Obesity,Fasting Plasma Insulin,and C‐Reactive Protein Levels in Healthy Children

Objective: Obesity is associated with hyperinsulinemia and increased level of C‐reactive protein in older children and adults, but little is known about these relationships in very young children. We examined these relationships in healthy 2‐ to 3‐year‐old children. Research Methods and Procedures: Analyses were performed on data from 491 healthy 2‐ to 3‐year‐old Hispanic children enrolled in a dietary study conducted in New York City, 1992 to 1995. Results: Body mass index (BMI), ponderal index, and sum of four skinfolds were highly correlated (r > 0.75) in both boys and girls. Fasting insulin and glucose levels were only modestly correlated (r = 0.37 for boys and r = 0.28 for girls; p < 0.001 for both), but essentially all of the variability in a calculated index of insulin resistance was attributable to variability in fasting insulin level. The correlations of BMI with fasting insulin level were r = 0.16 (p < 0.05) in boys and r = 0.14 (p < 0.05) in girls. In separate multivariate regression analyses adjusting for age and sex, BMI and ponderal index were associated with fasting plasma insulin level (p < 0.001 for both obesity measures). In multivariate regression analyses adjusting simultaneously for age, sex, and either BMI or ponderal index, fasting insulin level, but not these obesity measures, was associated with C‐reactive protein level. Discussion: Obesity is associated with higher fasting insulin level, and fasting insulin is associated with C‐reactive protein level, in healthy 2‐ to 3‐year‐old children.     

High‐Sensitivity C‐Reactive Protein in Japanese Patients with Type 2 Diabetes

Objective: To assess the relationship between high‐sensitivity (HS) C‐reactive protein (CRP) and metabolic syndrome (MetS) or atherosclerosis and to assess effects of strict metabolic control on the degree of inflammation and MetS in patients with type 2 diabetes. Research Methods and Procedures: Four hundred thirteen patients with diabetes were enrolled in the cross‐sectional study. Of these 413 patients, 161 patients were further admitted for 2.4 ± 0.4 weeks (mean ± SD) to investigate the change in HS‐CRP or other parameters under strict metabolic control. Results: Log‐transformed HS‐CRP value (log HS‐CRP) was strongly correlated with BMI (r = 0.448, p < 0.01). Log HS‐CRP was also correlated with the presence of MetS or each component of MetS. Furthermore, a positive significant trend in HS‐CRP levels was shown with an increasing number of MetS components (p < 0.05). Log HS‐CRP showed a significant positive correlation with carotid artery intima‐media thickness (IMT) (r = 0.152, p < 0.01). In multiple step‐wise regression analysis, BMI, hemoglobin A_1c, right IMT, duration of diabetes, and triglyceride were selected as explanatory variables for log HS‐CRP (R² = 0.412). Under strict metabolic control, HS‐CRP was significantly (p < 0.01) lower, together with lower levels of other markers for MetS. The change in HS‐CRP was significantly correlated with the change in BMI (r = 0.161, p = 0.04). Discussion: In subjects with type 2 diabetes, HS‐CRP levels are related to MetS and subclinical atherosclerosis. Strict weight management and metabolic control were associated with a reduction in HS‐CRP levels, and changes in HS‐CRP were related to changes in weight, supporting the hypothesis that lifestyle modification reduces inflammation and the risk of CHD.     

Association between high‐sensitivity C‐reactive protein,lipoprotein‐associated phospholipase A2 and carotid atherosclerosis: A cross‐sectional study

