Central Expressions of Ghrelin and Cholecystokinin in Rats with Gastric Electrical Stimulation

Background Gastric electrical stimulation (GES) has recently been proposed for the treatment of obesity. The aim of this study was to explore the possible central mechanisms involved in GES by investigating the expression of orexigenic and anorexigenic peptides in the rodent hypothalamus and hippocampus. Methods The experiment was designed in two parts: an acute experiment with 2 h GES and a chronic experiment with 14-day continuous GES. After stimulation, the expressions of an orexigenic hormone, ghrelin, in the hypothalamus and an anorexigenic hormone, cholecystokinin (CCK), in the hippocampus were detected by the immunohistochemical method. GES was performed using parameters similar to those used in clinical studies for treating obesity. Results Compared with the control group, 2 h GES resulted in a decrease in the number of ghrelin-immunoreactive (ghrelin-IR) neurons in the hypothalamic paraventricular nucleus (PVN, 34.8 ± 1.86 vs 57.2 ± 2.95, P = 0.02) and the supraoptic nucleus (SON, 51.2 ± 3.21 vs 82.8 ± 3.08, P = 0.01); the CCK-immunoreactive (CCK-IR) neurons in the hippocampus were of no changes (7.4 ± 0.87 vs 6.2 ± 0.58, P = 0.29). After the 14-day GES, the number of CCK-IR neurons in the hippocampus was increased compared with that of the control group (4.0 ± 0.32 vs 2.4 ± 0.51, P = 0.03). However, there were no changes in the number of ghrelin-IR neurons either in the PVN or in the SON. Conclusions These results indicate that the expression of ghrelin and CCK can be altered by GES. GES may be able to alter energy homeostasis by modulating the expressions of food intake-related hormones in the central nervous system: reducing the level of orexigenic ghrelin acutely and increasing the level of anorexigenic CCK chronically.     

巴斯德处理周围神经后的溃变和再生的实验研究

目的：为了研究本法的实用性，在组织学和定量方面评价巴斯德处理小白鼠坐骨神经后的神经溃变和再生。方法：将Wistar系雄性小白鼠左侧坐骨神经10mm的长度，进行60℃，30min的巴斯德处理，评价了对照部、处理部以及末梢部，评价时间在处理后1周（1周群），6周（6周群）各群分别为11只。结果：（1）有髓轴突数；末梢部的比较中，6周群的数比1周群显著增加了（P＜0．01）。（2）有髓轴突直径：末梢部的比较中，6周群的直径比1周群显著增加了（P＜0．01）。（3）有髓轴突面积经，末梢部的比较中，6周群的面积比比1周群显著增加了（P＜0．05）。（4）透射电子显微镜所见：1周群的处理部中，髓鞘陷入凝固坏死，雪旺细胞基底膜发生溃变。6周群的末梢部中，发现了多数的再生有髓轴。结论：从以上结果足能证明，巴斯德湿热处理小白鼠的坐骨神经一旦发生溃变但是再生是可能的，因此，在恶性骨、软组织肿瘤的手术之际，巴斯德湿热处理法作为神经保存的方法是极为有用的。     

Determination of Ghrelin Immunoreactivity in Kidney Tissues of Diabetic Rats

Backgrounds/Aims. Ghrelin, a recently discovered hormone, is released largely from stomach and might affect insulin secretion and glucose metabolism. The aim of this study was to determine the immunohistochemical localization of ghrelin in streptozotocin-induced diabetic rat kidneys. Methods. Fifty-four adult male Wistar rats were used in this study. All rats were divided into nine groups according to three time points of the study (2, 4, and 6 weeks) as control group, control group given 0.1 M phosphate-citrate, and diabetic group given 50 mg/kg streptozotocin intraperitoneally. The rats in all groups were decapitated at the end of 2, 4, and 6 weeks of the study. The kidneys of the rats were removed, and tissue samples were processed by using routine paraffin techniques. The samples were immunohistochemically stained using avidin-biotin-peroxidase method for ghrelin immunoreactivity. Results. There were no differences of ghrelin immunoreactivity between the control groups. Ghrelin immunoreactivity was observed in both distal tubulus and collecting ducts in the diabetic groups, while it was detected only in distal tubules of the control groups. The intensity of ghrelin immunoreactivity was increased at 4 and 6 weeks of the study in the diabetic groups. Conclusion. Increased ghrelin immunoreactivity in the diabetic rat kidney tissues suggests that ghrelin may contribute to the pathophysiological mechanism of diabetic nephropathy.     

