~1H-MRS对Ⅱ型糖尿病周围神经病变定性诊断的研究
摘要
目的
利用磁共振氢质子波谱(Proton Magnetic Resonance Spectroscopy,1H-MRS)技术,从分子影像学水平对Ⅱ型糖尿病患者下肢骨骼肌内的常见代谢物进行定量及半定量分析,研究Ⅱ型糖尿病患者骨骼肌的代谢改变,探讨糖尿病周围神经病变(DPN)与骨骼肌组织内代谢物变化的关联性,探讨磁共振氢质子波谱(1H-MRS)在糖尿病周围神经病变(DPN)诊断中的应用价值。
材料与方法
1、研究对象的选择
联系山东省立医院内分泌科,2010年3月至2010年10月间选取48例经完整资料诊断为Ⅱ型糖尿病的患者,其中男性24例,女性24例,平均年龄54.5±10.5岁,年龄范围40～84岁,病程7天～25年。所有患者均行小腿部位肌电图检查。根据肌电图结果是否存在周围神经损伤作为糖尿病周围神经病变(DPN)的诊断标准,将T2DM病例分成两组:有周围神经病变组(A组)23例(男性10例,女性13例,平均年龄56.7±8.7岁,年龄范围46-84岁)和无周围神经病变组(B组)25例(男性14例,女性11例,平均年龄54.7±9.3岁,年龄范围40-70岁)。所有受试对象均排除其他原因所致的周围神经病变。同时在健康查体者中随机选择年龄、性别相匹配的健康成年人作为对照组(C组)共24例,(男性11例,女性13例,平均年龄52.2±13.1岁,年龄范围30-77岁)。组间年龄(F=1.092,P=0.341)、性别(F=0.361,P=0.550)均无显著性差异。
2、设备与方法
采用德国西门子公司1.5T超导型全身MRI扫描仪(Magnetom Sonata Maestro Class)和标准膝关节线圈。扫描序列包括小腿部位常规序列和1H-MRS序列。检查时均取仰卧位,足先进。小腿比目鱼肌中心与线圈中心线重合。所有受试对象在检查前签署知情同意书。
常规扫描序列具体参数如下:横断位以及冠状位T1WI(TR 450ms,TE 13ms)、冠状FS-T2WI(TR 3540ms,TE 85ms)以及矢状位Pd+T2WI(TR 3000ms,TE 14ms)。FOV 200mm×200mm,层厚10mm,层间距5mm。
常规序列扫描完成后,以横断位、冠状位、矢状位三方位T1WI图像作为1H-MRS的定位像,进行磁共振波谱成像序列(1H-MRS)扫描。1H-MRS具体参数如下:单体素(SVS),激励回波探测法(stimulated-echo acquisition mode,STEAM),FOV 180mm,TR 1500ms,TE 30ms,采集次数128次,采集时间180s,带宽1000Hz,体素大小20mm×20mm×20mm。1H-MRS扫描前自动采用化学位移饱和法(chemical shift selective saturation,CHESS)进行水抑制,水抑制频率为35Hz。感兴趣区(ROI)定位在小腿比目鱼肌内,同时避开邻近血管、肌筋膜及周围脂肪等成分对数据采集的影响,以确保数据准确性。
扫描完成后,将1H-MRS原始数据调至工作站波谱选项卡中经后处理软件进行交互式处理得到包含所有待分析物质的谱线图以及各物质的峰值下面积积分值,主要有:肌酸(Cr)、胆碱复合物(Cho)、细胞外脂肪(EMCL)、细胞内脂肪(IMCL),并以Cr为内标准取得Cho/Cr、EMCL/Cr、IMCL/Cr的相对含量值。可以对谱线图进行手动后处理,使物质含量值更加精确。
3、统计分析
采用SPSS17.0统计分析软件包,所有计量资料均采用?χ±s表示。数据正态性检验和方差齐性检验分别采用单样本Kolmogorov-Smirnov检验和Levene检验。应用单因素方差分析(one-way ANOVA)对组间常见代谢物的含量及相对含量进行比较分析。P<0.05为有差异,P<0.01为有显著差异。
结果
各组间的Cho、Cr、EMCL、IMCL峰下的面积及Cho/Cr、EMCL/Cr、IMCL/Cr比值比较结果如下:
1、糖尿病周围神经病变组(A组)与糖尿病无周围神经病变组(B组)比较:Cr、Cho、EMCL、IMCL、Cho/Cr含量的差异没有统计学意义(P>0.05);EMCL/Cr、IMCL/Cr含量的差异有统计学意义(P<0.05);
2、糖尿病周围神经病变组(A组)与对照组(C组)比较:Cr、Cho、EMCL、EMCL/Cr含量的差异没有统计学意义(P>0.05);IMCL、Cho/Cr、IMCL/Cr含量的差异有统计学意义(P<0.05);
3、糖尿病无周围神经病变组(B组)与对照组(C组)比较:Cr、Cho、EMCL、Cho/Cr含量的差异没有统计学意义(P>0.05);IMCL、EMCL/Cr、IMCL/Cr含量的差异有统计学意义(P<0.05)。
结论
与正常人相比,糖尿病患者比目鱼肌内IMCL、IMCL/Cr升高,其中糖尿病无周围神经病变患者比目鱼肌中IMCL、EMCL/Cr、IMCL/Cr升高,糖尿病周围神经病变患者比目鱼肌中IMCL、Cho/Cr、IMCL/Cr升高。因此,利用1H-MRS对小腿骨骼肌组织内的常见代谢物进行定量分析,评价骨骼肌组织的代谢改变对Ⅱ型糖尿病周围神经病变的诊断具有一定的参考价值。
Objective
To investigate quantitatively common metabolites contents in lower limb skeletal muscle of patients with typeⅡdiabetes with diabetic peripheral neuropathy (DPN), typeⅡdiabetes without diabetic peripheral neuropathy (DPN) and healthy people from the level of molecular imaging using proton magnetic resonance spectroscopy techniques (1H-MRS). At the same time, discuss some changes of common metabolite contents in skeletal muscles among three groups, and to evaluate the value of magnetic resonance proton spectroscopy (1H-MRS) in diabetic peripheral neuropathy (DPN) diagnosis. Materials and Methods
1. The choice of subjects
Cooperation with the Department of Endocrinology, Shandong Provincial Hospital, 48 patients with typeⅡdiabetes diagnosed by the complete data (24 males, 24 females, mean age 54.5±10.5 years, range 40-84years old, course 7d-25 years) were selected in the study from March 2010 to October 2010. All patients were checked EMG examination in the calf, and were grouped into a peripheral neuropathy group (A group) 23 patients (10 males and 13 females, mean age 56.7±8.7 years, range 46-84 years) and without peripheral neuropathy group (B group), 25 cases (14 males and 11 female, mean age 54.7±9.3 years, range 40-70 years) according to EMG showed nerve damage as a diabetic peripheral neuropathy (DPN) in the diagnostic criteria.
At the same time, 24 healthy adults (11 males, 13 females, mean age 52.2±13.1 years, range 20-25 years old) without T2DM were randomly selected as a control group from people who are health check. All subjects were excluded peripheral nerve lesions due to other causes. Age (F=1.092, P=0.341), gender (F=0.361, P=.550) among the three groups were not significantly different.
