降糖方干预后,骨骼肌炎症细胞浸润减少,肌纤维排列趋于整齐。模型组大鼠FPG、FINS、HOMA-IR水平、血清TG、TC、LDL-C水平、骨骼肌IκB-α mRNA、NF-κBp65 mRNA和蛋白水平、骨骼肌组织IL-4、IL-12、TNF-α蛋白水平高于对照组(P<0.01);盐酸二甲双胍组、降糖方低、高剂量组大鼠FPG、FINS、HOMA-IR水平,血清TG、TC、LDL-C水平,骨骼肌IκB-α mRNA、NF-κBp65 mRNA和蛋白水平、骨骼肌组织IL-4、IL-12、TNF-α蛋白表达水平低于模型组(P<0.01)。结论:降糖方对糖耐量异常大鼠糖脂代谢具有明显改善作用,其机制可能与降糖方抑制骨骼肌IκB-α mRNA、NF-κBp65 mRNA和蛋白的表达有关。

北京市大兴区成人空腹血糖受损现状调查

目的调查北京市大兴区成人空腹血糖受损流行病学现状,在否认糖尿病病史人群中了解其空腹血糖异常的比例及其与血脂代谢的关系,为这部分人群的血糖体检筛查,以及预防发生糖尿病及心脑血管疾病提供参考.方法2018年1-10月在中国中医科学院广安门医院体检的北京市大兴区居民共805人,采用问卷调查了解糖尿病知晓率,并检测血糖、血脂等实验室项目.结果在698名否认糖尿病病史的受访者中,空腹血糖受损(IFG)103例(14.8%),空腹血糖(FBG)升高者130例(18.6%),与FBG正常组(541例,77.5%)相比,IFG组以及FBG升高组的三酰甘油(TG)、残粒脂蛋白(RLP)、小而密低密度脂蛋白(sdLDL-C)均显著升高(P<0.05),高密度脂蛋白(HDL-C)则显著降低(P<0.05).在年龄>60岁人群中,有糖尿病病史组的空腹血糖正常率显著高于否认有糖尿病病史组(80.8%vs.64.4%,P=0.026).结论在北京市大兴区受访人群中,空腹血糖受损等血糖代谢异常的比例依然较高,且在否认糖尿病病史受访者中更为明显,并容易伴随血脂代谢异常.对血糖代谢异常的知晓、健康教育并控制高血脂等危险因素,对他们可能是干预和治疗的关键.

2型糖尿病合并轻度认知障碍患者脑葡萄糖代谢连接网络拓扑结构分析

目的:分析2型糖尿病(T2DM)合并轻度认知障碍(MCI)(T2DM&MCI)患者脑葡萄糖代谢连接网络拓扑结构的改变情况。方法:选择阿尔茨海默病神经影像学倡议(ADNI)数据库收录的T2DM&MCI受试者(观察组)和健康受试者(对照组),每组35例。从数据库获取2组简易智能精神状态检查量表(MMSE)评分、患者报告日常认知量表的记忆评分(EcogPtMem)、患者亲属报告日常认知量表的记忆评分(EcogSPMem)以及氟代脱氧葡萄糖-电子发射断层扫描(FDG-PET)图像。利用SPM12将FDG-PET图像标准化到蒙特利尔神经病学研究所(MNI)空间脑模板上。以小脑作为参考区,提取每个受试者解剖自动标记法(AAL)模块脑区的标准摄取值比率(SUVR),构建葡萄糖代谢连接脑网络。采用GRETNA软件分析全局效率、度中心性、节点局部效率等脑网络拓扑属性;采用Spearman相关性分析差异脑区度中心性与EcogPtMem评分以及EcogSPMem评分的相关性、节点局部效率与EcogPtMem评分以及EcogSPMem评分的相关性。结果:与对照组比较,观察组MMSE评分明显更低,EcogPtMem和EcogSPMem评分均明显更高,差异具有统计学意义(P<0.05)。与对照组比较,观察组的全局效率组间差异无统计学意义(P>0.05)。与对照组比较,观察组左侧海马旁回(P=0.005)、左侧海马(P=0.013)、左侧顶下缘角回(P=0.031)、左侧角回(P=0.034)、右侧角回(P=0.013)、右侧顶下缘角回(P=0.044)、右侧海马旁回(P=0.024)度中心性明显降低;左侧直回(P=0.028)、左侧海马旁回(P=0.044)、左侧海马(P=0.026)、左侧顶下缘角回(P=0.031)、左侧角回(P=0.024)、右侧角回(P=0.004)、右侧顶下缘角回(P=0.039)节点局部效率明显降低。相关性分析结果显示,观察组左侧海马度中心性(r=-0.273,P=0.022)和左侧海马旁回度中心性(r=-0.341,P=0.004)与EcogPtMem评分呈负相关关系;左侧海马度中心性(r=-0.391,P=0.001)、左侧海马旁回度中心性(r=-0.410,P<0.001)、右侧海马旁回度中心性(r=-0.240,P=0.045)与EcogSPMem评分呈负相关关系。观察组左侧海马节点局部效率(r=-0.257,P=0.032)、左侧海马旁回节点局部效率(r=-0.251,P=0.036)、右侧角回节点局部效率(r=-0.265,P=0.027)与EcogPtMem评分呈负相关关系;左侧海马节点局部效率(r=-0.363,P=0.002)和左侧海马旁回节点局部效率(r=-0.362,P=0.002)与EcogSPMem评分呈负相关关系。结论:T2DM&MCI患者脑葡萄糖代谢连接网络拓扑结构异常可能是引起其记忆功能下降的原因之一,这可为探究T2DM&MCI神经机制提供参考。