High‐sensitivity C‐reactive protein (hs‐CRP) and lipoprotein‐associated phospholipase A2 (Lp‐PLA2) have been reported to be independent predictors of atherosclerosis. However, whether the combination of these two markers can improve the prediction of atherosclerosis is unknown. This study aimed to evaluate the association between combining hs‐CRP and Lp‐PLA2 and predicting carotid atherosclerosis. A total of 1982 participants aged ≥40 years were included in this study. Hs‐CRP and Lp‐PLA2 were measured by a high‐sensitivity nephelometry assay and quantitative sandwich enzyme‐linked immunosorbent assay, respectively. Ultrasonography was performed on the bilateral carotid arteries to evaluate stenosis and plaques. Multivariable logistic regression models were used to analyse the association between the combination of the hs‐CRP and Lp‐PLA2 levels and carotid plaques and stenosis. A total of 1579 (79.7%) and 181 (9.1%) subjects had carotid plaques and carotid stenosis, respectively. The group with high hs‐CRP and Lp‐PLA2 levels had the highest prevalence of carotid plaques (90.6%) and stenosis (20.8%). A significant association was found between high hs‐CRP and Lp‐PLA2 levels and carotid stenosis (adjusted odds ratio [OR]: 2.39; 95% confidence interval [CI]: 1.13‐5.09), but this combination was not associated with carotid plaques (OR: 2.62, 95% CI: 0.93‐7.38). The results suggested that the combination of hs‐CRP and Lp‐PLA2 were better predictors than either protein alone with regard to carotid atherosclerosis.     

Association of plasma acylcarnitines with insulin sensitivity, insulin secretion,and prediabetes in a biracial cohort

The ability to predict prediabetes, which affects ∼90 million adults in the US and ∼400 million adults worldwide, would be valuable to public health. Acylcarnitines, fatty acid metabolites, have been associated with type 2 diabetes risk in cross-sectional studies of mostly Caucasian subjects, but prospective studies on their link to prediabetes in diverse populations are lacking. Here, we determined the association of plasma acylcarnitines with incident prediabetes in African Americans and European Americans enrolled in a prospective study. We analyzed 45 acylcarnitines in baseline plasma samples from 70 adults (35 African-American, 35 European-American) with incident prediabetes (progressors) and 70 matched controls (non-progressors) during 5.5-year (mean 2.6 years) follow-up in the Pathobiology of Prediabetes in a Biracial Cohort (POP-ABC) study. Incident prediabetes (impaired fasting glucose/impaired glucose tolerance) was confirmed with OGTT. We measured acylcarnitines using tandem mass spectrometry, insulin sensitivity by hyperinsulinemic euglycemic clamp, and insulin secretion using intravenous glucose tolerance test. The results showed that progressors and non-progressors during POP-ABC study follow-up were concordant for 36 acylcarnitines and discordant for nine others. In logistic regression models, beta-hydroxy butyryl carnitine (C4-OH), 3-hydroxy-isovaleryl carnitine/malonyl carnitine (C5-OH/C3-DC), and octenoyl carnitine (C8:1) were the only significant predictors of incident prediabetes. The combined cut-off plasma levels of <0.03 micromol/L for C4-OH, <0.03 micromol/L for C5-OH/C3-DC, and >0.25 micromol/L for C8:1 acylcarnitines predicted incident prediabetes with 81.9% sensitivity and 65.2% specificity. Thus, circulating levels of one medium-chain and two short-chain acylcarnitines may be sensitive biomarkers for the risk of incident prediabetes among initially normoglycemic individuals with parental history of type 2 diabetes.     

An SNP in the Adiponectin Gene Is Associated with Decreased Serum Adiponectin Levels and Risk for Impaired Glucose Tolerance