1.5T superconducting magnetic resonance scanner (Germany Siemens Magnetom Sonota Maestro Class) and standard knee coil was used. Scanning Sequences include the conventional sequence and MRS sequences.
All subjects carried out axial and coronary T1-weighted imaging(TR 450ms, TE 13ms), coronary T2-weighted imaging(TR 3540ms, TE 85ms) and sagittal Proton density-weighted image (TR 3000ms, TE 14ms). FOV is 240mm×240mm, thickness is 10mm, with 5mm spacing.
When the conventional serial scan is complete, transverse, sagittal and coronal T1-weighted image was used for positioning magnetic resonance spectroscopy. Specific parameters are as follows: single-voxel (SVS), stimulated-echo acquisition mode (STEAM),FOV 180mm,TR 1500 ms,TE 30ms,acquisition 128 times, scan time 180s, bandwidth of 1000Hz, voxel 20mm×20mm×20mm. ROI (ROI) placed on the soleus muscle in the calf, avoiding the adjacent blood vessels, fascia and the surrounding fat in order to remove their impact on data collection to ensure that collected data is more accurate. Before MRS scanning, water suppression were automatically performed by chemical shift saturation method (chemical shift selective saturation, CHESS), and the frequency of the water suppression is 35Hz.
After scanning, the original spectral data was transferred to the spectrum tab of workstations, which were processed by the interactive processing software automatically. Finally, MRS curves containing all the substances to be analyzed and the peak integral areas under these materials were obtained, the most of them including creatine (Cr), choline (Cho), extra-myocellular liplids (EMCL), intra-myocellular liplids (IMCL) and relative content of Cho/Cr, EMCL/Cr, IMCL/Cr. Subsequently, if dissatisfactory, manual adjustment could be made on the MRS curves, in order to obtain more precise values of material content.
3. Statistical Analysis
SPSS 17.0 statistical analysis software package was used. All measurement data are indicated with?χ±s. Single-sample Kolmogorov-Smirnov test and Levene test were used to test data normality and homogeneity of variance. One-way analysis of variance (ANOVA) was used to analyze the content and relative content differences of a material among there groups. To make the P<0.05 as a difference and P <0.01 as the significant difference.
Results
Comparison results of areas under the peak Cho, Cr, EMCL, IMCL and the ratio of Cho/Cr, EMC /Cr, IMCL/Cr among there groups are as follows:
2. Equiment and Methods
1. Between diabetic peripheral neuropathy group (A group) and diabetic patients without peripheral neuropathy group (B group): Content differences of Cr, Cho, EMCL, IMCL and Cho/Cr was not statistically significant (P> 0.05); Content differences of EMCL/Cr and IMCL/Cr was statistically significant (P<0.05);
2. Between diabetic peripheral neuropathy group (A group) and control group (C group): Content differences of Cr, Cho, EMCL and EMCL/Cr was not statistically significant (P> 0.05); Content differences of IMCL, Cho/Cr and IMCL/Cr was statistically significant (P<0.05);
3. Between diabetic patients without peripheral neuropathy group (B group) and control group (C group): Content differences of Cr, Cho, EMCL and Cho/Cr was not statistically significant (P> 0.05); Content differences of IMCL, EMCL/Cr and IMCL/Cr was statistically significant (P<0.05). Conclusion
Compared with healthy people, IMCL, IMCL/Cr in soleus muscle increase in T2DM patients. IMCL, EMCL/Cr, IMCL/Cr increase in T2DM patients without peripheral neuro- pathy; IMCL, Cho/Cr, IMCL/Cr increase in T2DM patients with peripheral neuropat- hy. Therefore, 1H-MRS has some reference value in the diagnosis of peripheral neuropathy in T2DM patients by testing contents and relative contents of some common metabolites and by analyzing certain metabolic changes of the calf muscle tissue.
利用磁共振氢质子波谱(Proton Magnetic Resonance Spectroscopy,1H-MRS)技术,从分子影像学水平对Ⅱ型糖尿病患者下肢骨骼肌内的常见代谢物进行定量及半定量分析,研究Ⅱ型糖尿病患者骨骼肌的代谢改变,探讨糖尿病周围神经病变(DPN)与骨骼肌组织内代谢物变化的关联性,探讨磁共振氢质子波谱(1H-MRS)在糖尿病周围神经病变(DPN)诊断中的应用价值。
材料与方法
1、研究对象的选择
联系山东省立医院内分泌科,2010年3月至2010年10月间选取48例经完整资料诊断为Ⅱ型糖尿病的患者,其中男性24例,女性24例,平均年龄54.5±10.5岁,年龄范围40～84岁,病程7天～25年。所有患者均行小腿部位肌电图检查。根据肌电图结果是否存在周围神经损伤作为糖尿病周围神经病变(DPN)的诊断标准,将T2DM病例分成两组:有周围神经病变组(A组)23例(男性10例,女性13例,平均年龄56.7±8.7岁,年龄范围46-84岁)和无周围神经病变组(B组)25例(男性14例,女性11例,平均年龄54.7±9.3岁,年龄范围40-70岁)。所有受试对象均排除其他原因所致的周围神经病变。同时在健康查体者中随机选择年龄、性别相匹配的健康成年人作为对照组(C组)共24例,(男性11例,女性13例,平均年龄52.2±13.1岁,年龄范围30-77岁)。组间年龄(F=1.092,P=0.341)、性别(F=0.361,P=0.550)均无显著性差异。
2、设备与方法
采用德国西门子公司1.5T超导型全身MRI扫描仪(Magnetom Sonata Maestro Class)和标准膝关节线圈。扫描序列包括小腿部位常规序列和1H-MRS序列。检查时均取仰卧位,足先进。小腿比目鱼肌中心与线圈中心线重合。所有受试对象在检查前签署知情同意书。
常规扫描序列具体参数如下:横断位以及冠状位T1WI(TR 450ms,TE 13ms)、冠状FS-T2WI(TR 3540ms,TE 85ms)以及矢状位Pd+T2WI(TR 3000ms,TE 14ms)。FOV 200mm×200mm,层厚10mm,层间距5mm。
常规序列扫描完成后,以横断位、冠状位、矢状位三方位T1WI图像作为1H-MRS的定位像,进行磁共振波谱成像序列(1H-MRS)扫描。1H-MRS具体参数如下:单体素(SVS),激励回波探测法(stimulated-echo acquisition mode,STEAM),FOV 180mm,TR 1500ms,TE 30ms,采集次数128次,采集时间180s,带宽1000Hz,体素大小20mm×20mm×20mm。1H-MRS扫描前自动采用化学位移饱和法(chemical shift selective saturation,CHESS)进行水抑制,水抑制频率为35Hz。感兴趣区(ROI)定位在小腿比目鱼肌内,同时避开邻近血管、肌筋膜及周围脂肪等成分对数据采集的影响,以确保数据准确性。
扫描完成后,将1H-MRS原始数据调至工作站波谱选项卡中经后处理软件进行交互式处理得到包含所有待分析物质的谱线图以及各物质的峰值下面积积分值,主要有:肌酸(Cr)、胆碱复合物(Cho)、细胞外脂肪(EMCL)、细胞内脂肪(IMCL),并以Cr为内标准取得Cho/Cr、EMCL/Cr、IMCL/Cr的相对含量值。可以对谱线图进行手动后处理,使物质含量值更加精确。
3、统计分析
采用SPSS17.0统计分析软件包,所有计量资料均采用?χ±s表示。数据正态性检验和方差齐性检验分别采用单样本Kolmogorov-Smirnov检验和Levene检验。应用单因素方差分析(one-way ANOVA)对组间常见代谢物的含量及相对含量进行比较分析。P<0.05为有差异,P<0.01为有显著差异。
结果
各组间的Cho、Cr、EMCL、IMCL峰下的面积及Cho/Cr、EMCL/Cr、IMCL/Cr比值比较结果如下:
1、糖尿病周围神经病变组(A组)与糖尿病无周围神经病变组(B组)比较:Cr、Cho、EMCL、IMCL、Cho/Cr含量的差异没有统计学意义(P>0.05);EMCL/Cr、IMCL/Cr含量的差异有统计学意义(P<0.05);
2、糖尿病周围神经病变组(A组)与对照组(C组)比较:Cr、Cho、EMCL、EMCL/Cr含量的差异没有统计学意义(P>0.05);IMCL、Cho/Cr、IMCL/Cr含量的差异有统计学意义(P<0.05);
3、糖尿病无周围神经病变组(B组)与对照组(C组)比较:Cr、Cho、EMCL、Cho/Cr含量的差异没有统计学意义(P>0.05);IMCL、EMCL/Cr、IMCL/Cr含量的差异有统计学意义(P<0.05)。