糖代谢异常与血管性认知障碍的研究进展:联系与发病机制

糖代谢异常是包括糖尿病前期和糖尿病的一组疾病,糖尿病前期可进一步分为糖耐量异常和空腹血糖受损。血管性认知障碍是脑血管病变及其危险因素导致的临床卒中或亚临床血管性脑损伤,涉及至少一个认知域受损的临床综合征。本文讨论糖代谢异常与血管性认知障碍的联系,并详细分析糖代谢异常导致血管性认知障碍相关机制的最新进展。

糖耐量异常对PCOS患者雄激素、脂代谢及血管内皮相关因子的影响

目的探讨糖耐量异常(IGT)对多囊卵巢综合征(PCOS)患者雄激素、脂代谢及血管内皮相关因子的影响。方法回顾性分析2019年1月至2021年1月确诊并治疗的PCOS患者98例,根据是否存在IGT分组为IGT组(糖耐量受损组,n=36)和NGT组(糖耐量正常组,n=62)。比较两组年龄、体质量指数(BMI)、腰臀比(WHR)和文化程度等一般资料;比较两组雄激素、脂代谢及血管内皮相关因子水平,Pearson分析雄激素、脂代谢及血管内皮相关因子水平与IGT的关系。结果两组年龄、BMI、WHR、文化程度、存在多毛、痤疮、黑棘皮和溢脂所占比例无显著差异(P>0.05);IGT组脱氢表雄酮(DHEA)、睾酮(T)、雄烯二酮(A)、总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、血管内皮生长因子(VEGF)和内皮抑素(ES)水平显著高于NGT组(P<0.05);IGT组高密度脂蛋白胆固醇(HDL-C)水平显著低于NGT组(P<0.05)。PCOS患者DHEA、T、A、TC、TG、LDL-C、VEGF和ES水平与IGT水平呈正相关(P<0.05),HDL-C与IGT水平呈负相关(P<0.05)。结论PCOS伴IGT患者血糖水平与雄激素和血管内皮因子均呈正相关关系,且与脂代谢水平中TC、TG、LDL-C呈正相关,HDL-C呈负相关。

健胰方加减对糖调节受损患者血糖及胰岛素代谢水平的影响

目的分析健胰方加减对糖调节受损患者血糖、胰岛素代谢水平的影响。方法90例糖调节受损患者,采取随机法分为对照组和观察组,每组45例。对照组行生活方式干预,观察组在对照组的基础上应用健胰方加减辅助治疗。比较两组患者治疗前以及治疗3个月后的糖代谢指标[空腹血糖(FBG)、餐后2小时血糖(2 h PG)、糖化血红蛋白(HbA1c)]水平、胰岛素代谢指标[脂联素、胰岛β细胞功能指数(HOMA-β)、空腹胰岛素(FINS)、胰岛素抵抗指数(HOMA-IR)]水平。结果治疗后,观察组患者FBG(4.60±0.50)mmol/L、2 h PG(7.02±1.01)mmol/L、HbA1c(4.53±0.03)%均低于对照组的(5.70±0.60)mmol/L、(7.75±1.02)mmol/L、(5.75±0.50)%,差异均具有统计学意义(P<0.05)。治疗后,观察组患者脂联素(3.10±0.80)mg/L、HOMA-β(4.84±0.50)均高于对照组的(2.53±0.80)mg/L、(4.40±0.30),FINS(7.05±0.05)mIU/L、HOMA-IR(1.45±0.30)均低于对照组的(9.20±2.02)mIU/L、(2.33±0.20),差异均具有统计学意义(P<0.05)。结论生活方式干预配合健胰方加减治疗,有助于糖调节受损患者血糖、胰岛素代谢水平调节,有效阻断疾病发展。

