抗坏血酸对NIDDM患者红细胞山梨醇的影响

对２７例ＮＩＤＤＭ患者血浆抗坏血酸及红细胞山梨醇含量进行了测定，并观察了口服抗坏血酸对ＮＩＤＤＭ患者红细胞山梨醇的影响。提示ＮＩＤＤＭ患者抗坏血酸代谢紊乱是造成山梨醇在一些组织异常增高的原因之一，补充抗坏血酸有助于纠正ＮＩＤＤＭ患者多元醇代谢的异常。     

Caloric restriction counteracts age-related changes in the activities of sorbitol metabolizing enzymes from mouse liver

The influence of caloric restriction (CR) on hepatic sorbitol-metabolizing enzyme activities was investigated in young and old mice. Aldose reductase and sorbitol dehydrogenase activities were significantly lower in old CR mice than in old controls. Young CR mice showed decreased aldose reductase activity and a trend towards decreased sorbitol dehydrogenase when compared to controls. Metabolites of the pathway, namely sorbitol, glucose and fructose were decreased by CR in young and old mice. Pyruvate levels were decreased by CR in both young and old mice, while lactate decreased only in old CR. Malate levels increased in old CR but remained unchanged in young CR, when compared with controls. Accordingly, the lactate/pyruvate and malate/pyruvate ratios in young and old CR mice were increased, indicating increased NADH/NAD and NADPH/NADP redox couples, respectively. The results indicate that decreased glucose levels under CR conditions lead to decreased sorbitol pathway enzyme activities and metabolite levels, and could contribute to the beneficial effects of long-term CR through decreased sorbitol levels and NADPH sparing.     

Effects of exercise and ethanol ingestion on platelet thromboxane release in healthy men

We studied the effects of repeated bicycle exercises and ethanol ingestion (1.5 g/kg) on platelet aggregation and thromboxane (TxB2) release in 10 healthy male volunteers. After a bicycle exercise performed in the morning, the adenosine diphosphate (ADP)-induced platelet aggregation and the aggregation-associated thromboxane release were found to be decreased in fasting men. In contrast, after ingestion of fruit juice and a second exercise at noon, platelet aggregation and thromboxane release were increased. These latter changes were negligible when ethanol was ingested together with fruit juice. A third exercise, performed in the evening, again caused a decrease in the aggregation and associated thromboxane release during the control session, but provoked an increase during the ethanol session. Exercise increased the urinary excretion of 2,3-dinor-6-keto-PGF1 alpha. Changes in the plasma arachidonic acid (AA) concentration probably influenced the platelet thromboxane release. The results suggest that both physical exercise and ingestion of ethanol in fruit juice influence the ADP-stimulated platelet thromboxane release.     

筋脉通对糖尿病大鼠坐骨神经传导速度、醛糖还原酶及山梨醇浓度的影响

目的观察中药复方筋脉通对糖尿病大鼠坐骨神经传导速度、坐骨神经组织和红细胞内醛糖还原酶活性(AR)及山梨醇(SNS)浓度的影响,并探讨其作用机理。方法采用链脲佐菌素(STZ)糖尿病(DM)大鼠模型,给予中药复方筋脉通灌胃,并以氨基胍为对照,疗程8周。观察该制剂对糖尿病大鼠坐骨神经传导速度、坐骨神经组织和红细胞醛糖还原酶活性(AR)及对山梨醇(SNS)浓度的影响。结果经筋脉通治疗后,糖尿病大鼠坐骨神经传导速度增快,坐骨神经和红细胞SNS浓度、坐骨神经AR明显降低,和对照组比较有显著性差异(P<0.05～0.01)。红细胞内AR有降低的趋势,但无统计学意义。对血糖有下降作用。结论提示筋脉通对改善糖尿病神经病变有一定的疗效。     

Effects of short-term overfeeding with fructose,fat and fructose plus fat on plasma and hepatic lipids in healthy men

AimsThe present study aimed to assess the effects of excess fat, fructose and fat-plus-fructose intakes on intrahepatocellular lipid (IHCL).MethodsHealthy male subjects were studied after an isocaloric diet or a 7-day high-fructose (Fru: +3.5 g fructose/kg fat-free mass/day, +35% energy), high-fat (Fat: +30% energy as saturated-fat) or high-fructose, high-fat diet (FruFat: +3.5 g fructose/kg fat-free mass/day, +30% energy as fat, +65% total energy). IHCL was measured by ¹H magnetic resonance spectroscopy.ResultsAll hypercaloric diets increased IHCL (Fru: +16%; Fat: +86%; FruFat: +133%; P < 0.05). Very low-density lipoprotein (VLDL) triacylglycerols increased after Fru (+58%; P < 0.05), but decreased after Fat (−22%; P < 0.05), while no change was observed after FruFat.ConclusionFat and fructose both increased IHCL, but fructose increased, while fat decreased, VLDL triacylglycerols. However, excess fat and fructose combined had additive effects on IHCL and neutralizing effects on VLDL triglycerides. This suggests that fructose stimulates, while fat inhibits, hepatic VLDL triacylglycerol secretion.     