结论
与正常人相比,糖尿病患者比目鱼肌内IMCL、IMCL/Cr升高,其中糖尿病无周围神经病变患者比目鱼肌中IMCL、EMCL/Cr、IMCL/Cr升高,糖尿病周围神经病变患者比目鱼肌中IMCL、Cho/Cr、IMCL/Cr升高。因此,利用1H-MRS对小腿骨骼肌组织内的常见代谢物进行定量分析,评价骨骼肌组织的代谢改变对Ⅱ型糖尿病周围神经病变的诊断具有一定的参考价值。
Objective
To investigate quantitatively common metabolites contents in lower limb skeletal muscle of patients with typeⅡdiabetes with diabetic peripheral neuropathy (DPN), typeⅡdiabetes without diabetic peripheral neuropathy (DPN) and healthy people from the level of molecular imaging using proton magnetic resonance spectroscopy techniques (1H-MRS). At the same time, discuss some changes of common metabolite contents in skeletal muscles among three groups, and to evaluate the value of magnetic resonance proton spectroscopy (1H-MRS) in diabetic peripheral neuropathy (DPN) diagnosis. Materials and Methods
1. The choice of subjects
Cooperation with the Department of Endocrinology, Shandong Provincial Hospital, 48 patients with typeⅡdiabetes diagnosed by the complete data (24 males, 24 females, mean age 54.5±10.5 years, range 40-84years old, course 7d-25 years) were selected in the study from March 2010 to October 2010. All patients were checked EMG examination in the calf, and were grouped into a peripheral neuropathy group (A group) 23 patients (10 males and 13 females, mean age 56.7±8.7 years, range 46-84 years) and without peripheral neuropathy group (B group), 25 cases (14 males and 11 female, mean age 54.7±9.3 years, range 40-70 years) according to EMG showed nerve damage as a diabetic peripheral neuropathy (DPN) in the diagnostic criteria.
At the same time, 24 healthy adults (11 males, 13 females, mean age 52.2±13.1 years, range 20-25 years old) without T2DM were randomly selected as a control group from people who are health check. All subjects were excluded peripheral nerve lesions due to other causes. Age (F=1.092, P=0.341), gender (F=0.361, P=.550) among the three groups were not significantly different.
1.5T superconducting magnetic resonance scanner (Germany Siemens Magnetom Sonota Maestro Class) and standard knee coil was used. Scanning Sequences include the conventional sequence and MRS sequences.
All subjects carried out axial and coronary T1-weighted imaging(TR 450ms, TE 13ms), coronary T2-weighted imaging(TR 3540ms, TE 85ms) and sagittal Proton density-weighted image (TR 3000ms, TE 14ms). FOV is 240mm×240mm, thickness is 10mm, with 5mm spacing.
When the conventional serial scan is complete, transverse, sagittal and coronal T1-weighted image was used for positioning magnetic resonance spectroscopy. Specific parameters are as follows: single-voxel (SVS), stimulated-echo acquisition mode (STEAM),FOV 180mm,TR 1500 ms,TE 30ms,acquisition 128 times, scan time 180s, bandwidth of 1000Hz, voxel 20mm×20mm×20mm. ROI (ROI) placed on the soleus muscle in the calf, avoiding the adjacent blood vessels, fascia and the surrounding fat in order to remove their impact on data collection to ensure that collected data is more accurate. Before MRS scanning, water suppression were automatically performed by chemical shift saturation method (chemical shift selective saturation, CHESS), and the frequency of the water suppression is 35Hz.
After scanning, the original spectral data was transferred to the spectrum tab of workstations, which were processed by the interactive processing software automatically. Finally, MRS curves containing all the substances to be analyzed and the peak integral areas under these materials were obtained, the most of them including creatine (Cr), choline (Cho), extra-myocellular liplids (EMCL), intra-myocellular liplids (IMCL) and relative content of Cho/Cr, EMCL/Cr, IMCL/Cr. Subsequently, if dissatisfactory, manual adjustment could be made on the MRS curves, in order to obtain more precise values of material content.
3. Statistical Analysis
SPSS 17.0 statistical analysis software package was used. All measurement data are indicated with?χ±s. Single-sample Kolmogorov-Smirnov test and Levene test were used to test data normality and homogeneity of variance. One-way analysis of variance (ANOVA) was used to analyze the content and relative content differences of a material among there groups. To make the P<0.05 as a difference and P <0.01 as the significant difference.
Results
Comparison results of areas under the peak Cho, Cr, EMCL, IMCL and the ratio of Cho/Cr, EMC /Cr, IMCL/Cr among there groups are as follows:
2. Equiment and Methods
1. Between diabetic peripheral neuropathy group (A group) and diabetic patients without peripheral neuropathy group (B group): Content differences of Cr, Cho, EMCL, IMCL and Cho/Cr was not statistically significant (P> 0.05); Content differences of EMCL/Cr and IMCL/Cr was statistically significant (P<0.05);
2. Between diabetic peripheral neuropathy group (A group) and control group (C group): Content differences of Cr, Cho, EMCL and EMCL/Cr was not statistically significant (P> 0.05); Content differences of IMCL, Cho/Cr and IMCL/Cr was statistically significant (P<0.05);
3. Between diabetic patients without peripheral neuropathy group (B group) and control group (C group): Content differences of Cr, Cho, EMCL and Cho/Cr was not statistically significant (P> 0.05); Content differences of IMCL, EMCL/Cr and IMCL/Cr was statistically significant (P<0.05). Conclusion
Compared with healthy people, IMCL, IMCL/Cr in soleus muscle increase in T2DM patients. IMCL, EMCL/Cr, IMCL/Cr increase in T2DM patients without peripheral neuro- pathy; IMCL, Cho/Cr, IMCL/Cr increase in T2DM patients with peripheral neuropat- hy. Therefore, 1H-MRS has some reference value in the diagnosis of peripheral neuropathy in T2DM patients by testing contents and relative contents of some common metabolites and by analyzing certain metabolic changes of the calf muscle tissue.
