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1.
高脂饲料喂养时间及链脲佐菌素剂量对实验型2型糖尿病大鼠造模的影响 总被引:3,自引:0,他引:3
目的采用高脂饲料联合链脲佐菌素(STZ)诱导方法建立糖尿病大鼠模型,探讨模型死亡率和成模率的影响因素。方法 8周龄雄性Wistar大鼠在高脂饲料喂养0周、4周、6周或8周后分别腹腔注射30mg/kg STZ;雄性Wistar大鼠在高脂饲料喂养四周后分别腹腔注射20、30或60 mg/kg STZ建立糖尿病模型,做糖耐量实验及胰岛素耐量实验,并检测血清指标,然后再以罗格列酮作为阳性药物进行验证。结果大鼠在高脂饲料喂养4周后,腹腔注射STZ 30 mg/kg处理后,糖尿病大鼠模型成模率分别为85%和80%,高于20 mg/kg STZ组;死亡率为零,显著低于60 mg/kg STZ组(75%);高脂饲料喂养4周后注射30 mg/kg STZ组死亡率最低,而高脂饲料喂养8周模型组死亡率最高达65%。成模大鼠血清甘油三酯、游离脂肪酸显著升高(P<0.05),空腹血清胰岛素未明显下降,并出现糖耐量异常和胰岛素抵抗;罗格列酮治疗4周后血糖、血清甘油三酯及游离脂肪酸显著降低(P<0.05)。结论高脂饲料喂养时间、STZ剂量及鼠龄是影响糖尿病大鼠模型成模率和死亡率的重要因素。 相似文献
2.
目的研究巴马小型猪T1DM模型血清25-羟维生素D3[25(OH)D3]变化,探讨巴马小型猪T1DM空腹血糖(FBG)与血清25(OH)D3的相关性。方法选用健康雄性巴马小型猪12只,分为对照组6只和糖尿病模型组6只。糖尿病模型组腹腔注射链脲佐菌素(STZ),第一次腹腔注射STZ 75 mg/kg,1周后第二次腹腔注射STZ 150 mg/kg,对照组注射等量柠檬酸钠溶液;实验结束后行葡萄糖耐量试验(OGTT)、胰岛素释放实验(IRT)及检测空腹25(OH)D3水平,并行胰腺组织病理学检查、胰岛β细胞免疫组化染色分析。结果 (1)自链脲佐菌素给药后13 d开始,模型组空腹血糖明显升高并稳定维持在7.6~17.1 mmol/L水平。(2)造模成功1周后,模型组OGTT各时点血糖水平均高于正常对照组(P<0.01),IRT各时点胰岛素水平均低于正常对照组(P<0.01)。(3)胰岛β细胞免疫组化结果提示,模型组胰岛中胰岛素染色阳性面积[(10.68±2.78)%]显著低于对照组[(43.63±2.83)%](P<0.01)。(4)模型组血清25(OH)D3[(29.67±4.41)ng/ml]低于对照组[(35.83±+3.25)ng/ml](P<0.05)。(5)模型组25(OH)D3水平与FBG成负相关(r=-0.338,P<0.05)。结论 (1)采用腹腔多次注射STZ可以成功构建巴马小型猪1型糖尿病模型。(2)模型组小型猪血清25(OH)D3水平降低与T1DM的发生有关。 相似文献
3.
目的观察补镁对2型糖尿病大鼠胰岛素受体(insulin receptor,IR)表达水平的影响。方法将高脂饲料喂养加链脲佐菌素注射方法诱发的2型糖尿病大鼠随机分为4个组,高、中、低剂量组在高脂饲料中分别加入氧化镁2000、1000、200mg/kg(以镁离子计),糖尿病对照组只喂饲高脂饲料,正常对照组喂饲普通饲料。动物自由进食,连续4周,用葡萄糖氧化酶法测定空腹尾尖血的血糖含量,腹主动脉取血用放免法测定血清胰岛素含量,用免疫组化法测定胰腺和骨骼肌组织IR表达水平。结果经Image-Pro Plus图像分析,高剂量组的胰腺和骨骼肌组织中IR表达水平分别为0.341±0.001和0.346±0.002,均较糖尿病对照组升高,而血糖水平则较糖尿病对照组降低,差异均有显著性意义(P<0.05)。结论镁补充可以提高2型糖尿病大鼠胰腺和骨骼肌组织中IR的表达水平,降低空腹血糖水平。 相似文献
4.