参麦活血饮对糖尿病大鼠坐骨神经和红细胞山梨醇水平及神经功能的影响

目的 探讨糖尿病（DM）大鼠坐骨神经和红细胞山梨醇含量与神经功能之间的关系。观察参麦活血饮进行短期干预的作用和可能机制。方法 采用链脲佐菌素诱发DM大鼠模型。造模1周后用中成药参麦活血饮（成分为红参，麦冬，红花）治疗。用药4周后测定神经电生理，坐骨神经和红细胞山梨醇水平。结果 DM大鼠神经传导速度减慢，坐骨神经和红细胞山梨醇水平升高；经参麦活血饮治疗后上述改变减轻。同时，红细胞和坐骨神经山梨醇水平呈正相关；感觉神经传导速度与坐骨神经和红细胞山梨醇水平呈负相关，H反射与坐骨神经和红细胞山梨醇水平呈正相关。运动神经传导速度与坐骨神经和红细胞山梨醇水平无明显相关。结论 DM时红细胞山梨醇水平可反映坐骨神经山梨醇水平，亦能反映周围神经的病变程度，中药参麦活血饮可明显缓解DM大鼠周围神经的早期病变。     

1-磷酸鞘氨醇受体3在心血管系统中的作用

1-磷酸鞘氨醇受体是1-磷酸鞘氨醇在细胞内发挥作用的重要靶点,包括5种亚型,广泛存在于包括心血管系统在内的各系统。近年来,许多研究发现1-磷酸鞘氨醇受体3在血管舒张、血管屏障功能、缺血再灌注损伤和动脉粥样硬化等过程中具有重要的生物学作用。现就1-磷酸鞘氨醇受体3在心血管系统中的作用及其机制做一综述。     

Erythrocyte membrane n-3 fatty acid levels and carotid atherosclerosis in Chinese men and women

Objective

Prospective studies have supported the beneficial effects of n-3 fatty acid consumption on cardiac deaths, but limited data focused on atherosclerosis. We investigated the associations between n-3 fatty acids in erythrocytes and atherosclerosis in middle-aged and older Chinese.

Methods

847 subjects (285 men and 562 women), aged 40–65 years, from Guangzhou, China were included in this community-based cross-sectional study between December 2005 and January 2008. The levels of α-linolenic acid (ALA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in erythrocytes were measured by gas chromatography. Carotid ultrasound examination was conducted to obtain intima–media thickness of the common carotid artery and the carotid bifurcation. Dietary data and other covariates were collected using interviewer-administered questionnaires.

Results

After adjustment for age, sex, and other confounders, negative dose–response associations between the contents of individual n-3 polyunsaturated fatty acids in the erythrocyte membrane and the prevalence of carotid artery wall thickening and plaque were observed. A comparison in the highest and lowest tertiles gave odds ratios (95% confidence interval) for thickening in the walls of the common carotid artery of 0.58 (0. 34–0.97; P-trend = 0. 037) for DHA, and 0.39 (0.23–0.67; P-trend < 0.001) for ALA. However, EPA was not significantly associated with carotid atherosclerosis. Similar results were found for thickening at the carotid bifurcation and the occurrence of carotid artery plaque.

Conclusions

Higher levels of DHA and ALA in the erythrocyte membrane were significantly associated with a lower burden of subclinical atherosclerosis.     