生长激素对大鼠海绵体神经移植后再生的影响

目的:研究腓肠神经移植替代损伤的双侧海绵体神经(CN)后,生长激素(GH)对大鼠勃起功能恢复的影响。方法:24只雄性SD大鼠(3~4个月,300~400 g)随机均分为2组:神经移植组(腓肠神经移植替代损伤的双侧CN);GH组(神经移植后皮下注射GH)。2个月及4个月后,CN电刺激检测大鼠阴茎勃起功能,免疫组化SP法检测阴茎海绵体内神经元型一氧化氮合酶(nNOS)神经纤维并图像分析计算阳性像素值。结果:2个月后GH组有31.25%CN对电刺激有勃起反应,较神经移植组0%差异有显著性(P<0.05),nNOS阳性神经纤维的像素值在GH组为38 971±7 692,而神经移植组为16 538±3 179,差异同样具有显著性(P<0.05);而4个月后GH组有75%的CN对电刺激有勃起反应,神经移植组43.75%的CN有反应,差异无显著性(P>0.05);nNOS阳性神经纤维的像素值分别为91 348±18 965,79 276±12 021,差异亦无显著性(P>0.05)。结论:GH能促进CN移植后的再生,有利于盆腔根治性手术后勃起功能的恢复。     

大鼠胰腺部分切除后导管细胞增殖规律研究

目的　探讨大鼠胰腺大部分切除术后残余胰腺组织导管上皮细胞增殖的时空规律 ,明确胰腺干细胞组织定位。方法　手术切除大鼠胰腺 90 %组织 ,不同时间点处死动物后取材 ,免疫组织化学染色 ,5 溴脱氧嘧啶核苷 (BrdU )标记 ,观察不同分类胰腺导管上皮细胞以及腺泡细胞着色并计算染色指数。结果　建模后第 1天主胰管、大胰管、小胰管细胞均出现增殖高峰 ,其中小胰管增殖持续到大鼠建模后第 5天 ,与对照组比较差异有非常显著性 (P <0 .0 0 1) ;腺泡细胞仅在建模后第 5天出现小的增殖峰 ;建模后第 7天破坏的小叶结构基本恢复 ,胰腺导管周围有新生胰岛形成。结论　大鼠胰腺大部分切除后 ,胰腺再生过程中出现了胰腺干细胞增生与分化 ,而且胰腺干细胞主要位于导管上皮细胞中。     

胰十二指肠及肾一期联合移植三例体会

报告３例Ⅰ型糖尿病并发尿毒症患者接受全胰十二指肠及肾一期联合移植，术后术移植胰及肾功能恢复良好，停用胰岛素后，停用胰岛素后，血肌酐、尿素氮降至正常。本组其中２例胰肾有功能存活分别为３年和２年。例３因移植肾急性排斥，多器官衰竭于术后第２２天死亡。作者认为胰肾一期联合移植可同时纠正糖尿病和尿毒症。     

胰腺内分泌肿瘤外科诊治现状及进展

目的 探讨胰腺内分泌肿瘤外科诊断及治疗新进展.方法 搜集有关胰腺内分泌肿瘤相关文献并进行复习.结果 胰腺内分泌肿瘤可以过量分泌激素而引起相关临床症状.由于发病率低、临床症状复杂,常引起胰腺内分泌肿瘤的漏诊和误诊.最近影像学的进展及对血清激素水平的检测提高了胰腺内分泌肿瘤的早期诊断率.随着对胰腺内分泌肿瘤的了解及对其分子遗传机理的研究,其临床治疗观念也发生了重大变化.结论 正确诊断是胰腺内分泌肿瘤治疗的前提.外科干预仍是目前胰腺内分泌肿瘤治疗的首选方案,可以延长患者生存时间,改善和控制临床症状.     