引文
[1]张惠芬,迟家敏,王瑞萍.实用糖尿病学[M].第2版,北京:人民出版社,2001:1.
[2]Boulton NJM, Vinik A I, Arezzo JC, et al. Diabetic Neuropathies: a statement by the American Diabetes Association[J]. Diabetes Care, 2005, 28(4):956-962.
[3]宁光.糖尿病神经病变的诊断和治疗[J].国际内分泌代谢杂志, 2006, 26(3):附录-3-2-3-4.
[4] Bendszus M, Wessig C, Solymosi L, et al. MRI of peripheral nerve de-generation and regeneration: correlation with electrophysiology and histology[J]. Exp Neurol 2004,188(1):171-177.
[5]Danielson ER, Ross B. Magnetic resonance spectroscopy diagnosis of neurological diseases. New York: Maral Dekker, 1999:5-22.
[6]刘兆爱,甲吉芳,刘艳霞,等.脂代谢紊乱与2型糖尿病慢性并发症关系分析[J].实用心电学杂志,2008,17(3):187-188.
[7]陈金仲,邵豪脂.脂代谢紊乱与胰岛素抵抗的相关研究进展[J].中国实用医药,2008(7):147-148.
[8]朱翠英.脂毒性的形成机制及其干预策略[J].国际检验医学杂志,2006,27(1):24-26.
[9]张静,张建华.初诊糖尿病患者β细胞功能状况与血糖水平的相关性分析[J].临床内科杂志,2007,21(8):553-554.
[10] Feldman EL, Cornblath DR, Porter J,et al.NINDS:Advances in undertanding and treating neuropathy. J Peripher Nerv Syst,2008,13(1):1-6.
[11] Jensen TS, Bach FW, Kastrup J, et a.l Vibratory and thermal thresholds in diabetics with and without clinical neuropathy. Acta NeurolScand,1991,84(4):326-333.
[12]吴佩娴,张帆,孙凤芹.糖尿病周围神经病变的临床分析及震动感觉阈值测定.中国实用医药,2009,4(21):22-23.
[13]Summer CJ,Sheth S,Griffin JW,et al. The spectrum of neuropathy in diabetic and impaired glucose tolerance[J].Neurology,2003,60:108-111.
[14]王盼,吴仲敏,凡馨.糖尿病周围神经病及其检测技术.四川医学,2009,30(6):978-980.
[15]唐彦,谈跃.糖尿病周围神经病变的诊断进展. 2010,48(1):9-11.
[16]Li F, Abatan OI, KimH, et al. Taurine reverses neurological and neurovascular deficits in Zucker diabetic fatty rats[J].Neurobiol Dis,2006,22(3):669-676.
[17]马叶萍,孙新芳.糖尿病周围神经病变的药物治疗进展[J].中风与神经疾病杂志,2006,23(5):631-632.
[18]Cameron NE, Eaton SE, Cotter MA, et al. Vascular factors and metabolic interactions in the pathogenesis of diabetic neuropathy[J]. Diabetologia,2001,44(11):1973-1988.
[19]谢华,王清秀,肖敏.糖尿病周围神经痛研究进展.郧阳医学院学报[J],2008,27(1):85-87.
[20]Freeman R. Not all neuropathy in diabetes is of diabetic etiology:differential diagnosis of diabetic neuropathy〔J〕.Curr fasting plasma Diab Rep,2009,9:423-431.
[21]王萌,王瑞英,王素星.氧化应激与糖尿病周围神经病变〔J〕.临床荟萃,2009,24(5):449-450.
[22]Cheng HT, Dauch JR,Hayes JM,et al.Nerve growth factor mediates mechanical allodynia in a mouse model of type 2 diabetes〔J〕.Neuropathol Exp Neurol,2009,68:1229-1243.
[23]张雪兰,谢云,职心乐.糖尿病周围神经病变相关危险因素分析.中国慢性病预防与控制,2010,18(2):115-117.
[24]Tesfaye S,Chaturvedi N,Eaton SE,et al.Vascular risk factors and diabetic neuropathy. N Engl Med,2005,352(4):341-350.
[24]程璇,卢祖能.周围神经病临床诊疗新进展.卒中与神经疾病,2009,16(3):185-188.
[25] Yagihashi S, Yamagishi S, Wada R. Pathology and pathogenetic mechanisms of diabetic neuropathy: correlation with clinical signs and symptoms[J].Diabetes Res Clin Parct,2007,77(1):184-189.
[26] Malik R A, Tesfaye S, Newrick P G, et al. Sural nerve pathology in diabetic patients with minimal but progressive neuropathy. Diabetologia. 2005, 48: 578-585.
[27] Kiziltan ME, Gunduz A, Kiziltan G,et al.Peripheral neuropathy in patientswith diabetic footulcers: clinical and nerve conduction study[J]. Neurol Sci,2007, 258(1-2): 75-79.
[28]张大红,刘淑娣,李涛.糖尿病周围神经病变的临床特点及药物治疗.中国医药导报,2009年,6(10):224.
[29]Douglas W.Diabetes mellitus and the peripheral nervous system:manifestations and mechanisms[J].Muscle Nerve,2007,36:145.
[30]汤晓芙,陈学诗,主编.中国现代神经精神病学发展概况[M].北京:中国科学技术出版社,1995.159.
[31]朱一浩.糖尿病周围神经病患者的神经传导速度分析[J].临床脑电学杂志,1998,7:232.
[32]尹凤琼,唐一平,朱榆红.糖尿病周围神经病肌电图检查与临床分析.云南医药,2008,29(1):17-21.
[33]吕海莉,吴建民,刘宽芝.糖尿病周围神经病变及其康复治疗.中国康复医学杂志,2009,24(3):287-9.
[34]PERKINSBA, BERILR. Diagnosis and management of diabebic neuropathy[J].Curr Diab Rep,2002,2(6):495-500.
[35]陈妙玲,李新春.周围神经损伤的磁共振成像研究进展.国际医学放射学杂志, 2010,33(4): 325-328.
[36] Sinnreich M, Taylor BV, Dyck PJ. Diabetic neuropathies. Classification, clinical features, and pathophysiological basis[J]. Neurologist, 2005,11(2): 63-79.
[37]Said G. Diabetic neuropathy-a review[J]. Nat Clin Pract Neurol,2007, 3(6):331-340.
[38]郭军红,蒲传强.糖尿病周围神经病的病理与电生理研究进展.中国康复理论与实践,2009,15(1):8-10.
[39]Gary LP, PatriciaMN,Madhumita R,etal.Intraepidermal nerve fibers are indicators of small-fiber neuropathy in both diabetic and nondiabetic patients[J].Diabetes Care, 2004, 27(8): 1974-1979.
[40] Ruiz-Pena JL, Pinero P, Sellers G, et al. Magnetic resonance spectroscopy of normal appearing white matter in early relapsing-remitting multiple sclerosis: correlations between disability and spectroscopy. J Neurol, 2002, 249(10): 1382-1390.