华支睾吸虫3-磷酸甘油醛脱氢酶重组蛋白的纯化、酶学活性及免疫学研究

目的体外制备华支睾吸虫3-磷酸甘油醛脱氢酶重组蛋白(CsGAPDH),分析其酶学活性及免疫学特性。方法常规表达重组质粒pGEX-4T-1-GAPDH,用谷胱甘肽-S-转移酶(GST)亲和纯化试剂盒纯化重组蛋白,经十二烷基磺酸钠-聚丙烯酰胺凝胶电泳(SDS-PAGE),用凝血酶和纯化柱酶切、纯化的CsGAPDH免疫BALB/c小鼠,制备抗血清。ELISA检测抗IgG抗体滴度,浓缩型S-P免疫组化3步法检测CsGAPDH抗原在免疫小鼠体内的分布和表达。蛋白质印迹法(Western blotting)鉴定其抗血清的特异性。建立酶反应体系测定重组蛋白CsGAPDH的酶催化活性。结果纯化蛋白样品呈单一条带。免疫动物获取CsGAPDH抗血清,在免疫过程中抗体滴度呈连续上升趋势。CsGAPDH抗原分布和表达于小鼠肌细胞膜部位。免疫小鼠血清具有抗CsGAPDH特异性抗体。重组蛋白CsGAPDH具有酶生理活性,其酶活力单位为2 872 U min^-1.ml^-1。结论制备的重组蛋白CsGAPD H具有较好的酶活性和免疫原性。     

Effects of low fructose diet on glycemic control,lipid profile and systemic inflammation in patients with type 2 diabetes: A single-blind randomized controlled trial

Background and aimType 2 diabetes is one of the global epidemic disorders, which causes many side effects on the body. Fructose is a lipogenic monosaccharide. Recent studies have reported the adverse effects of this carbohydrate on diabetes. This study aimed to evaluate the clinical efficacy of a low-fructose diet on the metabolic alterations in patients with type 2 diabetes.MethodsThis study was a randomized, single-blind clinical trial on 50 patients with type 2 diabetes. Participants randomly allocated to two groups, to receive either diabetic-diet or diabetic-diet with low-fructose for 8-weeks. Anthropometric measurements, systolic blood pressure (SBP), Diastolic blood pressure (DBP) and metabolic factors were assessed at baseline and the end of the trial.ResultsAt the end of trial, reduction in body weight, waist circumference, and blood pressure were not significant except for DBP (P = 0.013). Statistical analysis showed that low-fructose diet compared to control group significantly declined fasting blood glucose (FBG), Hemoglobin A1c (HbA1c), Triglyceride (TG), high-density lipoprotein-cholesterol (HDL-C) and high-sensitivity C-reactive protein (hs-CRP) (P = 0.015, P = 0.001, P=<0.0001, P= <0.0001 and P= <0.0001 respectively).ConclusionOur results showed that eight weeks of low-fructose diet results in a significant improvement in FBG, HbA1c, TG, HDL-C and hs-CRP in patients with type 2 diabetes.     

阿托伐他汀在1-磷酸鞘氨醇诱导心肌细胞肥大中的作用

目的研究阿托伐他汀对1-磷酸鞘氨醇(S1P)诱导乳鼠心肌细胞肥大反应中的作用。方法原代培养乳鼠心肌细胞,测定心肌细胞体积和[3H]-亮氨酸掺入量作为心肌细胞肥大的指标。乳鼠心肌细胞使用不同浓度的阿托伐他汀(atorvastatin),加入S1P,[3H]-亮氨酸掺入量作为心肌细胞蛋白摄取量;分别用qPCR和Western blot法检测心肌细胞的β-肌球蛋白(β-MHC)的mRNA和蛋白质表达水平;用qPCR检测心肌细胞的心房利钠肽(ANF)的mRNA表达水平。结果与S1P组比较,阿托伐他汀10μmol/L处理组[3H]-亮氨酸掺入率减少[(234.89%±31.23%)比(342.23%±31.60%),P=0.205],β-MHC的mRNA和蛋白表达水平下降[(0.59±0.14)比(0.84±0.20),P=0.318]和[(0.55±0.09)比(0.98±0.15),P=0.223],ANF的mRNA表达水平降低[(0.51±0.13)比(0.76±0.19),P=0.445];与S1P组比较,阿托伐他汀20μmol/L处理组[3H]-亮氨酸掺入率明显减少[(189.07%±17.69%)比(342.23%±31.60%),P<0.01],β-MHC的mRNA和蛋白表达水平显著下降[(0.50±0.12)比(0.84±0.20),P<0.01]和[(0.35±0.08)比(0.98±0.15),P<0.01],ANF的mRNA水平明显降低[(0.47±0.12)比(0.76±0.19),P<0.01]。结论阿托伐他汀可抑制S1P诱导的心肌细胞肥大,并可减少S1P诱导的β-MHC和ANF表达。     