2型糖尿病大鼠后肢缺血模型的建立及评价

目的建立2型糖尿病大鼠后肢缺血模型并进行评价,为后续的干预实验提供研究平台。方法将15只SD大鼠随机分为正常对照组、糖尿病组及糖尿病后肢缺血组,每组5只。糖尿病组及糖尿病后肢缺血组的10只大鼠均给予高脂饮食喂养4周后,腹腔注射链脲佐菌素（STZ,40mg／kg）以建立2型糖尿病模型。糖尿病后肢缺血组大鼠建模成功后行双侧髂总动脉结扎术以建立后肢缺血模型,正常对照组和糖尿病组大鼠仅分离髂总动脉,不予结扎。2周后对3组大鼠股动脉的起始段行彩色多普勒超声检查,以检测股动脉的血流峰值速度和血流加速时间;取缺血部位的小腿三头肌及大腿股四头肌组织,分别行HE染色及免疫组化SP染色,以观察3组大鼠肌细胞的营养状况及血管再生情况。结果后肢缺血模型建模2周后,正常对照组、糖尿病组和糖尿病后肢缺血组大鼠的血流峰值速度分别为（22．49±3．02）cm／s、（17．36±2．60）cm／s和（11．23±1．26）cm／s,血流加速时间分别为（0．080±0．009）S、（0．120±0．009）S和（0．160±0．020）s,糖尿病后肢缺血组大鼠的股动脉血流峰值速度小于正常对照组和糖尿病组（P〈0．05）,而血流加速时间较长（P〈0．05）。HE染色结果显示：糖尿病后肢缺血组大鼠小腿三头肌的结构破坏,有大量炎症细胞浸润,肌肉损伤程度重于正常对照组和糖尿病组。免疫组化sP染色结果显示：糖尿病后肢缺血组大鼠大腿股四头肌的毛细血管密度[（1．40±0．55）个／HPF]小于正常对照组[（6．80±0．84）个／HPF]及糖尿病组[（4．60±0．55）个／HPF],差异均有统计学意义伊〈O．05）。结论对SD大鼠给予高脂饮食联合小剂量STZ注射可以成功诱导2型糖尿病模型,在此模型基础上结扎髂总动脉可以成功制备糖尿病后肢缺血模型。     

银杏叶提取物对2型糖尿病大鼠睾丸间质细胞雄激素合成的影响

目的:研究银杏叶提取物(EGB)对2型糖尿病大鼠睾丸间质细胞雄激素合成的影响。方法:雄性SD大鼠30只,随机均分成3组:正常对照组、2型糖尿病组、EGB治疗组。用光镜和透射电镜观察EGB对2型糖尿病大鼠睾丸的形态学改变;ELISA法检测血清LH、T水平;半定量RT-PCR检测睾丸间质细胞类固醇激素合成急性调节蛋白(StAR)、细胞色素P450侧链裂解酶(P450scc)、细胞色素P45017a-羟化酶(P450c17)、3β-羟基类固醇脱氢酶Ⅰ型(3β-HSD1)、17β-羟基类固醇脱氢酶Ⅲ型(17β-HSD3)的mRNA水平。结果:糖尿病组光镜下睾丸间质细胞较正常对照组缩小;透射电镜下见到间质细胞核固缩,胞质内内质网减少。糖尿病组血清LH及T水平显著低于正常对照组(P<0.05);睾丸组织P450scc的mRNA水平显著低于正常对照组(P<0.01),StAR、17β-HSD3及3β-HSD1的mRNA水平也明显低于正常对照组(P<0.05),P450c17基因表达呈下降趋势(P>0.05);EGB治疗12周与糖尿病组比较睾丸组织病理改变较轻,血清LH、T含量升高(P<0.05),StAR、P450scc的mRNA水平升高(P<0.05),P450c17、17β-HSD3及3β-HSD1的mRNA水平呈上升趋势(P>0.05)。结论:EGB能减轻糖尿病大鼠睾丸损害并使2型糖尿病大鼠睾丸间质细胞合成和分泌T能力增强。     

