2 型糖尿病患者胰高血糖素及胰岛素水平检测及临床意义

目的:探讨2型糖尿病患者经标准馒头餐试验后胰高血糖素、胰岛素水平变化及其临床意义。方法:选取我院2014年3月至2015年3月收治的80例2型糖尿病患者为试验组,均接受标准馒头餐试验,对其餐前及餐后0.5 h、1 h、2 h胰高血糖素及胰岛素水平进行检测,并与同期80例血糖无异常的健康对照组作比较。结果:健康对照组餐前及餐后胰高血糖素水平无明显变化(P0.05),而试验组餐前胰高血糖素水平明显高于健康对照组(P0.05),且餐后明显升高,在餐后1 h达到峰值,餐后0.5 h、1h、2 h均明显高于健康对照组(P0.01)。健康对照组餐后胰岛素水平明显升高,在餐后1 h达到峰值后开始降低,较餐前略高,但差异平无统计学意义(P0.05);试验组餐前胰岛素水平明显低于健康对照组(P0.05),且餐后水平升高幅度缓慢,餐后0.5 h、1 h、2h均明显低于健康对照组(P0.05);实验组胰岛素抵抗指数(HOMA-IR)明显高于健康对照组,经Pearson相关分析,试验组餐后0.5 h、1 h、2 h胰高血糖素水平与HOMA-IR均呈明显的正相关(r=0.273、0.335、0.368,P0.05)。结论:2型糖尿病患者血糖高表达与胰高血糖素、胰岛素水平密切相关,胰高血糖素可拮抗胰岛素,及时检测二者的水平对临床准确评估病情具有重要的意义。     

肌肉肌醇对HepG2 胰岛素抵抗模型葡萄糖消耗量影响的细胞实验研究

目的:研究肌肉肌醇(myo-inositol,MI)对胰岛素抵抗细胞(IR-HepG2)细胞外葡萄糖消耗量的影响。方法:采用CCK-8法观察MI、高糖对HepG2细胞活力的影响,通过高糖持续作用,胰岛素刺激诱导HepG2细胞建立胰岛素抵抗细胞模型,葡萄糖氧化酶法(GOD-POD法)鉴定模型是否成立,并用GOD-POD法检测正常HepG2细胞和MI对HepG2胰岛素抵抗细胞葡萄糖消耗量的变化。结果:在对HepG2细胞活性没有影响的情况下,MI增加了胰岛素抵抗模型的葡萄糖消耗量。与模型对照组相比,葡萄糖氧化酶法结果显示,MI可显著增加胰岛素抵抗模型葡糖糖的消耗量(P0.01)。结论:MI可明显增加IR-HepG2细胞模型葡萄糖的消耗量,对IR-HepG2细胞模型胰岛素抵抗有显著的改善作用。     

二甲双胍联合西格列汀对2型糖尿病患者氧化应激、胰岛素抵抗的影响

目的:探讨二甲双胍联合西格列汀对2型糖尿病患者氧化应激、胰岛素抵抗的影响。方法:收集我院就诊或住院治疗的80例2型糖尿病患者,随机分为实验组和对照组,每组40例。两组患者入院后均给予相应的治疗措施,对照组患者给予二甲双胍250 mg/次,2次/d;实验组患者在对照组的基础上给予西格列汀100 mg/次,1次/d,治疗均连续8周。治疗结束后对患者血清丙二醛(MDA)、8异前列腺素F2α(8-iso-PGF2α)、空腹血糖(FBG)、空腹胰岛素(FINS)、胰岛素抵抗指数(HOMA-IR)以及患者临床治疗效果进行检测并比较。结果:与治疗前相比,治疗后两组患者MDA、8-iso-PGF2α、FBG、FINS以及HOMA-IR水平均下降(P0.05);与对照组相比,实验组患者MDA、8-iso-PGF2α、FBG、FINS以及HOMA-IR水平较低(P0.05),临床治疗总有效率较高(P0.05)。结论:二甲双胍联合西格列汀能够降低2型糖尿病患者血糖水平,降低MDA、8-iso-PGF2α水平,减轻氧化应激反应,降低胰岛素抵抗,临床疗效较好。     