Adiponectin is a plasma protein produced by the adipose tissue. Hypoadiponectinemia has been associated with insulin resistance and several components of the metabolic syndrome (MS): type 2 diabetes, obesity, and dyslipidemia. We investigated whether single nucleotide polymorphisms (SNPs) at positions 45 and 276 in the adiponectin gene were associated with features of the MS in 747 unrelated Spanish subjects. The G allele of SNP45 and the G/G genotype of SNP276 were associated with impaired glucose tolerance (p = 0.020 and 0.042, respectively). The G/G genotype for SNP276 was associated with lower serum adiponectin levels as compared with the G/T and T/T genotypes (G/G, 10.10 ± 0.24 μg/mL; G/T, 10.98 ± 0.32 μg/mL; T/T, 12.00 ± 0.92 μg/mL; p = 0.015) even after adjustment for sex, age, BMI, waist‐to‐hip ratio, homeostasis model assessment index, and the degree of glucose tolerance (p = 0.040). We found a significant negative association of circulating adiponectin levels with waist‐to‐hip ratio (r = ?0.42, p < 0.001), sagittal abdominal diameter (r = ?0.24, p < 0.001), triglycerides (r = ?0.32, p < 0.001), homeostasis model assessment index (r = ?0.14, p = 0.001), and uric acid (r = ?0.36, p < 0.001) and positive association with high‐density lipoprotein‐cholesterol (r = 0.41, p < 0.001). Our findings indicate that serum adiponectin levels are associated with several components of the MS. The SNP276 of the adiponectin gene may affect impaired glucose tolerance and hypoadiponectinemia.     

Hsp74/14‐3‐3σ Complex Mediates Centrosome Amplification by High Glucose,Insulin, and Palmitic Acid

It has been reported recently that type 2 diabetes promotes centrosome amplification via 14‐3‐3σ/ROCK1 complex. In the present study, 14‐3‐3σ interacting proteins are characterized and their roles in the centrosome amplification by high glucose, insulin, and palmitic acid are investigated. Co‐immunoprecipitation in combination with MS analysis identified 134 proteins that interact with 14‐3‐3σ, which include heat shock 70 kDa protein 4 (Hsp74). Gene ontology analyses reveal that many of them are enriched in binding activity. Kyoto Encyclopedia of Genes and Genomes analysis shows that the top three enriched pathways are ribosome, carbon metabolism, and biosynthesis of amino acids. Molecular and functional investigations show that the high glucose, insulin, and palmitic acid increase the expression and binding of 14‐3‐3σ and Hsp74 as well as centrosome amplification, all of which are inhibited by knockdown of 14‐3‐3σ or Hsp74. Moreover, molecular docking analysis shows that the interaction between the 14‐3‐3σ and the Hsp74 is mainly through hydrophobic contacts and a lesser degree ionic interactions and hydrogen bond by different amino acids residues. In conclusion, the results suggest that the experimental treatment triggers centrosome amplification via upregulations of expression and binding of 14‐3‐3σ and Hsp74.     

Circulating miR‐145 is associated with plasma high‐sensitivity C‐reactive protein in acute ischemic stroke patients

Stroke is a major cerebrovascular disease threatening human health and life with high morbidity, disability and mortality. We aimed to find effective biomarkers for the early diagnosis on stroke. Nine previously reported stroke‐associated miRNAs (miR‐21, miR‐23a, miR‐29b, miR‐124, miR‐145, miR‐210, miR‐221, miR‐223 and miR‐483‐5p) were measured by quantitative real time‐PCR, and plasma high‐sensitivity C‐reactive protein (hs‐CRP) and serum interleukin 6 (IL‐6), the pro‐inflammation markers in brain injury, were examined by enzyme‐linked immunosorbent assay in 146 acute ischemic stroke patients and 96 healthy blood donors. We found that serum miR‐145 was significantly increased within 24 h after stroke onset and serum miR‐23a and miR‐221 were decreased in patients. Moreover, serum miR‐145 was strong positively correlated with plasma hs‐CRP and moderate positively correlated with serum IL‐6. Meanwhile, serum miR‐23a and miR‐221 were moderate negatively correlated with plasma hs‐CRP but not serum IL‐6. Importantly, the combination of hs‐CRP and serum miR‐145 gained a better sensitivity/spectivity for prediction of acute ischemia stroke (area under receiver operating characteristic curve from 0.794 to 0.896). Conclusively, our preliminary findings indicate that serum miR‐145 upregulated in acute ischemic stroke might be a new biomarker for acute ischemia stroke evaluation. Copyright © 2015 John Wiley & Sons, Ltd.     