目的研究番石榴叶水提取物(WE)灌胃处理后,糖尿病小鼠胰岛形态结构及其胰岛素合成表达功能的改变。方法通过腹腔注射链脲佐菌素(STZ)诱导糖尿病小鼠模型,水提取物灌胃处理,4周后进行口服葡萄糖耐量试验(OGTT),HE染色观察胰腺组织病理形态学改变,免疫组化(IHC)和图像分析技术观察分析胰岛β细胞胰岛素表达量,试剂盒法检测肝脏组织中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和还原型谷胱甘肽(GSH)水平。结果与糖尿病模型对照组(DM)相比,水提取物组糖尿病小鼠禁食3h空腹血糖水平下降33.4%,葡萄糖耐量明显改善;胰岛体积缩小、形状不规则及β细胞变性等病理改变明显减轻,β细胞数量增多,单位面积内胰岛素表达量明显上升;肝脏组织GSH水平显著升高。结论番石榴叶水提取物对糖尿病小鼠胰岛具有保护作用,作用机制可能是通过抗氧化作用减轻小鼠胰岛β细胞结构和功能的损伤。 相似文献
5.
苦瓜多糖对链脲佐菌素诱导糖尿病小鼠的降血糖效果 总被引:10,自引:0,他引:10
目的:研究苦瓜水提多糖(watersolublepolysaccharidesofMomordicacharantiaL.MCW)和苦瓜碱提多糖(alkalinesolublepolysaccharidesofMomordicacharantiaL.MCB)对STZ诱导糖尿病小鼠的降血糖作用。方法:昆明种小鼠120只,随机抽取12只作空白对照,余下108只,禁食后于次日晨腹腔注射链脲佐菌素(STZ)200mg/kgbw。取血糖值在11.1mmol/L以上者随机分组,共4组:模型组、MCW组(300mg/kgbw)、MCB组(300mg/kgbw)和优降糖组(15mg/kgbw)。连续灌胃10d后,禁食,次日晨眼眶取血,测定血糖及血清胰岛素含量。解剖取胰腺,观察小鼠胰岛组织形态。结果:MCW和MCB都可以降低糖尿病小鼠空腹血糖,MCB组分的降血糖效果最佳,不但可以显著降低糖尿病小鼠空腹血糖值,而且可以提高糖尿病小鼠血清胰岛素水平。结论:苦瓜多糖能帮助恢复受损胰岛组织,促进胰岛素的分泌,从而降低血糖。 相似文献
6.
目的研究镁补充对2型糖尿病大鼠红细胞胰岛素受体亲和力的影响。方法将高脂饲料喂饲加链脲佐菌素腹腔注射诱发的2型糖尿病大鼠随机分成糖尿病对照及高、中、低剂量组,饲料中分别加入氧化镁(以镁计)0、2000、1000、200mg/kg,正常对照组喂饲普通饲料,共喂养4周。检测红细胞胰岛素受体结合常数、结合容量、受体数目、空腹血糖及空腹胰岛素等指标,计算胰岛素抵抗指数与敏感指数。结果高剂量组高亲和力胰岛素受体结合常数、结合容量和受体数目分别为(1.24±0.47)×109L/mol、(1.26±0.53)×1014/L和80.23±0.47,均高于糖尿病对照组;胰岛素抵抗指数较糖尿病对照组降低而胰岛素敏感指数升高。结论镁补充能提高2型糖尿病大鼠红细胞胰岛素受体亲和力,改善胰岛素抵抗。 相似文献
7.