[41]彭洪娟,赵斌. 1H-MRS基本原理及成像技术[J].医学影像学杂志,2004, 12:1033-1035.
[42]李克,于同刚.磁共振波谱技术在肌骨疾病中的应用.中国医学计算机成像杂志[J],2003,9(5):332-337.
[43] GajewiczW,PapierzW,SzymczakW,etal.The use of proton MRS in the differential diagnosis of brain and tumor-like processes. MedSci Monit,2003,9:97-105.
[44] Castilo M,Kwock L,ukherji SK.Clinical application of proton MR spectroscopy. AJNR,1996,17:1-15.
[45] Burtscher IM,Holtas S. Proton MR spectroscopy in clinical routine. J Mag Reson Imaging,2001,13:560-567.
[46]郭红云,牛广明. 1H磁共振波谱分析在脑肿瘤诊断中的应用现状.医学综述,2008,14(11):1728-9.
[47] Jeffry RA , S ophia CS , Albert B ,et al . Abs olute quantitation of short TE brain1H2MR spectra and spectroscopic imaging data[J] . Journal of Computer Assisted Tomography ,1993 ,17 :191.
[48] Fisher E, Rudick RA, Simon JH, et al. Eight year follow up study of brain atrophy in patients with MS[J].Neurology,2002;59(9):1412-1420.
[49] Pouwels PJ, Frahm J. Regional metabolite concentrations in human brain as determined by quantitative localized proton MRS. Magn Reson Med, 1998; 39: 53-60.
[50]林艳,饶海冰,吴仁华.1H-MRS定量测定脑代谢物的研究.国外医学放射医学核医学分册2005,29(2):85-88.
[51] Pfefferbaum A, Adalsteinsson E, Spielman D et al. In vivo spectroscopic quantification of the N-acetylmoiety, creatine, and choline from large volumes of brain gray and white matter: effects of normal aging. Magn Reson Med, 1999; 41: 276- 284.
[52]Schulze S.Humoral and neural medicutors of the systemic respome to surgery[J].Dan Nod Bull,1993,40(3):365-477.
[53]邝菲,王飞.氢质子磁共振波谱(1H-MRS)技术应用.医学影像学杂志, 2007,17 (8) :871-4.
[54]Zancanaro C, Nano R, Marchioro C, et al. Magnetic resonance spectroscopy investigations of brown adipose tissue and isolated brown adipocytes[J]. J Lipid Res, 1994, 35(12):2191-2199.
[55]薛江苗,林祥涛,李吉昌等.磁共振氢质子波谱及弥散加权成像在诊断良、恶性骨病变中的对比应用.山东大学学报(医学版),2008,46(3):309-12.
[56] Boesch C , Slotboom J , Hoppeler H , et al . In vivo determinationof int ra2myocellular lipids in human skeletal muscle by means of lo2calized 1H2MR2spect roscopy[J] . Magn Reson Med ,1997 ,37 (4) :484-493.
[57]Schick F , Eismann B , J ung WI , et al . Comparison of localized proton NMR signals of skeletal muscle and fat tissue in vivo : two lipid compartment s in muscle tissue[J ] . Magn Reson Med ,1993 ,29 (2) :158-167.
[58]Sachin KC,Sharad M,et al.Magnetic resonance spectroscopy[J].Neuro Oplthalmol,2005,25:217-226.
[59] RicoSanz J,Thomas EL,Jenkinson G,et al.Diversity in Levels of Intracellular Total Creatine and Triglycerides in Human Skeletal Muscles Observed by 1H-MRS[J].J ApplPhysiol,1999,87(6):2068-2072.
[60]Brechtel K, Jacob S, Machann J, et al. Acquired Generalized Lipoatrophy(AGL):Highly Selective MR Lipid Imaging and Localized 1H-MRS[J].J Magn Reson Imaging,2000,12(2):306-310.
[61]蔡明江,成杰,张南雁.胰岛素抵抗与2型糖尿病直立性低血压的关系[J].中国临床康复,2003,7(27):3684-5.
[62]Pan DA, Lillioja S,Kriketos AD,et al.Skeletal Muscle Triglyceride Levels are Inversely Related to Insulin Action[J]. Diabetes, 1997,46(6):983-988.
[63]张磊,刘彦君.磁共振氢谱对胰岛素抵抗及Ⅱ型糖尿病的研究.放射学实践,2005,20(3):272-274.
[64] Perseghin G,Scifo P,De Cobelli F,et al.Intramyocellular Triglyceride Content Is a Determinant of in Vivo Insulin Resistance in Humans:a1H-13C Nuclear Magnetic Resonance Spectroscopy Assessment in Offspring of Type 2 Diabetic Parents[J]. Diabetes,1999,48(8):1600-1606.
[65] Jacob S,Machann J,Rett K.Association of Increased Intramyocellular Lipid Content with Insulin Resistance in Lean Nondiabetic Offspring of Type 2 Diabetic Subjects[J]. Diabetes,1999,48(5):1113-1119.
[66] Kuhlmann J,Neumann-Haefelin C,Belz U,et al.Intramyocellular Lipid and Insulin Resistance:a Longitudinal in Vivo1H-Spectroscopic Study in Zucker Diabetic Fatty Rats[J].Diabetes,2003,52(1):138-144.
[67]邸蕴华.2型糖尿病脂质代谢与胰岛素抵抗的相关性研究.中外医疗,2010,6:44.
[1]张祥,洪梅,陈萍,等.糖尿病视网膜病变的视皮层和视辐射区1H-MRS波谱初探.中华放射学杂志,2009,43(1):46-49.
[2] Lupien SB, Bluhm EJ, Ishil DN. Systemic insulin-like growth f actor I administrationprevents cognitive impairment in diabetic rats, and b rain IGF regulates l earning/memory in normal adult rats. J Neurosci Res, 2003, 74(4): 512-523.
[3]Gispen WH,Biessels GJ.Cognition and synaptic plasticity in diabetes mellitus.Trends Neurosci,2000,23(11):542-549.
[4]王悦,徐晓云.2型糖尿病患者高级脑功能与脑磁共振质子波谱研究。同济大学医学院硕士学位论文.
[5] den Heijer T , Vermeer SE, van Dijk EJ, et al. Type 2 diabetes and atrophy of medial temporal lobe structures on brain MRI. Diabetologia, 2003, 46(12):1604-1610. [ 6] Gold SM , Dziobek I, Sweat V, et al. Hippocampal damage and memory im pairments as possible early brain complications of type 2 diabetes. Diabetologia, 2007, 50(4) : 711-719.
[7]Rivera EJ,Goldin A,Fulmer N,et a1.Insulin and insulin—like growth factor expression and function deteriorate with progression of Alzheimer’s disease:link to brain reductions in acebrlcholine.J Alzheimers Dis,2005;8(3):247-268.
[8]叶任高,陆再英,主编.内科学.6版.北京:人民卫生出版社,2004:797—798.
[9] Schaefer M,Heinze HJ,Rotte M. Verbal memory encoding in patients with left-sided hippocampal sclerosis.Neuroreport,2006,17(11):1219-1223.