Effect of Glucose Tolerance Status on PAI‐1 Plasma Levels in Overweight and Obese Subjects

Objective: The aim of our study was to examine whether plasminogen activator inhibitor‐1 (PAI‐1) plasma levels varied as a function of differences in glucose tolerance status independently of body fatness, body‐fat distribution, and insulin sensitivity. Research Methods and Procedures: Plasma PAI‐1 antigen levels, along with insulin resistance [measured by homeostatic model assessment (HOMA_IR)], central fat accumulation, body composition, blood pressure, and fasting concentrations of glucose, insulin, and lipids, were measured in 229 overweight and obese [body mass index (BMI) ≥25 kg/m²) subjects with normal glucose tolerance (NGT) and in 44 age‐ and BMI‐matched subjects with impaired glucose tolerance (IGT). Results: Plasma PAI‐1 antigen levels were significantly higher in IGT than in NGT subjects. Log PAI‐1 was positively correlated with BMI, HOMA_IR, and log insulin, and inversely associated with high‐density lipoprotein‐cholesterol both in IGT and in NGT individuals. On the other hand, log PAI‐1 was positively correlated with waist circumference, fat mass (FM), fat‐free mass, systolic and diastolic blood pressure, and log triglycerides only in the NGT group. After multivariate analyses, the strongest determinants of PAI‐1 levels were BMI, FM, waist circumference, and high‐density lipoprotein cholesterol in the NGT group and only HOMA_IR in the IGT cohort. Discussion: This study demonstrates that PAI‐1 concentrations are higher in IGT than in NGT subjects. Furthermore, we suggest that the influences of total adiposity, central fat, and insulin resistance, main determinants of PAI‐1 concentrations, are different according to the degree of glucose tolerance.     

An Approach to Incorporate Multi‐Enzyme Digestion into C‐TAILS for C‐Terminomics Studies

Protein C‐termini study is still a challenging task and far behind its counterpart, N‐termini study. MS based C‐terminomics study is often hampered by the low ionization efficiency of C‐terminal peptides and the lack of efficient enrichment methods. We previously optimized the C‐terminal amine‐based isotope labeling of substrates (C‐TAILS) method and identified 369 genuine protein C‐termini in Escherichia coli. A key limitation of C‐TAILS is that the prior protection of amines and carboxylic groups at protein level makes Arg‐C as the only specific enzyme in practice. Herein, we report an approach combining multi‐enzyme digestion and C‐TAILS, which significantly increases the identification rate of C‐terminal peptides and consequently improves the applicability of C‐TAILS in biological studies. We carry out a systematic study and confirm that the omission of the prior amine protection at protein level has a negligible influence and allows the application of multi‐enzyme digestion. We successfully apply five different enzyme digestions to C‐TAILS, including trypsin, Arg‐C, Lys‐C, Lys‐N, and Lysarginase. As a result, we identify a total of 722 protein C‐termini in E. coli, which is at least 66% more than the results using any single enzyme. Moreover, the favored enzyme and enzyme combination are discovered. Data are available via ProteomeXchange with identifier PXD004275.     

TAZ Is a Negative Regulator of PPARγ Activity in Adipocytes and TAZ Deletion Improves Insulin Sensitivity and Glucose Tolerance

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Glucose‐6‐phosphate dehydrogenase is posttranslationally regulated in the larvae of the freeze‐tolerant gall fly,Eurosta solidaginis,in response to freezing