目的探讨不同链脲佐菌素(STZ)注射剂量和方法对大鼠血糖值、血糖稳定性和胰岛损害的影响。方法75只SPF级6周龄雄性Wistar大鼠高脂高糖、饲养8周后,分别给予20、25、30mg/kg的STZ腹腔注射。造模后连续7周每周观察各组大鼠的体重、空腹血糖和餐后2h血糖。评价各组大鼠血糖变化和成模率。实验结束时测定血清胰岛素(INS)、甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白(HDL)、低密度脂蛋白(LDL)等。HE染色和胰岛素免疫组化观察胰岛细胞形态学特点。结果20mg/kg注射组成模率较低(30%);25mg/kg注射组成模率较高(73.3%),血糖中度升高并且稳定,胰岛结构完整,β细胞数量和细胞质内棕色颗粒有所减少;30mg/kg的STZ注射组血糖较高,死亡率较高,并且胰岛和β细胞数量极少,小胰岛多见,形状不规则,出现空泡样变性。结论高脂、高糖饲养8周后联合小剂量STZ25mg/kg能够造成更具有代表人类2型糖尿病病理生理特征的大鼠模型。 相似文献
8.
目的 探讨2型糖尿病动物模型建立的方法.方法 根据体重将35只Wistar大鼠随机分为对照组(10只)和糖尿病组(25只);糖尿病组喂高糖高脂饲料,对照组喂普通饲料,喂养1个月后,糖尿病组大鼠一次性腹腔注射链脲佐菌素(STZ) 25 mg/kg.bw,对照组注射相同剂量柠檬酸钠缓冲液,72 h后以随机血糖≥16.7 mmol/L确定为糖尿病模型.结果 STZ注射后72 h,与对照组相比糖尿病组大鼠血糖明显升高(P<0.05),葡萄糖耐量,胰岛素耐受均异常,血清TG,TC,LDL-C显著升高(P<0.05),同时伴有多饮、多食、多尿等糖尿病症状.结论 高糖高脂饲料联合小剂量腹腔注射STZ可致大鼠血糖明显上升,血脂紊乱等2型糖尿病症状. 相似文献
9.
目的观察镁补充对2型糖尿病大鼠胰岛素受体亲和力的影响。方法将用高脂饮食联合链脲佐菌素(STZ)方法诱发的2型糖尿病大鼠随机分为4个组,糖尿病对照组喂饲高脂饲料,高、中、低剂量组在高脂饲料中分别加入2000、1000、200mg/kg的镁(以镁离子计)。每周检测空腹血糖1次。自由饮食喂养4 w,处死动物。用放射性受体分析法测肝细胞胰岛素受体亲和力、放射免疫法测血清胰岛素(Ins)水平、比色法检测糖化血红蛋白(HbA1c)和血浆丙二醛(MDA)、葡萄糖氧化酶法测空腹血浆葡萄糖(FPG),并计算胰岛素敏感指数(ISI)和抵抗指数(IRI)。结果高剂量组的高亲和力胰岛素受体结合常数(K1)为(4.76±0.08)×108L/mol,低亲和力胰岛素受体结合常数(K2)与结合容量(R2)分别为(1.10±0.14)×106L/mol,(8.49±0.43)×1013/mg蛋白,均较糖尿病对照组显著性升高(P<0.05)。补镁第3 w开始高剂量组空腹血糖较糖尿病对照组显著性降低,高剂量组的胰岛素敏感指数较糖尿病对照组显著性升高,而胰岛素抵抗指数则显著性降低。结论镁补充可以提高2型糖尿病大鼠胰岛素受体亲和力,降低胰岛素抵抗。 相似文献
10.