Overexpression of mitochondrial FAD-linked glycerol-3-phosphate dehydrogenase does not correct glucose-stimulated insulin secretion from diabetic GK rat pancreatic islets

Summary Glucose-stimulated insulin secretion is impaired in GK (Goto-Kakizaki) rats, perhaps because of abnormalities in glucose metabolism in pancreatic islet beta cells. The glycerol phosphate shuttle plays a major role in glucose metabolism by reoxidizing cytosolic NADH generated by glycolysis. In the pancreatic islets of GK rats, the activity of mitochondrial FAD-linked glycerol-3-phosphate dehydrogenase (mGPDH), the key enzyme of the glycerol phosphate shuttle, is decreased and this abnormality may be responsible, at least in part, for impaired glucose-stimulated insulin secretion. To investigate this possibility, we overexpressed mGPDH in islets isolated from GK rats via recombinant adenovirus-mediated gene transduction, and examined glucose-stimulated insulin secretion. In islets isolated from diabetic GK rats at 8 to 10 weeks of age, glucose-stimulated insulin secretion was severely impaired, and mGPDH activity was decreased to 79 % of that in non-diabetic Wistar rats. When mGPDH was overexpressed in islets from GK rats, enzyme activity and protein content increased 2- and 6-fold, respectively. Basal (3 mmol/l glucose) and glucose-stimulated (20 mmol/l) insulin secretion from the Adex1CAlacZ-infected GK rat islets were, respectively, 4.4 ± 0.7 and 8.1 ± 0.7 ng · islet⁻¹· 30 min⁻¹, and those from mGPDH-overexpressed GK rat islets 4.7 ± 0.3 and 9.1 ± 0.8 ng · islet⁻¹· 30 min⁻¹, in contrast to those from the Adex1CAlacZ-infected non-diabetic Wistar rat islets (4.7 ± 1.6 and 47.6 ± 11.9 ng · islet⁻¹· 30 min⁻¹). Thus, glucose-stimulated insulin secretion is severely impaired in GK rats even in the stage when mGPDH activity is modestly decreased, and at this stage, overexpression of mGPDH cannot restore glucose-stimulated insulin secretion. We conclude that decreased mGPDH activity in GK rat islets is not the defect primarily responsible for impaired glucose-stimulated insulin secretion. [Diabetologia (1998) 41: 649–653] Received: 20 October 1997 and in revised form: 22 December 1997     

周期型马来丝虫3-磷酸甘油醛脱氢酶编码基因的克隆与真核表达

目的 克隆和表达周期型马来丝虫3-磷酸甘油醛脱氢酶(BmGAPDH)的编码基因.方法 依据公布的BmGAPDH基因序列设计引物,以周期型马来丝虫总RNA为模板,反转录PCR(RT-PCR)扩增目的 编码基因.PCR产物经TA克隆后,克隆至载体pGEM-T Easy中,经PCR和双酶切鉴定后,亚克隆至真核表达质粒pcDNA3.1(+),构建真核表达载体pcDNA3.1(+)/BmGAPDH,转染COS-7细胞后进行RT-PCR验证.用十二烷基磺酸钠-聚丙烯酰胺电泳(SDS-PAGE)对获得重组蛋白(rBmGAPDH)进行分析和鉴定.结果 转染的COS-7细胞高水平表达BmGAPDH的mRNA,根据克隆的目的 基因序列推导的氨基酸序列与GenBank登录的结果 一致.SDS-PAGE分析显示重组蛋白rBmGAPDH相对分子质量(Mr)约为43 000.结论 成功进行了BmGAPDH编码基因的克降和真核表达.Cloning,weukaryotic expremion of the gene encoding glyceraidehydes-3-phosphate dehydrogenase from periodic Brugia malayi XIE Dong-fimg,FANG Zheng,HUANG Wei-qun,SHEN Qin,TONG Hai-yan,XUBang-sheng.     