The freeze‐tolerant larvae of the goldenrod gall fly (Eurosta solidaginis) undergo substantial alterations to their molecular physiology during the winter including the production of elevated quantities of glycerol and sorbitol, which function as cryoprotectants to survive whole body freezing. Production of these cryoprotectants depends on cytosolic pools of nicotinamide adenine dinucleotide phosphate H (NADPH), a major source being the pentose phosphate pathway (PPP). Glucose‐6‐phosphate dehydrogenase (G6PDH) mediates the rate‐limiting and committed step of the PPP and therefore its molecular properties were explored in larvae sampled from control versus frozen states. G6PDH was purified from control (5°C) and frozen (?15°C) E. solidaginis larvae by a single‐step chromatography method utilizing 2′,5′‐ADP agarose and analyzed to determine its enzymatic parameters. Studies revealed a decrease in K_m for G6P in the frozen animals (to 50% of control values) suggesting an increased flux through the PPP. Immunoblotting of the purified enzyme showed differences in the relative extent of several posttranslational modifications, notably ubiquitination (95% decrease in frozen larvae), cysteine nitrosylation (61% decrease), threonine (4.1 fold increase), and serine phosphorylation (59% decrease). Together these data suggested that the increased flux through the PPP needed to generate NADPH for cryoprotectants synthesis is regulated, at least in part, through posttranslational alterations of G6PDH.     

SPR‐based plastic optical fibre biosensor for the detection of C‐reactive protein in serum

A plastic optical fibre biosensor based on surface plasmon resonance for the detection of C‐reactive protein (CRP) in serum is proposed. The biosensor was integrated into a home‐made thermo‐stabilized microfluidic system that allows avoiding any thermal and/or mechanical fluctuation and maintaining the best stable conditions during the measurements. A working range of 0.006–70 mg L^–1 and a limit of detection of 0.009 mg L^–1 were achieved. These results are among the best compared to other SPR‐based biosensors for CRP detection, especially considering that they were achieved in a real and complex medium, i.e. serum. In addition, since the sensor performances satisfy those requested in physiologically‐relevant clinical applications, the whole biosensing platform could well address high sensitive, easy to realize, real‐time, label‐free, portable and low cost diagnosis of CRP for future lab‐on‐a‐chip applications.

3D sketch (left) of the thermo‐stabilized home‐made flow cell developed to house the SPR‐based plastic optical fibre biosensor. Exemplary response curve (shift of the SPR wavelength versus time) of the proposed biosensor (right) for the detection of C‐reactive protein in serum.     

The effects of the dietary glycemic load on type 2 diabetes risk factors during weight loss

Objective: To compare the effects of two calorie-restricted diets that differ in glycemic load (GL) on glucose tolerance and inflammation. Research Methods and Procedures: Thirty-four healthy overweight adults, ages 24 to 42 years, were randomized to 30% provided calorie-restricted diets with high (HG) or low (LG) glycemic load for 6 months. Outcomes were changes in glucose-insulin dynamics and C-reactive protein (CRP) levels. Results: Compared with baseline, levels of fasting insulin, homeostasis model assessment of insulin resistance, post-load insulin at 30 minutes, and incremental area-under-the-curve-insulin during the oral glucose tolerance test were significantly lower in both groups at 6 months (p range, 0.01 to 0.05), but after adjustment for baseline values and weight change, there were no differences between the two groups with regard to changes over time in any parameter. The mean percentage change in insulin sensitivity by a frequently sampled intravenous glucose tolerance test was +26% in the HG group and +24% in the LG group (p = 0.83); first-phase acute insulin release was −20% in the HG group and −21% in the LG group (p = 0.77). More participants on the LG diet (14 of 16 subjects) had a decline in serum CRP, compared with those on the HG diet (7 of 16 subjects) (p < 0.05). Discussion: In healthy overweight adults provided with food for 6 months, the dietary GL did not seem to influence chronic adaptations in glucose-insulin dynamics above that associated with weight loss. This finding highlights the importance of absolute weight loss over the dietary macronutrient composition used to achieve weight loss. The finding of greater declines in CRP concentration after consumption of a low-GL diet warrants further investigation.     