[10]周红,卢万俊,滕皋军等.2型糖尿病患者认知功能及海马氢质子磁共振波谱研究.中国医学影像技术2009,25(8):1367-1370.
[11]马晓臣,王桂芝,王元.2型糖尿病患者脑海马区氢质子波谱的临床分析.现代中西医结合杂,2010,19(10):1174-.
[12]张祥,洪梅,陈萍等.糖尿病视网膜病变的视皮层和视辐射区1H—MR波谱初探.中华放射学杂志,2009,43(1):46-49.
[13]张海燕,宋滇平.老年2型糖尿病患者认知功能障碍的研究——磁共振波谱技术在早期诊断中的运用.昆明医学院2008硕士.
[14] Finck BN, Han XL, Courtois M, et al. A critical role for PPAR alpha-mediated lipotoxicity in the pathogenesis of betic cardiomyopathy: modulation by dietary fat content, PNAS, 2003,100:1226-1231.
[15]王南,董慧,陆付耳等.应用在体磁共振氢谱测定2型糖尿病患者心肌甘油三酯含量.中国糖尿病杂志,2010,18(10):761-763.
[16]Van Herpen NA, Schrauwen-Hinderling VB. Lipid accumulation in non-adipose tissue and lipotoxicity. Physiol Behav, 2008,94:231-241.
[17] Szczepaniak LS,Nurenberg P,Leonard D,et al.Magnetic resonance spectroscopy to measure hepatic triglyceride content:prevalence of hepatic steatosis in the general population.Am J Physiol Endocrinol Metab. 2005,288:E462-E468.
[18]Mehta SR,Thomas EL,Bell JD,et al.Non-invasive means of measuring hepatic fat content.World J Gastroenterol,2008,14:3476-3483.
[19]王南,董慧,陆付耳.2型糖尿病大鼠肝脏甘油三酯含量的磁共振氢谱研究.放射学实践,2009,24(8):820-824.
[20]董慧,陆付耳,王南等.2型糖尿病患者肝脏甘油三酯含量的相关因素分析:磁共振波谱研究.华中科技大学报(医学版),2010,39(1):64-68.
[21]Maarten E. Tushuizena, Petra J.Postprandial lipid and apolipoprotein responses following three consecutive meals associate with liver fat content in type 2 diabetes and the metabolic syndrome. Atherosclerosis, 2010, (211) :308–314.
[22]邸蕴华.2型糖尿病脂质代谢与胰岛素抵抗的相关性研究.中外医疗,2010,6:44.
[23]张磊,刘彦君.磁共振氢谱对胰岛素抵抗及Ⅱ型糖尿病的研究.放射学实践,2005,20(3):272-274.
[24]Pan DA,Lillioja S,Kriketos AD,et al.Skeletal Muscle Triglyceride Levels are Inversely Related to Insulin Action[J]. Diabetes, 1997,46(6):983-988.
[25]Krssak M, Falk Petersen K, Dresner A et al. Intramyocellular Lipid Concentrations are Correlated with Insulin Sensitivity in Humans:a 1H NMR Spectroscopy Study[J].Diabetologia,1999,42(1):113-116. ,
[26] Perseghin G,Scifo P,De Cobelli F,et al.Intramyocellular Triglyceride Content Is a Determinant of in Vivo Insulin Resistance in Humans:a1H-13C Nuclear Magnetic Resonance Spectroscopy Assessment in Offspring of Type 2 Diabetic Parents[J]. Diabetes,1999,48(8):1600-1606.
[27] Jacob S,Machann J,Rett K.Association of Increased Intramyocellular Lipid Content with Insulin Resistance in Lean Nondiabetic Offspring of Type 2 Diabetic Subjects[J]. Diabetes,1999,48(5):1113-1119.
[28] Kautzky-Willer A, Krssak M, Winzer C, et al. Increased Intramyocellular Lipid Concentration Identifies Impaired Glucose Metabolism in Women with Previous Gestational Diabetes[J]. Diabetes,2003,52(2):244-251.
[29] Anderwald C,Bernroider E,Krssak M,et al.Effects of Insulin Treatment in Type 2 Diabetic Patients on Intracellular Lipid Content in Liver and Skeletal Muscle[J].Diabetes,2002,51(10): 3025-3032.
[30]张磊,金真,刘彦君等.小腿骨骼肌细胞内脂质的磁共振氢谱测定在2型糖尿病评估中的应用.中国临床康复,2004,8(21):4230-4231.
[2]Boulton NJM, Vinik A I, Arezzo JC, et al. Diabetic Neuropathies: a statement by the American Diabetes Association[J]. Diabetes Care, 2005, 28(4):956-962.
[3]宁光.糖尿病神经病变的诊断和治疗[J].国际内分泌代谢杂志, 2006, 26(3):附录-3-2-3-4.
[4] Bendszus M, Wessig C, Solymosi L, et al. MRI of peripheral nerve de-generation and regeneration: correlation with electrophysiology and histology[J]. Exp Neurol 2004,188(1):171-177.
[5]Danielson ER, Ross B. Magnetic resonance spectroscopy diagnosis of neurological diseases. New York: Maral Dekker, 1999:5-22.
[6]刘兆爱,甲吉芳,刘艳霞,等.脂代谢紊乱与2型糖尿病慢性并发症关系分析[J].实用心电学杂志,2008,17(3):187-188.
[7]陈金仲,邵豪脂.脂代谢紊乱与胰岛素抵抗的相关研究进展[J].中国实用医药,2008(7):147-148.
[8]朱翠英.脂毒性的形成机制及其干预策略[J].国际检验医学杂志,2006,27(1):24-26.
[9]张静,张建华.初诊糖尿病患者β细胞功能状况与血糖水平的相关性分析[J].临床内科杂志,2007,21(8):553-554.
[10] Feldman EL, Cornblath DR, Porter J,et al.NINDS:Advances in undertanding and treating neuropathy. J Peripher Nerv Syst,2008,13(1):1-6.
[11] Jensen TS, Bach FW, Kastrup J, et a.l Vibratory and thermal thresholds in diabetics with and without clinical neuropathy. Acta NeurolScand,1991,84(4):326-333.
[12]吴佩娴,张帆,孙凤芹.糖尿病周围神经病变的临床分析及震动感觉阈值测定.中国实用医药,2009,4(21):22-23.
[13]Summer CJ,Sheth S,Griffin JW,et al. The spectrum of neuropathy in diabetic and impaired glucose tolerance[J].Neurology,2003,60:108-111.
[14]王盼,吴仲敏,凡馨.糖尿病周围神经病及其检测技术.四川医学,2009,30(6):978-980.
[15]唐彦,谈跃.糖尿病周围神经病变的诊断进展. 2010,48(1):9-11.
[16]Li F, Abatan OI, KimH, et al. Taurine reverses neurological and neurovascular deficits in Zucker diabetic fatty rats[J].Neurobiol Dis,2006,22(3):669-676.
[17]马叶萍,孙新芳.糖尿病周围神经病变的药物治疗进展[J].中风与神经疾病杂志,2006,23(5):631-632.
[18]Cameron NE, Eaton SE, Cotter MA, et al. Vascular factors and metabolic interactions in the pathogenesis of diabetic neuropathy[J]. Diabetologia,2001,44(11):1973-1988.