[目的]观察胰升糖素样肽-1长期作用对2型糖尿病大鼠血糖和胰岛素水平的影响. [方法]采用高脂高糖饲料喂养结合小剂量链脲佐菌素注射的方法成功建立2型糖尿病动物模型.用高、中、低3个剂量GLP-1对2型糖尿病大鼠进行长期干预(4周),比较干预组与未干预组糖尿病大鼠血糖、血脂和胰岛素水平的变化. [结果]GLP-1高剂量组较糖尿病组大鼠血糖及血脂明显降低(P<0.01),胰岛素水平明显升高(P<0.01). [结论]一定剂量的GLP-1长期作用.可以明显降低2型塘尿病大鼠的血糖,增加胰岛素分泌,并有效地控制体重和降低甘油三酯水平. 相似文献
11.
目的 系统评价维生素D(VD)和钙联合补充对糖尿病患者及其高危人群的空腹血糖、胰岛素抵抗、炎症标志物等指标的影响。方法 检索4个主要数据库,搜索联合补充VD和钙相关的随机对照试验,检索时间限定均建库开始至2017年1月1日。结果 Meta分析结果显示,VD+钙补充组与对照组相比空腹血糖的浓度降低,此外,维生素D+钙补充组的HOMA - IR也显著下降。但对于高敏C反应蛋白和白介素 - 6,2组不存在统计学差异。结论 糖尿病人及其高危人群补充VD和钙可改善空腹血糖和胰岛素抵抗,但对炎症标志物的影响并不显著。 相似文献
12.
长期酒精摄入对大鼠胰岛的影响及与氧化应激关系的探讨 总被引:6,自引:0,他引:6
目的 探讨了活性氧和一氧化氮 (NO)在其中的可能作用 ,以研究长期酒精摄入对胰岛影响的机制。方法 对照组灌以 6ml kgBW的蒸馏水 ,低、中、高各剂量组的无水乙醇剂量分别为 0 4 8、1 4 4及 2 4 0g kgBW ,时间为 1 3周。实验结束时检测了血糖和血胰岛素 ,用免疫组化及图象分析法分析了大鼠的胰岛结构参数 (从各组随机选 1 0只 ) ,并检测了其余大鼠血清和胰腺组织中的自由基反应水平。结果 (1 )与对照组相比 ,高剂量组雌雄大鼠的血糖升高 ,血胰岛素下降 ,胰岛素免疫反应阳性物面积与胰腺组织面积百分比(Ins+ panc)及胰岛素免疫反应阳性物面积与胰岛组织面积百分比 (Ins+ Isl)均降低 (P <0 0 5 )。 (2 )与对照组相比 ,高剂量组雌雄大鼠血清和胰腺组织中的总超氧化物歧化酶 (T SOD)降低 ,NO、活性氧及丙二醛 (MDA)含量升高 ;而低剂量组雌雄大鼠血清中的T SOD和谷胱甘肽过氧化物酶 (GSH Px)升高 ,NO、活性氧及MDA含量下降 (P <0 0 5 )。结论 长期过量饮酒可通过引起胰腺氧化损伤而使胰岛功能受损 ,这可能是酒精引起患糖尿病危险性增高的原因之一。而长期适量饮酒可使抗氧化能力增强 ,对机体有一定的保护作用 相似文献
13.
目的 分析孕中期预防性应用维生素D降低妊娠期糖尿病发病率的临床效果.方法 选取佛山市勒流医院自2014年8月到2015年3月期间收治的妊娠12周以前的妇女120例,采用连续随机数字表法随机分为干预组和对照组,每组60例,从妊娠12周开始,干预组给予维生素D,20万IU,肌肉注射,每月一次,连续三个月,对照组则给予安慰剂,治疗至妊娠足24周,复测空腹血糖、空腹胰岛素浓度、血清25羟维生素D3水平并通过糖耐量试验(OGTT)实验,明确两组的妊娠期糖尿病(GDM)发病人数.观察与对比两组孕妇干预前后血清25羟维生素D3 水平及血糖、GDM发生情况.结果 两组患者怀孕12周时,血清25羟维生素D3水平的妇女120例,采用连续随机数字法随机分为干预组和对照组,每组60例,从妊娠12周开比较无显著性差异(t=1.32,P>0.05),干预组行维生素D补充治疗后,其24周时血清25羟维生素D3水平显著高于对照组(t=5.31,P<0.05),干预组24周血清25羟维生素D3水平高于12周,而对照组24周血清25羟维生素D3水平低于12周,但两组组内比较均无显著性差异(t值分别为-1.79、1.83,均P>0.05).12周时,两组患者空腹血糖水平、空腹胰岛素水平、胰岛素抵抗指数均无显著性差异(t值分别为0.93、0.77、0.46,均P>0.05),干预组24周空腹血糖水平、空腹胰岛素水平、胰岛素抵抗指数均显著低于对照组(t值分别为-4.54、-5.31、-5.57,均P<0.05),且糖尿病发病率显著低于对照组(χ2=17.42,P<0.05).结论 孕中期预防性应用维生素D降低妊娠期糖尿病发病率具有显著的临床效果显著,值得推广与应用. 相似文献
14.