微生态制剂改善非酒精性脂肪性肝病患者胰岛素抵抗的临床研究

目的:观察美常安对非酒精性脂肪性肝病(NAFLD)患者临床症状及胰岛素抵抗(IR)的作用。方法:选取2009年4月至2013年3月我院收治的88例NAFLD患者,随机分为治疗组和对照组。对照组给予基础治疗,治疗组在对照组的基础上,加用美常安胶囊进行治疗。比较两组疗效及治疗前后两组血清谷丙转氨酶(ALT)、甘油三酯(TG)及稳态胰岛素抵抗指数(HOMA-IR)水平,并分析血浆D乳酸、TNF-α、内毒素与HOMA-IR的相关性,观察两组不良反应情况。结果:治疗组治疗有效率为52.3%,明显高于对照组的29.5%(P0.05)。治疗后治疗组ALT、TG、HOMA-IR下降幅度,均明显优于对照组(P0.05)。治疗后治疗组患者血浆D乳酸、TNF-α、内毒素水平明显低于对照组(P0.05),且治疗组患者HOMA-IR与患者血浆D乳酸、血清TNF-α、内毒素水平呈正相关(r=0.352,0.44,0.48;均P0.05)。不良反应发生率低,且两组不良反应发生率无显著差异(P0.05)。结论:美常安治疗NAFLD疗效显著,可降低ALT、TG水平,降低肠道通透性,改善肠源性内毒素血症,改善IR,且安全性较高。     

Cytokines and their association with insulin resistance in obese pregnant women with different levels of physical activity

BackgroundCytokines contribute to insulin resistance in pregnancy, but the role of distinct cytokines is not fully understood.ObjectivesTo study whether cytokines produced by tissues other than skeletal muscle are associated with glucose and insulin metabolism activity in overweight and obese women and to study whether these associations can be modified by physical activity.MethodsA longitudinal study with 44 overweight and obese pregnant women was conducted. Changes in cytokines levels (IFN-γ, IP-10, IL1-α, MIP1-α, adiponectin and leptin) and ICAM1 from early (15 wk) to late (32 wk) pregnancy were determined. Physical activity was measured objectively with accelerometers. In linear regression models, the associations between (changes in) cytokine levels and fasting glucose, fasting insulin and HOMA-IR were studied.ResultsBoth IFN-γ and IP-10 levels increased from early to late pregnancy, and adiponectin levels decreased. IFN-γ and IP-10 were positively associated with fasting glucose, whereas IL-1α, ICAM1 and adiponectin were inversely associated with insulin and insulin resistance. The association of IL-1α with insulin and insulin resistance was only found in women with low levels of physical activity.ConclusionsIFN-γ, IP-10, IL1-α, ICAM1, and adiponectin may play a role in glucose and insulin metabolism in pregnancy. The relationship of IL-1α with insulin and insulin resistance might be moderated by levels of physical activity. Further studies are required to confirm the role of these cytokines in glucose and insulin metabolism in obese pregnant women.     

2型糖尿病内脏脂肪含量与胰岛β细胞功能及胰岛素抵抗的关系研究

目的:研究2型糖尿病患者内脏脂肪含量与胰岛β细胞功能及胰岛素抵抗的关系。方法:对65例初诊2型糖尿病患者采用256 CT平脐经L4、5水平进行扫描并测量皮下及内脏脂肪含量,并以BMI不同进行分组,即体重正常组、超重组、肥胖组。采用稳态模式评估法(HOMA)计算胰岛素抵抗指数、胰岛B细胞分泌功能,测量入组患者的相关人体指标、空腹血生化检查指标。结果:超体重组、肥胖组患者腰围、体重指数(body mass index, BMI)、甘油三酯(triglyceride, TG)、低密度脂蛋白胆固醇(low density lipoprotein cholesterol, LDL-C)、空腹血糖,(fasting blood-glucose, FBG)、空腹胰岛素(fasting insulin, FINS)INS、稳态模型胰岛素抵抗指数(Homeostatic Model Assessment for Insulin Resistance, HOMA-IR)、胰岛β细胞功能指数(Homeostasis model assessment-β,HOMA-β)指标肥胖组、超重组均明显高于正常体重组(P0.05),超体重组、肥胖组内脏脂肪含量、内脏脂肪面积、皮下脂肪含量、脂肪总含量、脂肪百分比,超重组、肥胖组均明显高于正常体重组(P0.05),且肥胖组各项指标明显高于超重组(P0.05)。多元回归分析显示腹部脂肪总含量、内脏脂肪含量、皮下脂肪含量、内脏脂肪面积、BMI与胰岛素抵抗呈正相关,而其中内脏脂肪含量及面积关系最密切。结论:内脏脂肪含量是2型糖尿病胰岛素抵抗及B细胞功能变化的独立影响因素。     