胃袖带切除术对GK大鼠2型糖尿病的影响及其机理

目的研究胃袖带切除术（sleevegastrectomy,SG）对GK大鼠2型糖尿病（type2diabetesmellitus,T2DM）的治疗作用及其可能机理。方法将13只12周龄的GK大鼠随机分为2组：SG组7只和假手术组（SO组）6只,分别行SG术和假手术。于术前及术后1、4、10和26周测量2组大鼠的体质量、24h进食量、空腹血糖值、血清胰高血糖素样肽-1（glucagon-likepeptide-1,GLP-1）和血清生长激素释放肽（Ghrelin）浓度;于术后10周检测2组大鼠的粪便能量含量,并进行口服葡萄糖耐量实验（OGTT）和胰岛素耐受性实验（ITT）。结果①体质量：各时点2组大鼠的体质量比较差异均无统计学意义（P〉0．05）;与术前比较,术后1周2组大鼠的体质量均降低（P〈0．01）,术后10和26周的体质量均增加（P〈0．01）。②24h进食量：与SO组比较,术后4和10周SG组大鼠的24h进食量均较低（P〈0。05）。与术前比较,SG组大鼠术后1、4及10周的进食量均较低（P〈0．05）,SO组大鼠术后1周的进食量低于术前（P〈0．05）。③空腹血糖值：与SO组比较,术后各时点SG组大鼠的空腹血糖值均较低（P〈0．01）。与术前比较,SG组大鼠术后各时点的空腹血糖值均较低（P〈0．01）,而SO组大鼠仅术后1周明显低于术前∽〈0．OD。④血清GLP-1水平：与SO组比较,术后4、10及26周SG组大鼠的血清GLP．1水平均较高（P〈0．05）。与术前比较,术后4、10及26周SG组大鼠的血清GLP-1水平较高（P〈0．05）,而术后SO组大鼠的血清GLP．1水平无明显变化（P〉0．05）。⑤血清Ghrelin水平：与SO组比较,术后各时点SG组大鼠的血清Ghrelin水平均较低（P〈0．01）。与术前比较,术后各时点SG组大鼠的血清Ghrelin水平均较低（P〈0．001）,而SO组大鼠的血清Ghrelin水平无明显变化（P〉0．05）。⑥曲线下面积（AUC）：SG组大鼠的AUC（OGTT和ITT）均较SO组低（P〈0．01）。结论SG术可以明显降低GK大鼠的空腹血糖值,改善葡萄糖耐量及增强胰岛素敏感性,该作用可能是GLP．1、Grelin等多种胃肠道激素共同作用的结果。SG术可能是潜在的非肥胖型T2DM的治疗方法。     

The Relationship of Ghrelin and Adiponectin with Bone Mineral Density and Bone Turnover Markers in Elderly Men

Body weight is commonly considered a significant predictor of bone mineral density (BMD). Adiponectin, an adipocyte-derived hormone, could modulate BMD. Moreover, recent studies have reported that ghrelin is able to stimulate bone formation. In this study, we investigated any associations of adiponectin and ghrelin serum levels with bone turnover markers and BMD in elderly men. In 137 men aged 55 years and older (mean age 67.4 +/- 5.4 years, mean body mass index [BMI] 26.6 +/- 3.4 kg/m(2)), we evaluated serum adiponectin, serum ghrelin, body composition (fat mass and lean mass), BMD, bone alkaline phosphatase (ALP), and the carboxy-terminal telopeptide of type I collagen (betaCTX). Ghrelin showed significant correlations with BMD at the femoral neck (r = 0.25, P < 0.01), total femur (r = 0.22, P < 0.05), and whole body (r = 0.18, P < 0.05). However, after adjusting for age, BMI, and calcium intake, the correlation remained significant only for femoral neck BMD. Ghrelin showed a significant correlation with lean mass but not with fat mass and bone turnover markers. Adiponectin showed a positive association with both bone ALP and betaCTX; the correlation between adiponectin and bone ALP (r = 0.25, P < 0.01) remained significant after adjusting for confounding variables. No significant correlations between adiponectin and BMD at all skeletal sites were observed. In conclusion, our study suggests that in elderly Italian men serum ghrelin was significantly associated with femoral neck BMD and that adiponectin was positively associated with bone ALP. Further studies are needed to elucidate the role of adipocytokines in bone metabolism.     

Molecular and biochemical trajectories from diabetes to Alzheimer&rsquo;s disease: A critical appraisal

Diabetes mellitus (DM), a metabolic disorder is a major orchestra influencing brain and behavioral responses via direct or indirect mechanisms. Many lines of evidence suggest that diabetic patients apparently face severe brain complications, but the story is far from being fully understood. Type 2 diabetes, an ever increasing epidemic and its chronic brain complications are implicated in the development of Alzheimer’s disease (AD). Evidences from clinical and experimental studies suggest that insulin draws a clear trajectory from the peripheral system to the central nervous system. This review is a spot light on striking pathological, biochemical, molecular and behavioral commonalities of AD and DM. Incidence of cognitive decline in diabetic patients and diabetic symptoms in AD patients has brought the concept of brain diabetes to attention. Brain diabetes reflects insulin resistant brain state with oxidative stress, cognitive impairment, activation of various inflammatory cascade and mitochondrial vulnerability as a shared footprint of AD and DM. It has become extremely important for the investigators to understand the patho-physiology of brain complications in diabetes and put intensive pursuits for therapeutic interventions. Although, decades of research have yielded a range of molecules with potential beneficial effects, but they are yet to meet the expectations.     