硒、锌对链脲佐菌素所致胰岛氧化损伤的保护作用 总被引:11,自引:0,他引:11
用离体培养的新生大鼠胰岛,观察链脲佐菌素(STZ)对胰岛过氧化氢(H2O2)释放和葡萄糖刺激胰岛素分泌的影响以及硒、锌的保护作用。结果显示:0.5~4mmol/LSTZ增加胰岛H2O2释放和抑制胰岛素分泌,均呈剂量依赖关系,且两者有负相关关系。硒可明显减少STZ诱导的H2O2释放,而锌则无该效应,但硒和锌均能明显减轻STZ和外源性H2O2抑制胰岛素分泌的作用。结果表明:H2O2在STZ所致胰岛损伤中起重要作用,硒和锌对STZ所致胰岛氧化损伤具有一定的防护作用。 相似文献
15.
This study investigated the effects of magnetized water supplementation on blood glucose, DNA damage, antioxidant status, and lipid profiles in streptozotocin (STZ)-induced diabetic rats. There were three groups of 4-week-old male Sprague-Dawley rats used in the study: control group (normal control group without diabetes); diabetes group (STZ-induced diabetes control); and magnetized water group (magnetized water supplemented after the induction of diabetes using STZ). Before initiating the study, diabetes was confirmed by measuring fasting blood glucose (FBS > 200 dl), and the magnetized water group received magnetized water for 8 weeks instead of general water. After 8 weeks, rats were sacrificed to measure the fasting blood glucose, insulin concentration, glycated hemoglobin level, degree of DNA damage, antioxidant status, and lipid profiles. From the fourth week of magnetized water supplementation, blood glucose was decreased in the magnetized water group compared to the diabetes group, and such effect continued to the 8th week. The glycated hemoglobin content in the blood was increased in the diabetes group compared to the control group, but decreased significantly in the magnetized water group. However, decreased plasma insulin level due to induced diabetes was not increased by magnetized water supplementation. Increased blood and liver DNA damages in diabetes rats did significantly decrease after the administration of magnetized water. In addition, antioxidant enzyme activities and plasma lipid profiles were not different among the three groups. In conclusion, the supplementation of magnetized water not only decreased the blood glucose and glycated hemoglobin levels but also reduced blood and liver DNA damages in STZ-induced diabetic rats. From the above results, it is suggested that the long-term intake of the magnetized water over 8 weeks may be beneficial in both prevention and treatment of complications in diabetic patients. 相似文献
16.