Plasma Adiponectin Levels in High Risk African‐Americans with Normal Glucose Tolerance,Impaired Glucose Tolerance,and Type 2 Diabetes**

Objective: We studied plasma adiponectin, insulin sensitivity, and insulin secretion before and after oral glucose challenge in normal glucose tolerant, impaired glucose tolerant, and type 2 diabetic first degree relatives of African‐American patients with type 2 diabetes. Research Methods and Procedures: We studied 19 subjects with normal glucose tolerance (NGT), 8 with impaired glucose tolerance (IGT), and 14 with type 2 diabetes. Serum glucose, insulin, C‐peptide, and plasma adiponectin levels were measured before and 2 hours after oral glucose tolerance test. Homeostasis model assessment‐insulin resistance index (HOMA‐IR) and HOMA‐β cell function were calculated in each subject using HOMA. We empirically defined insulin sensitivity as HOMA‐IR < 2.68 and insulin resistance as HOMA‐IR > 2.68. Results: Subjects with IGT and type 2 diabetes were more insulin resistant (as assessed by HOMA‐IR) when compared with NGT subjects. Mean plasma fasting adiponectin levels were significantly lower in the type 2 diabetes group when compared with NGT and IGT groups. Plasma adiponectin levels were 2‐fold greater (11.09 ± 4.98 vs. 6.42 ± 3.3811 μg/mL) in insulin‐sensitive (HOMA‐IR, 1.74 ± 0.65) than in insulin‐resistant (HOMA‐IR, 5.12 ± 2.14) NGT subjects. Mean plasma adiponectin levels were significantly lower in the glucose tolerant, insulin‐resistant subjects than in the insulin sensitive NGT subjects and were comparable with those of the patients with newly diagnosed type 2 diabetes. We found significant inverse relationships of adiponectin with HOMA‐IR (r = ?0.502, p = 0.046) and with HOMA‐β cell function (r = ?0.498, p = 0.042) but not with the percentage body fat (r = ?0.368, p = 0.063), serum glucose, BMI, age, and glycosylated hemoglobin A1C (%A1C). Discussion: In summary, we found that plasma adiponectin levels were significantly lower in insulin‐resistant, non‐diabetic first degree relatives of African‐American patients with type 2 diabetes and in those with newly diagnosed type 2 diabetes. We conclude that a decreased plasma adiponectin and insulin resistance coexist in a genetically prone subset of first degree African‐American relatives before development of IGT and type 2 diabetes.     

Clinical association of metabolic syndrome,C‐reactive protein and testosterone levels with clinically significant prostate cancer

Recently, the influence that metabolic syndrome (MetS), hormonal alterations and inflammation might have on prostate cancer (PCa) risk has been a subject of controversial debate. Herein, we aimed to investigate the association between MetS‐components, C‐reactive protein (CRP) and testosterone levels, and the risk of clinically significant PCa (Sig‐PCa) at the time of prostate biopsy. For that, men scheduled for transrectal ultrasound guided biopsy of the prostate were studied. Clinical, laboratory parameters and criteria for MetS characterization just before the biopsy were collected. A total of 524 patients were analysed, being 195 (37.2%) subsequently diagnosed with PCa and 240 (45.8%) meet the diagnostic criteria for MetS. Among patients with PCa, MetS‐diagnosis was present in 94 (48.2%). Remarkably, a higher risk of Sig‐PCa was associated to MetS, greater number of MetS‐components and higher CRP levels (odds‐ratio: 1.83, 1.30 and 2.00, respectively; P < 0.05). Moreover, higher circulating CRP levels were also associated with a more aggressive Gleason score in PCa patients. Altogether, our data reveal a clear association between the presence of MetS, a greater number of MetS‐components or CRP levels >2.5 mg/L with an increased Sig‐PCa diagnosis and/or with aggressive features, suggesting that MetS and/or CRP levels might influence PCa pathophysiology.     