Ghrelin对大鼠离体胰腺胰岛素分泌及Glut-2蛋白表达的影响

目的探讨Ghrelin对大鼠离体胰腺组织胰岛素分泌及葡萄糖转运蛋白-2（Glut-2）表达的影响。方法将25只Wistar大鼠随机分为正常对照组（NC组）、高糖组（HCG组）、高糖＋高浓度Ghrelin（10-8mol/L）组（HCG＋HCGh组）、高糖＋中浓度Ghrelin（10-9mol/L）组（HCG＋MCGh组）及高糖＋低浓度Ghrelin（10-10mol/L）组（HCG＋LCGh组）,每组5只。建立大鼠离体胰腺灌注模型,经腹主动脉远端相应灌注低糖（5.5 mmol/L）、单纯高糖（33.3 mmol/L）溶液或加入上述不同浓度Ghrelin的高糖（33.3 mmol/L）溶液。采用ELISA法测定门静脉流出液的胰岛素水平,采用免疫组化染色方法半定量测定Glut-2蛋白在离体胰腺组织中的表达水平,采用透射电镜观察胰岛β细胞的超微结构改变。结果 5组大鼠的空腹血浆葡萄糖（FBG）、空腹血浆胰岛素（FINS）、胰岛素抵抗指数（HOMA-IR）及胰岛素分泌指数（HOMA-β）比较差异均无统计学意义（P〉0.05）。用低糖溶液灌注时,5组大鼠门静脉流出液的胰岛素水平比较差异无统计学意义（P〉0.05）;而用高糖溶液灌注后,胰岛素的分泌在3 min和10～12 min时出现了2个高峰（以HCG＋HCGh组最高）。NC组大鼠胰岛β细胞Glut-2蛋白的平均光密度值高于其余4组（P〈0.05）。透射电镜观察结果显示,高糖各组大鼠离体胰腺的凋亡征象较NC组严重,但HCG＋HCGh组的细胞器损害程度较HCG＋MCGh组及HCG＋LCGh组轻。结论在大鼠离体胰腺中,Ghrelin可促进高浓度葡萄糖诱导的胰岛素分泌,对胰岛β细胞起保护作用。     

牵拉对兔耳软骨愈合和再生影响的实验研究

目的建立可靠的兔耳软骨牵引模型,对牵引后软骨的生长方式、愈合方式进行研究。方法 20只新西兰大白兔随机分组,每只兔随机选取一侧兔耳制作模型,实验组10只,对照组10只。实验组横向截断兔耳软骨,安装软骨牵引器,预固定2周,持续牵引2周,再固定1周;对照组术后不作牵引。于手术后即刻、预固定后、牵引后及再固定后分别取材,行HE、Masson染色,观察软骨组织生长愈合情况。对照组术后不作牵引。结果依靠外加牵引器进行持续牵引可促进兔耳软骨横向截断后产生新生的软骨细胞并修复组织缺损,基本恢复解剖形态。结论软骨截断后,通过外固定组织牵引技术能够促进软骨细胞再生和组织愈合,有望为软骨移植修复缺损提供更多的组织量。     

胃旁路术对非肥胖型2型糖尿病大鼠糖代谢的影响

目的:观察胃旁路术对非肥胖型2型糖尿病大鼠(GK大鼠)糖代谢的影响.方法:GK大鼠20只,Wistar大鼠10只,随机分为GK手术组、GK假手术组和Wistar假手术组,每组10只;手术组行胃旁路术;测定术前1周及术后第1、2、4、8、12周各组体质量、空腹血糖(FPG)、糖化血红蛋白(HbA1c)水平和血清胰岛素(INS)含量.结果:术后12周,GK手术组大鼠体质量由术前的(255.10±21.09)g上升到(364.55±25.73)g,FPG和HbA1c分别由术前的(11.36±1.14)mmol/L和(8.91±0.36)%下降到(8.36±0.62)mmol/L和(6.35±0.46)%,而血清INS由术前(32.76±2.37)μIU/mL上升到(55.14±5.45)μIU/mL.结论:胃旁路术可以明显降低GK大鼠的空腹血糖,改善糖代谢障碍.     