Insulin resistance is one of the most common features of polycystic ovary syndrome (PCOS). Some studies suggest that vitamin D deficiency may have a role in insulin resistance; thus, the aim of the current study was to determine the effect of vitamin D supplementation on insulin resistance in women with PCOS and a vitamin D deficiency. We hypothesized that vitamin D supplementation would lower the glucose level and insulin resistance in women with PCOS and a vitamin D deficiency. The current study was a randomized, placebo-controlled, double-blinded trial with 50 women with PCOS and a vitamin D deficiency, 20 to 40 years old, assigned to receive 3 oral treatments consisting of 50?000 IU of vitamin D3 or a placebo (1 every 20 days) for 2 months (vitamin D, n = 24; placebo, n = 26). The fasting blood glucose, insulin, 25-hydroxyvitamin D, and parathyroid hormone levels, as well as the homeostasis model assessment of insulin resistance and quantitative insulin sensitivity check index were measured at baseline and after treatment. In the vitamin D group, the serum level of 25-hydroxyvitamin D increased (6.9 ± 2.8 to 23.4 ± 6.1 ng/mL, P < .0001), and the parathyroid hormone level decreased (70.02 ± 43.04 to 50.33 ± 21.99 μIU/mL, P = .02). There were no significant changes in the placebo group. There was a significant increase in insulin secretion in the vitamin D group (P = .01), but this was not significant compared with the placebo group. The fasting serum insulin and glucose levels and the insulin sensitivity and homeostasis model assessment of insulin resistance did not change significantly by the end of the study. We were not able to demonstrate the effect of vitamin D supplementation on insulin sensitivity and insulin resistance in women with PCOS and vitamin D deficiency. 相似文献
17.
目的探讨骨化三醇[1,25(OH)2D3]对链脲佐菌素(streptozocin,STZ)所致SD大鼠糖尿病发生过程的影响,为人类1型糖尿病的预防提供实验依据。方法将28只雄性SD大鼠随机分为3组。20只大鼠采用STZ造成糖尿病模型,其中1,25(OH)2D3组(n=10)造模前4周接受1,25(OH)2D31μg/(kg·d)溶于0.05 ml花生油灌胃,STZ对照组(n=10)造模前4周采用花生油灌胃,0.05ml/d。STZ对照组和1,25(OH)2D3组均于实验第5周开始第1天腹腔注射福氏完全佐剂(CFA),0.5 ml/只,第2天按30 mg/kg STZ枸椽酸溶液腹腔注射,以STZ对照组全部成模为准,停止造模;成模后2周处死。其余8只为正常对照组,采用花生油灌胃,0.05ml/d,灌胃4周,不注射STZ。观察1,25(OH)2D3对STZ所致SD大鼠糖尿病发病情况及对胰岛素、血糖的影响。结果 STZ对照组10只大鼠全部造模成功,1,25(OH)2D3组10只大鼠中6只成模,造模成功率差异有统计学意义(P〈0.05)。1,25(OH)2D3组血糖曲线下面积(AUC)为(21.301±4.699)mmol·h/L,明显低于STZ对照组[(31.183±4.567)mmol·h/L],差异有统计学意义(P〈0.05)。1,25(OH)2D3组胰岛素AUC为(1.105±0.356)μg·h/L,明显高于STZ对照组[(0.472±0.162)μg·h/L],差异有统计学意义(P〈0.05)。血清1,25(OH)2D3水平与胰岛素AUC呈正相关,而与血糖AUC呈负相关,有统计学意义(r=0.517,P=0.04;r=-0.562,P=0.02)。结论 1,25(OH)2D3对STZ所致SD大鼠糖尿病的发生有一定的预防作用。 相似文献
18.
目的:分析妊娠早期25-羟维生素D不足对妊娠期糖尿病(GDM)的预测价值。方法:选取妊娠早期于本院就诊的孕妇作为研究对象,于确诊妊娠时检测空腹血糖(FPG)、血清25-羟维生素D[25-(OH)D]及空腹胰岛素(FIns),于孕24~28周行75g口服葡萄糖耐量试验(OGTT),按照血清25-(OH)D水平分为25-(OH)D正常及不足组,比较GDM的发生率及胰岛素相关指标的差异;按照OGTT的血糖值,将GDM孕妇分为不同时间点血糖正常及异常组,分析血清25-(OH)D水平与OGTT血糖值的关系。结果:血清25-(OH)D不足组中的GDM发生率及HOMA-IR均高于25-(OH)D正常组,胰岛素分泌指数(HOMA)-β低于25-(OH)D正常组(P0.05);糖耐量指标中,服糖后1、2h血糖异常组的血清25-(OH)D水平低于血糖正常组(P0.05),而空腹血糖异常组与正常组间血清25-(OH)D水平无统计学差异(P0.05)。结论:孕妇血清25-(OH)D不足可以降低机体胰岛素的敏感性,加重胰岛素抵抗,在妊娠早期检测,对GDM的发生可起到一定的预测作用。 相似文献
19.