Reciprocal Contribution of Pentraxin 3 and C‐Reactive Protein to Obesity and Metabolic Syndrome

Pentraxin 3 (PTX3) is an acute‐phase protein that shares structural homology with C‐reactive protein (CRP). PTX3 is produced in macrophages, endothelial cells, and adipocytes in response to inflammatory stimuli, whereas hepatocytes are the main source of CRP. Because obesity and metabolic syndrome (MetS) are considered chronic inflammatory states, PTX3 might be involved in the pathogenesis of obesity and MetS as well as CRP. Levels of CRP correlated positively with body weight, BMI, waist circumference (WC), fasting plasma glucose and interleukin (IL)‐6, and negatively with high‐density lipoprotein cholesterol and adiponectin in healthy males. In contrast, PTX3 correlated positively with adiponectin, and negatively with body weight, BMI, WC, and triglyceride. Plasma CRP significantly increased, whereas plasma PTX3 significantly decreased with increasing BMI. Plasma CRP and PTX3 levels were significantly higher and lower, respectively, in individuals who had more than one MetS component compared with those who had none. In conclusion, PTX3 and CRP antagonistically participate in the development of obesity or MetS.     

冠心病患者血清尿酸、高敏C 反应蛋白、纤维蛋白原水平变化 的临床研究

目的:观察冠心病患者血清中尿酸、高敏C反应蛋白、纤维蛋白原水平的变化.方法:选取2010年11月至2011年11月于我院就诊的68例冠心病患者(稳定型心绞痛21例,不稳定型心绞痛24例,急性心肌梗死13例)作为研究对象,并选取同期于我院体检中心体检的62例健康人为对照组,检测受试者血清中尿酸、高敏C反应蛋白、纤维蛋白原的水平.结果:研究组患者血清中UA、CRP和FBG水平显著高于对照组(P＜0.05).与稳定型心绞痛组比,不稳定型心绞痛的CRP水平增高(5.34±1.98 mg/L vs.11.36±2.73 mg/L,P＜0.05),急性心肌梗死组的UA (345.63±86.4 μmol/L vs.493.76±101.2 μmol/L,P＜0.05)、CRP (5.34±1.98mg/L vs.21.3±2.24 mg/L,P＜0.05)和FBG(3.86±1.34 g/L vs.6.85±2.36 g/L,P＜0.05)水平显著增高,与不稳定型心绞痛组比,急性心肌梗死组的UA(378.91±89.7 μmol/L vs.493.76±101.2 μmol/L,P＜0.05)、CRP(11.36±2.73 mg/L vs.21.3±2.24 mg/L,P＜0.05)和FBG(4.27±2.08 g/L vs.6.85±2.36 g/L,P＜0.05)水平显著增高(P＜0.05).结论:冠心病患者血清中尿酸、高敏C反应蛋白和纤维蛋白原的水平升高,3个指标可用于评估治疗效果和预后.     

血清镁、血小板聚集率在糖耐量减低患者微血管病变中的临床意义

目的:观察糖耐量减低患者微血管病变与血清镁、血小板聚集率(PAR)的相关性。方法:将2012年11月-2014年1月在本院内分泌科和体检中心的120例研究对象随机均分为糖耐量减低合并微血管病变组(n=30),糖耐量减低无微血管病变组(n=30),糖尿病组(n=30),正常对照组(n=30)。比较各组患者的生化指标、血清镁与PAR的相关性、血镁水平以及PAR与FPG、HbA1C相关性。结果:糖尿病组和糖耐量减低合并微血管病变组患者的所有生化指标与对照组相比,差异有显著性(P0.05);血清镁水平与PAR之间呈显著负相关(P0.01);血镁水平与糖耐量减低合并微血管病变组、糖耐量减低无微血管病变组、糖尿病组中FPG、HbA1C呈负相关关系(P0.05);PAR与糖耐量减低合并微血管病变组、糖耐量减低无微血管病变组、糖尿病组中FPG、HbA1C呈正相关关系(P0.05)。结论:血清镁与PAR在预测糖耐量患者微血管病变中有一定的临床意义,值得临床推广。