Roux-en-Y胃旁路术对GK大鼠骨骼肌组织胰岛素抵抗影响的机制研究

目的探讨Roux-en-Y胃旁路术（RYGB）改善2型糖尿病大鼠（Goto-Kakizaki大鼠,GK大鼠）骨骼肌胰岛素抵抗的可能机制。方法30只GK大鼠随机分为GK-RYGB组、GK-假手术组、GK．对照组,另取10只Wistar大鼠作为正常对照组。术后28d时处死实验动物。ELISA法检测血浆ghrelin浓度,免疫印迹法检测骨骼肌组织的磷酸化（p）-／总（t）。P13Kp85ct、p-／t．Akt／PKB及细胞膜（m）-／t．GLUT4蛋白的相对表达量,实时荧光定量PCR法检测骨骼肌组织中P13Kp85a、Akt／PKB及GLUT4mRNA的表达。结果①血浆ghrelin浓度在正常对照组明显高于GK。对照组（P〈0．01）和GK-假手术组（P〈O．01）;GK-RYGB组也明显高于GK．对照组∽〈0．01）及GK．假手术组（尸〈0．01）,但与正常对照组相比差异无统计学意义（尸〉0．05）。②p-／t．P13Kp85tt、p-／t．Akt／PKB及m-／t-GLUT4蛋白相对表达量在正常对照组均较GK-对照组（分别P〈0．01、P〈0．05、P〈0．01）和GK．假手术组（分别P〈0．01、P〈0．05、P〈0．01）明显上升;GK-RYGB组亦较GK-对照组（分别P〈0．01、P〈0．05、JP〈0．01）和GK．假手术组（分别尸〈0．01、P〈0．05、P〈0．01）均分别明显上升。③骨骼肌组织中P13Kp85ct、Akt／PKB及GLUT4mRNA的表达在正常对照组均较GK．对照组（分别P〈0．01、P〈0．05、P〈0．05）和GK．假手术组（分别P〈0．01、P〈0．05、P〈0．05）明显上升;GK．RYGB组较GK．对照组（分别P〈0．01、P〈0．05、P〈0．05）和GK-假手术组（分别P〈0．0l、P〈0．05、P〈0．05）也均分别明显上升。结论①RYGB术后GK大鼠血浆ghrelin水平显著升高。②RYGB术能够上调GK大鼠骨骼肌组织中P13Kp85a、Akt／PKBmRNA和磷酸化蛋白的表达,并上调GLUT4的转录和翻译,促使更多的GLUT4在细胞膜表达,增加骨骼肌组织对葡萄糖的摄取,从而改善骨骼肌组织的胰岛素抵抗。     

Liver blood supply after a modified Appleby procedure in classical and aberrant arterial anatomy

Reported here are two cases of a modified Appleby operation for borderline resectable ductal adenocarcinoma of the pancreatic body, in one of which a R0 distal resection was attended to by excision, not only of the celiac axis, but also of the common and left hepatic arteries in the presence of arterial anatomic variation Michels, type VIIIb. The possibility and avenues of the maintenance of the blood supply to the left hepatic lobe after surgical aggression of this kind are demonstrated employing computed tomography (CT) and 3-D CT angiography. Furthermore, both cases highlight all important worrisome aspects of pancreatic cancer resectability prediction.     

25 羟维生素D3与糖尿病骨质疏松患者的相关性研究

目的 观察 2 型糖尿病(T2DM)患者骨质疏松与25 羟维生素D3(25-OH-D3)的关系? 方法 测定186 例2 型糖尿病(T2DM)患者及65例年龄?性别相匹配健康对照者血(Ca) ?磷(P),采用酶联免疫法测定各组血清骨特异性碱性磷酸酶(ALP)?血清骨钙素(BGP)? (25-OH-D3)的浓度? 结果 2型糖尿病组BGP?25-OH-D3浓度低于对照组,差异显著(P<0.05),血清Ca?P?血浆ALP浓度与对照组之间无显著差异(P>0.05)? 女型糖尿病患者骨质疏松症的发病率高于男性,女性OP组BGP?25-OH-D3的浓度显著低于男性OP组(P<0.05)? 结论 2 型糖尿病患者 25-OH-D3的减少可影响钙?磷代谢,从而导致骨质疏松,因此对于 2 型糖尿病患者应早期适量补充钙剂及维生素D3?