Eftekhari MH Akbarzadeh M Dabbaghmanesh MH Hasanzadeh J 《Asia Pacific journal of clinical nutrition》2011,20(4):521-526
Introduction: Type 2 diabetes is a major public health problem. Recent epidemiological evidence also points to a potential association of vitamin D insufficiency with adverse metabolic risks, including that for type 2 diabetes. Subjects and method: A double-blind randomized placebo-controlled trial was carried out. Seventy subjects with type 2 diabetes, age 30-75 years old, were randomly assigned in a double-blind fashion to two groups. One group received two capsules of calcitriol (0.25 μg 1,25-dihydroxy cholecalciferol per each capsule) per day. The second group received placebo tablets. At the beginning, middle and the end of the 12 week supplementation trial, serum glucose, insulin, calcium and phosphorous, HbA1c and 25(OH) vitamin D were measured. Results: There was no significant difference between two groups at baseline. At the end of the study, fasting plasma glucose increased in the control group (p=0.038), while it remained unchanged in calcitriol group. Level of insulin and HbA1c increased significantly in both groups (p=0.013 and 0.0004 in treatment and control group). Regarding insulin resistance indices, there was a significant change in HOMA-IR and QUICKI in both groups (p=0.023 and 0.002 in treatment and 0.001 and <0.001 in control group respectively). Insulin secretion as assessed by HOMA-%β, remained relatively unchanged in the control group, while it increased significantly in the treatment group at the end of study (p=0.009). Conclusion: Vitamin D supplementation attenuated the increase in glycemia, and increased insulin secretion, but had no effect on insulin resistance. 相似文献
20.
BACKGROUNDThe role of vitamin D supplementation in gestational diabetes mellitus (GDM) patients is unclear.AIMTo determine the burden and risk of post-randomization GDM patient attrition from vitamin D-supplemented arms of randomized controlled trials (RCTs). The auxiliary aim was to compare the effects of nutritional supplements on their fasting blood glucose (FPG) levels and perinatal outcomes.METHODSRCTs were searched in the PubMed, Embase, and Scopus databases. Random-effect prevalence and pairwise meta-analysis were performed for the primary objective. The auxiliary aim was to compare the effects of nutritional supplements on their fasting blood glucose (FPG) levels and perinatal outcomes. Fixed-effect network meta-analyses were undertaken for the secondary goals. All analyses were performed using Stata software, and statistical significance was determined at P < 0.05.RESULTSThirteen RCTs from Iran and China were reviewed. The participant attrition burden in vitamin D recipients was 6% [95% confidence interval (CI): 0.03, 0.10], and its risk did not vary from non-recipients. Vitamin D and calcium co-supplementation reduced the cesarean section incidence in GDM patients [risk ratio (RR): 0.37; 95%CI: 0.18, 0.74]. The hyperbilirubinemia or hospitalization risk in their newborns decreased with vitamin D supplementation (RR: 0.47; 95%CI: 0.27, 0.83) and co-supplementation with calcium (RR: 0.35; 95%CI: 0.16, 0.77) or omega-3 fatty acids (RR: 0.25; 95%CI: 0.08, 0.77). Vitamin D and probiotics co-supplementation decreased newborn hyperbilirubinemia risk (RR: 0.28; 95%CI: 0.09, 0.91). FPG levels and macrosomia risk did not vary across interventions.CONCLUSIONIn RCTs, vitamin D supplementation or co-supplementation in GDM patients showed a low participant attrition burden and low risk of cesarean section, newborn hyperbilirubinemia, and newborn hospitalization. 相似文献