[19]谢华,王清秀,肖敏.糖尿病周围神经痛研究进展.郧阳医学院学报[J],2008,27(1):85-87.
[20]Freeman R. Not all neuropathy in diabetes is of diabetic etiology:differential diagnosis of diabetic neuropathy〔J〕.Curr fasting plasma Diab Rep,2009,9:423-431.
[21]王萌,王瑞英,王素星.氧化应激与糖尿病周围神经病变〔J〕.临床荟萃,2009,24(5):449-450.
[22]Cheng HT, Dauch JR,Hayes JM,et al.Nerve growth factor mediates mechanical allodynia in a mouse model of type 2 diabetes〔J〕.Neuropathol Exp Neurol,2009,68:1229-1243.
[23]张雪兰,谢云,职心乐.糖尿病周围神经病变相关危险因素分析.中国慢性病预防与控制,2010,18(2):115-117.
[24]Tesfaye S,Chaturvedi N,Eaton SE,et al.Vascular risk factors and diabetic neuropathy. N Engl Med,2005,352(4):341-350.
[24]程璇,卢祖能.周围神经病临床诊疗新进展.卒中与神经疾病,2009,16(3):185-188.
[25] Yagihashi S, Yamagishi S, Wada R. Pathology and pathogenetic mechanisms of diabetic neuropathy: correlation with clinical signs and symptoms[J].Diabetes Res Clin Parct,2007,77(1):184-189.
[26] Malik R A, Tesfaye S, Newrick P G, et al. Sural nerve pathology in diabetic patients with minimal but progressive neuropathy. Diabetologia. 2005, 48: 578-585.
[27] Kiziltan ME, Gunduz A, Kiziltan G,et al.Peripheral neuropathy in patientswith diabetic footulcers: clinical and nerve conduction study[J]. Neurol Sci,2007, 258(1-2): 75-79.
[28]张大红,刘淑娣,李涛.糖尿病周围神经病变的临床特点及药物治疗.中国医药导报,2009年,6(10):224.
[29]Douglas W.Diabetes mellitus and the peripheral nervous system:manifestations and mechanisms[J].Muscle Nerve,2007,36:145.
[30]汤晓芙,陈学诗,主编.中国现代神经精神病学发展概况[M].北京:中国科学技术出版社,1995.159.
[31]朱一浩.糖尿病周围神经病患者的神经传导速度分析[J].临床脑电学杂志,1998,7:232.
[32]尹凤琼,唐一平,朱榆红.糖尿病周围神经病肌电图检查与临床分析.云南医药,2008,29(1):17-21.
[33]吕海莉,吴建民,刘宽芝.糖尿病周围神经病变及其康复治疗.中国康复医学杂志,2009,24(3):287-9.
[34]PERKINSBA, BERILR. Diagnosis and management of diabebic neuropathy[J].Curr Diab Rep,2002,2(6):495-500.
[35]陈妙玲,李新春.周围神经损伤的磁共振成像研究进展.国际医学放射学杂志, 2010,33(4): 325-328.
[36] Sinnreich M, Taylor BV, Dyck PJ. Diabetic neuropathies. Classification, clinical features, and pathophysiological basis[J]. Neurologist, 2005,11(2): 63-79.
[37]Said G. Diabetic neuropathy-a review[J]. Nat Clin Pract Neurol,2007, 3(6):331-340.
[38]郭军红,蒲传强.糖尿病周围神经病的病理与电生理研究进展.中国康复理论与实践,2009,15(1):8-10.
[39]Gary LP, PatriciaMN,Madhumita R,etal.Intraepidermal nerve fibers are indicators of small-fiber neuropathy in both diabetic and nondiabetic patients[J].Diabetes Care, 2004, 27(8): 1974-1979.
[40] Ruiz-Pena JL, Pinero P, Sellers G, et al. Magnetic resonance spectroscopy of normal appearing white matter in early relapsing-remitting multiple sclerosis: correlations between disability and spectroscopy. J Neurol, 2002, 249(10): 1382-1390.
[41]彭洪娟,赵斌. 1H-MRS基本原理及成像技术[J].医学影像学杂志,2004, 12:1033-1035.
[42]李克,于同刚.磁共振波谱技术在肌骨疾病中的应用.中国医学计算机成像杂志[J],2003,9(5):332-337.
[43] GajewiczW,PapierzW,SzymczakW,etal.The use of proton MRS in the differential diagnosis of brain and tumor-like processes. MedSci Monit,2003,9:97-105.
[44] Castilo M,Kwock L,ukherji SK.Clinical application of proton MR spectroscopy. AJNR,1996,17:1-15.
[45] Burtscher IM,Holtas S. Proton MR spectroscopy in clinical routine. J Mag Reson Imaging,2001,13:560-567.
[46]郭红云,牛广明. 1H磁共振波谱分析在脑肿瘤诊断中的应用现状.医学综述,2008,14(11):1728-9.
[47] Jeffry RA , S ophia CS , Albert B ,et al . Abs olute quantitation of short TE brain1H2MR spectra and spectroscopic imaging data[J] . Journal of Computer Assisted Tomography ,1993 ,17 :191.
[48] Fisher E, Rudick RA, Simon JH, et al. Eight year follow up study of brain atrophy in patients with MS[J].Neurology,2002;59(9):1412-1420.
[49] Pouwels PJ, Frahm J. Regional metabolite concentrations in human brain as determined by quantitative localized proton MRS. Magn Reson Med, 1998; 39: 53-60.
[50]林艳,饶海冰,吴仁华.1H-MRS定量测定脑代谢物的研究.国外医学放射医学核医学分册2005,29(2):85-88.
[51] Pfefferbaum A, Adalsteinsson E, Spielman D et al. In vivo spectroscopic quantification of the N-acetylmoiety, creatine, and choline from large volumes of brain gray and white matter: effects of normal aging. Magn Reson Med, 1999; 41: 276- 284.
[52]Schulze S.Humoral and neural medicutors of the systemic respome to surgery[J].Dan Nod Bull,1993,40(3):365-477.
[53]邝菲,王飞.氢质子磁共振波谱(1H-MRS)技术应用.医学影像学杂志, 2007,17 (8) :871-4.
[54]Zancanaro C, Nano R, Marchioro C, et al. Magnetic resonance spectroscopy investigations of brown adipose tissue and isolated brown adipocytes[J]. J Lipid Res, 1994, 35(12):2191-2199.
[55]薛江苗,林祥涛,李吉昌等.磁共振氢质子波谱及弥散加权成像在诊断良、恶性骨病变中的对比应用.山东大学学报(医学版),2008,46(3):309-12.
[56] Boesch C , Slotboom J , Hoppeler H , et al . In vivo determinationof int ra2myocellular lipids in human skeletal muscle by means of lo2calized 1H2MR2spect roscopy[J] . Magn Reson Med ,1997 ,37 (4) :484-493.
[57]Schick F , Eismann B , J ung WI , et al . Comparison of localized proton NMR signals of skeletal muscle and fat tissue in vivo : two lipid compartment s in muscle tissue[J ] . Magn Reson Med ,1993 ,29 (2) :158-167.