果糖联合高脂饮食对金黄地鼠糖脂代谢的影响

目的通过果糖或葡萄糖联合高脂饮食喂养叙利亚金黄地鼠,比较不同饮食成分喂养对地鼠糖脂代谢的不同影响。方法将金黄地鼠随机分成正常对照组（NC）、高脂组（HF）、果糖高脂组（FRU＋HF）、葡萄糖高脂组（Glu＋HF）,喂养12周,测定体重、血脂、血糖、胰岛素、肝指数,观察肝脏及胰腺形态及组织学变化。结果各高脂喂养组地鼠与对照组比较TC、TG、血糖、LDL-C、HDL-C、肝指数升高,胰岛素水平降低,肝脂肪样变,胰岛增生,其中FRU＋HF组TG、胰岛素敏感性降低,肝指数升高,肝及胰岛病理变化更明显（P〈0．05）。结论果糖高脂喂养的金黄地鼠模型特点为TG显著增高、糖耐量减低、胰岛素抵抗及脂肪肝,更适合作为现代人高果糖高脂饮食导致糖脂代谢紊乱的研究模型。     

The effects of one month high fructose intake on plasma glucose and lipid levels in non-insulin-dependent diabetes

The effects of a high fructose diet on the control of blood glucose and serum lipids were studied in 10 non-insulin-dependent diabetic patients (mean age 64.4 years, mean duration of diabetes 5.6 years). Comparison was made following 28 days on the usual diabetic diet and 28 days during which 25% of the usual carbohydrate was substituted with fructose. There was no change in mean (+/- SEM) fasting plasma glucose (on usual diet 9.2 +/- 0.5 mmol/l, on fructose diet, 9.1 +/- 0.4 mmol/l), but there was a fall in mean plasma glucose levels at 30, 60, and 120 min in a 75 g OGTT following the fructose diet. There was no significant change in fasting lipids: on usual diet mean serum cholesterol 5.8 +/- 0.2 mmol/l, on fructose diet 5.6 +/- 0.2 mmol/l; serum triglyceride, on usual diet 1.3 +/- 0.1 mmol/l, on fructose diet 1.3 +/- 0.1 mmol/l; HDL cholesterol on usual diet 1.4 +/- 0.1 mmol/l, on fructose diet 1.4 +/- 0.1 mmol/l. Mean body weight did not vary significantly between the two diets. Incorporation of fructose into the diabetic diet may lower post-prandial glucose levels without disturbing serum lipids.     

乳果糖口服液与妈咪爱颗粒治疗婴儿功能性便秘的疗效比较

目的观察比较乳果糖口服液与妈咪爱颗粒治疗婴儿功能性便秘的疗效。方法选取2016-01~2016-07到该院门诊就诊的功能性便秘患儿46例随机分为观察组(21例)和对照组(25例),观察组口服乳果糖口服液,对照组口服妈咪爱颗粒,比较两组缓解婴儿功能性便秘的疗效。结果观察组显效13例,有效5例,无效3例;对照组显效5例,有效5例,无效15例。观察组疗效优于对照组(Z=-3.309,P=0.001)。结论乳果糖口服液治疗婴儿功能性便秘疗效优于妈咪爱颗粒,对于维持婴儿肠道正常的生理功能有较好的临床疗效。     

氧化苦参碱对高果糖饮食诱导小鼠脂肪肝和肝胰岛素抵抗的影响

目的 观察氧化苦参碱对高果糖饮食诱导小鼠肝脏脂质沉积和肝胰岛素敏感性的影响.方法 雄性C57BL/J6小鼠分为对照组、高果糖组和氧化苦参碱组(自高果糖喂养第4周后给予氧化苦参碱40 mg/kg),喂养8 w后对小鼠行腹膜下葡萄糖耐量试验(ipGTT),处死小鼠后测定各组空腹血糖、血胰岛素及肝脏甘油三酯(TG)含量,通过比较各组小鼠注射胰岛素后肝脏的磷酸化Akt/总Akt (p-Akt/t-Akt)和磷酸化GSK-3α/β/总GSK-3 α/β(p-GSK-3 α/β/t-GSK-3α/β)表达的比值变化评估肝脏胰岛素敏感性.结果 与对照组相比,高果糖组的血葡萄糖、血胰岛素、ipGTT曲线下面积及肝TG均显著增加(均P＜0.01);氧化苦参碱干预组的血葡萄糖、血胰岛素、葡萄糖耐量试验曲线下面积及肝TG均较高果糖组减低(均P＜0.01);与对照组相比,高果糖组胰岛素注射肝内的p-Akt/t-Akt及p-GSK-3 α/β/t-GSK-3 α/β均显著降低(均P＜0.01),而氧化苦参碱组胰岛素注射后肝内的p-Akt/t-Akt及p-GSK-3β/t-GSK-3β较高果糖组显著升高(均P＜0.01).结论 慢性高果糖喂养可引起小鼠肝脏脂质沉积和肝胰岛素抵抗,氧化苦参碱治疗可改善高果糖喂养诱导的脂肪肝和肝胰岛素敏感性.