中药益糖康干预并有糖调节受损的代谢综合征临床研究

目的:观察中药益糖康干预并有并有糖调节受损的代谢综合征的临床疗效。方法:通过对患者空腹血糖(fasting plasma glucose,FPG)、餐后2h血糖(2 hours plasma glucose;postprandial blood glucose;2hPG,PBG)、糖化血红蛋白(HbAlc)、体重(body weight,BW)、总胆固醇(total cholesterol,TC)、甘油三酯(triglyceride,TG)、高密度脂蛋白(high density lipoprotein,HDL-C)、低密度脂蛋白(low density lipoprotein,LDL-C)等主要指标进行分析。结果:①中药益糖康组FPG降低,与西药组(二甲双胍)相比,具有显著差异(P<0.05)。②中药益糖康组HbAlc、2hPG降低,与西药组(二甲双胍)相比,无显著差异(P>0.05)。③1年后中药益糖康组患者HbAlc较基线下降(P<0.005)。④1年后中药益糖康组患者的血脂谱与基线相比:TG下降16%(P<0.005),TC下降10%(P<0.005),LDL-C下降8%(P<0.0001),而HDL-C升高24%(P<0.0001)。⑤患者FPG每下降0.8mmol/L,BW平均下降0.9kg,与西药组(二甲双胍)相比,具有显著差异(P<0.005)。结论:中药益糖康可降糖、减轻体重,改善血脂谱,具有潜在的心血管收益。

非酒精性脂肪肝与代谢综合征关系的研究

目的分析无糖尿病(DM)史的非酒精性脂肪性肝(NAFL)患者糖代谢异常及代谢综合征(MS)的伴随情况,探讨NAFL与MS的关系。方法测量NAFL组(118例)和对照组(56例)的形体参数、血压、血脂谱、OGTT等,MS采用NCEP-ATPⅢ定义。结果NAFL组糖代谢异常的比率达43·2%,明显高于对照组12·5%(P<0·01)。NAFL组中MS伴有率明显高于对照组(31·4%vs5·4%,P=0·000)。Logistic回归分析显示2hPG、NAFL、肥胖家族史是MS的独立危险因素。以NAFL取代MS五个组分中的任何一个后,与原诊断定义相比一致性均很高(Kappa值均>0·6,P<0·0001)。结论无DM病史的NAFL患者糖代谢异常的比率、MS的伴有率明显增高。NAFL可以作为MS组成成分之一。

合并糖代谢异常的冠心病患者血浆脂联素水平变化及其临床意义

目的:检测脂联素(adiponectin,ADPN)在合并糖代谢异常的冠心病患者血浆中浓度的变化,探讨其临床意义。方法:收集2009年8月至2010年4月在湘雅医院心内科经冠状动脉造影(coronary angiography,CAG)检查证实为冠心病的患者87名,根据糖代谢情况分为单纯冠心病组(coronary heart disease group,CHD组,n=31)、冠心病合并糖耐量异常组(CHD combine with impaired glucose tolerance group,CHD+IGT组,n=28)和冠心病合并糖尿病组(CHDcombine with diabetes mellitus group,CHD+DM组,n=28),另选健康体检者31例为正常对照组(normal control group,NC组)。采用酶联免疫吸附法检测血浆ADPN水平;为所有受试对象测身高、体质量、腰围、血压;测空腹血糖、胰岛素、血脂、高敏C反应蛋白(high-sensitivity C-reactive protein,hs-CRP)、游离脂肪酸(free fatty acid,FFA)和肝、肾功能等,计算体质量指数(body mass index,BMI)和胰岛素抵抗指数(homeostasis model assessment for insulin resistance,HOMA-IR)。结果:1)CHD组、CHD+IGT组、CHD+DM组患者血浆ADPN水平均低于NC组(P<0.05);2)与CHD组相比,CHD+DM组ADPN水平最低,CHD+IGT组次之,各组间差异有统计学意义(P<0.05);3)ADPN与HDL-C呈正相关(r=0.483,P<0.01),与hs-CRP和冠脉Gensini积分呈负相关(r=–0.489,P<0.05;r=–0.252,P<0.05)。结论:冠心病患者血浆ADPN浓度降低;合并糖代谢异常的冠心病患者血浆ADPN浓度更低,且随着糖代谢异常程度加重降低更显著;冠心病与糖代谢异常是影响血浆ADPN浓度改变的两个重要因素,血浆ADPN水平显著降低反映了上述两种疾病状态的叠加作用。ADPN联合HDL-C,hs-CRP,Gensini积分等血清学指标可为判断合并糖代谢异常的冠心病患者的疾病严重程度提供一定参考。