不同强度有氧跑有助于改善IGR老年人的症状

为了探讨不同强度持续跑步干预对糖调节受损(impaired glucose regulation,IGR)人群胰岛素敏感性、骨密度、糖调节、激素分泌的影响效果差异,为研发促进IGR人群糖调节能力恢复的运动处方提供实证参考,本研究选定90名糖调节受损老年人为本研究实验对象,进行随机分组,随机分为Fatmax强度跑步组(F组,n=30);AT强度跑步组(A组,n=30);对照组(C组,n=30)。在干预开始前1周内对受试者进行前测(BMD,骨代谢,FPG,OGTT-2h,HOMA-IR,IGF-1,生长激素分泌指标)。干预前3天,F组进行FATMAX强度测试、A组进行AT强度测试,各组按照运动计划进行为期24周的干预,运动干预结束后测。通过24周干预,F组和A组受试者的BMI、体脂率后测结果显著低于前测结果(p<0.05),而C组BMI和体脂率前后测结果对比没有显著性差异(p>0.05);F组、A组的FPG和OGTT-2h后测结果显著低于前测,且显著低于C组后测结果(p<0.05);F组和A组受试者的血清GH、IGF-1以及BGP的后测结果明显高于其前测结果和C组后测结果(p<0.05),而C组GH、IGF-1和BGP前后测结果对比没有显著性差异(p>0.05)。F组和A组受试者股骨颈BMD、大转子骨BMD、Ward’s三角区BMD后测结果显著高于前测结果和C组后测结果(p<0.05)。IGR老年人长期进行以Fatmax和AT强度进行长时间有氧跑步,不仅能够增加其下肢骨密度、促进骨生产和改善骨代谢,而且降低FPG、缓解胰岛素抵抗、促进GH、IGF-1分泌。其机制可能是IGR老年人长期进行中低强度有氧跑会提升血清GH、IGF-1浓度,而GH和IGF-1能够促进胰岛素的分泌合成以及促进成骨细胞工作,从而缓解IGR老年人的胰岛素抵抗和增加下肢BMD。     

胰岛素不同给药方式对妊娠期糖尿病患者围手术期血糖控制的效果研究

目的:研究胰岛素不同给药方式对妊娠期糖尿病患者围手术期血糖控制的效果与安全性。方法:选择2013年11月～2016年11月于我院接受治疗的92例妊娠期糖尿病患者,所有患者按随机数字表法分为对照组和研究组,每组46例。对照组围手术期予以皮下注射胰岛素治疗,研究组围手术期予以胰岛素泵治疗。比较两组空腹血糖(FBG),餐后2 h血糖(2hPBG),血糖达标情况,抗生素使用情况,切口愈合情况、住院时间及并发症的发生情况。结果:治疗后12 h、24 h及36 h,两组FBG、2hPBG水平均较治疗前显著下降,且研究组以上指标均低于对照组(P0.05)。研究组血糖达标、抗生素使用、切口愈合及住院时间均明显短于对照组(P0.05)。两组均有低血糖、切口感染发生,研究组并发症发生率低于对照组(P0.05)。结论:胰岛素泵输注胰岛素对妊娠期糖尿病患者围手术血糖的控制效果明显优于皮下注射胰岛素,且其安全性更高。     

Insulin Induces Microtubule Stabilization and Regulates the Microtubule Plus-end Tracking Protein Network in Adipocytes

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Highlights

• •Insulin Affects the Phosphorylation of G2L1, MARK2, CLIP2, EB1, AGAP3, and CKAP5.
• •Insulin Increases CLASP2 +TIP Density and Decreases CLASP2 +TIP Velocity.
• •Insulin Stimulates CLASP2 and G2L1 Trailing Along Microtubules.
• •Insulin Stimulates α-Tubulin Acetylation at Lysine 40 and Microtubule Stabilization.

     

Insulin-like growth factor binding proteins and angiogenesis: from cancer to cardiovascular disease

Angiogenesis is a tightly regulated activity that is vital during embryonic development and for normal physiological repair processes and reproduction in healthy adults. Pathological angiogenesis is a driving force behind a variety of diseases including cancer and retinopathies, and inhibition of angiogenesis is a therapeutic option that has been the subject of much research, with several inhibitory agents now available for medical therapy. Conversely, therapeutic angiogenesis has been mooted as having significant potential in the treatment of ischemic conditions such as angina pectoris and peripheral arterial disease, but so far there has been less translation from lab to bedside.The insulin-like growth factor binding proteins (IGFBP) are a family of seven proteins essential for the binding and transport of the insulin-like growth factors (IGF). It is being increasingly recognised that IGFBPs have a significant role beyond simply modulating IGF activity, with evidence of both IGF dependent and independent actions through a variety of mechanisms. Moreover, the action of the IGFBPs can be stimulatory or inhibitory depending on the cell type and environment. Specifically the IGFBPs have been heavily implicated in angiogenesis, both pathological and physiological, and they have significant promise as targeted cell therapy agents for both pathological angiogenesis inhibition and therapeutic angiogenesis following ischemic injury. In this short review we will explore the current understanding of the individual impact of each IGFBP on angiogenesis, and the pathways through which these effects occur.