[58]Sachin KC,Sharad M,et al.Magnetic resonance spectroscopy[J].Neuro Oplthalmol,2005,25:217-226.
[59] RicoSanz J,Thomas EL,Jenkinson G,et al.Diversity in Levels of Intracellular Total Creatine and Triglycerides in Human Skeletal Muscles Observed by 1H-MRS[J].J ApplPhysiol,1999,87(6):2068-2072.
[60]Brechtel K, Jacob S, Machann J, et al. Acquired Generalized Lipoatrophy(AGL):Highly Selective MR Lipid Imaging and Localized 1H-MRS[J].J Magn Reson Imaging,2000,12(2):306-310.
[61]蔡明江,成杰,张南雁.胰岛素抵抗与2型糖尿病直立性低血压的关系[J].中国临床康复,2003,7(27):3684-5.
[62]Pan DA, Lillioja S,Kriketos AD,et al.Skeletal Muscle Triglyceride Levels are Inversely Related to Insulin Action[J]. Diabetes, 1997,46(6):983-988.
[63]张磊,刘彦君.磁共振氢谱对胰岛素抵抗及Ⅱ型糖尿病的研究.放射学实践,2005,20(3):272-274.
[64] Perseghin G,Scifo P,De Cobelli F,et al.Intramyocellular Triglyceride Content Is a Determinant of in Vivo Insulin Resistance in Humans:a1H-13C Nuclear Magnetic Resonance Spectroscopy Assessment in Offspring of Type 2 Diabetic Parents[J]. Diabetes,1999,48(8):1600-1606.
[65] Jacob S,Machann J,Rett K.Association of Increased Intramyocellular Lipid Content with Insulin Resistance in Lean Nondiabetic Offspring of Type 2 Diabetic Subjects[J]. Diabetes,1999,48(5):1113-1119.
[66] Kuhlmann J,Neumann-Haefelin C,Belz U,et al.Intramyocellular Lipid and Insulin Resistance:a Longitudinal in Vivo1H-Spectroscopic Study in Zucker Diabetic Fatty Rats[J].Diabetes,2003,52(1):138-144.
[67]邸蕴华.2型糖尿病脂质代谢与胰岛素抵抗的相关性研究.中外医疗,2010,6:44.
[1]张祥,洪梅,陈萍,等.糖尿病视网膜病变的视皮层和视辐射区1H-MRS波谱初探.中华放射学杂志,2009,43(1):46-49.
[2] Lupien SB, Bluhm EJ, Ishil DN. Systemic insulin-like growth f actor I administrationprevents cognitive impairment in diabetic rats, and b rain IGF regulates l earning/memory in normal adult rats. J Neurosci Res, 2003, 74(4): 512-523.
[3]Gispen WH,Biessels GJ.Cognition and synaptic plasticity in diabetes mellitus.Trends Neurosci,2000,23(11):542-549.
[4]王悦,徐晓云.2型糖尿病患者高级脑功能与脑磁共振质子波谱研究。同济大学医学院硕士学位论文.
[5] den Heijer T , Vermeer SE, van Dijk EJ, et al. Type 2 diabetes and atrophy of medial temporal lobe structures on brain MRI. Diabetologia, 2003, 46(12):1604-1610. [ 6] Gold SM , Dziobek I, Sweat V, et al. Hippocampal damage and memory im pairments as possible early brain complications of type 2 diabetes. Diabetologia, 2007, 50(4) : 711-719.
[7]Rivera EJ,Goldin A,Fulmer N,et a1.Insulin and insulin—like growth factor expression and function deteriorate with progression of Alzheimer’s disease:link to brain reductions in acebrlcholine.J Alzheimers Dis,2005;8(3):247-268.
[8]叶任高,陆再英,主编.内科学.6版.北京:人民卫生出版社,2004:797—798.
[9] Schaefer M,Heinze HJ,Rotte M. Verbal memory encoding in patients with left-sided hippocampal sclerosis.Neuroreport,2006,17(11):1219-1223.
[10]周红,卢万俊,滕皋军等.2型糖尿病患者认知功能及海马氢质子磁共振波谱研究.中国医学影像技术2009,25(8):1367-1370.
[11]马晓臣,王桂芝,王元.2型糖尿病患者脑海马区氢质子波谱的临床分析.现代中西医结合杂,2010,19(10):1174-.
[12]张祥,洪梅,陈萍等.糖尿病视网膜病变的视皮层和视辐射区1H—MR波谱初探.中华放射学杂志,2009,43(1):46-49.
[13]张海燕,宋滇平.老年2型糖尿病患者认知功能障碍的研究——磁共振波谱技术在早期诊断中的运用.昆明医学院2008硕士.
[14] Finck BN, Han XL, Courtois M, et al. A critical role for PPAR alpha-mediated lipotoxicity in the pathogenesis of betic cardiomyopathy: modulation by dietary fat content, PNAS, 2003,100:1226-1231.
[15]王南,董慧,陆付耳等.应用在体磁共振氢谱测定2型糖尿病患者心肌甘油三酯含量.中国糖尿病杂志,2010,18(10):761-763.
[16]Van Herpen NA, Schrauwen-Hinderling VB. Lipid accumulation in non-adipose tissue and lipotoxicity. Physiol Behav, 2008,94:231-241.
[17] Szczepaniak LS,Nurenberg P,Leonard D,et al.Magnetic resonance spectroscopy to measure hepatic triglyceride content:prevalence of hepatic steatosis in the general population.Am J Physiol Endocrinol Metab. 2005,288:E462-E468.
[18]Mehta SR,Thomas EL,Bell JD,et al.Non-invasive means of measuring hepatic fat content.World J Gastroenterol,2008,14:3476-3483.
[19]王南,董慧,陆付耳.2型糖尿病大鼠肝脏甘油三酯含量的磁共振氢谱研究.放射学实践,2009,24(8):820-824.
[20]董慧,陆付耳,王南等.2型糖尿病患者肝脏甘油三酯含量的相关因素分析:磁共振波谱研究.华中科技大学报(医学版),2010,39(1):64-68.
[21]Maarten E. Tushuizena, Petra J.Postprandial lipid and apolipoprotein responses following three consecutive meals associate with liver fat content in type 2 diabetes and the metabolic syndrome. Atherosclerosis, 2010, (211) :308–314.
[22]邸蕴华.2型糖尿病脂质代谢与胰岛素抵抗的相关性研究.中外医疗,2010,6:44.
[23]张磊,刘彦君.磁共振氢谱对胰岛素抵抗及Ⅱ型糖尿病的研究.放射学实践,2005,20(3):272-274.
[24]Pan DA,Lillioja S,Kriketos AD,et al.Skeletal Muscle Triglyceride Levels are Inversely Related to Insulin Action[J]. Diabetes, 1997,46(6):983-988.
[25]Krssak M, Falk Petersen K, Dresner A et al. Intramyocellular Lipid Concentrations are Correlated with Insulin Sensitivity in Humans:a 1H NMR Spectroscopy Study[J].Diabetologia,1999,42(1):113-116. ,
[26] Perseghin G,Scifo P,De Cobelli F,et al.Intramyocellular Triglyceride Content Is a Determinant of in Vivo Insulin Resistance in Humans:a1H-13C Nuclear Magnetic Resonance Spectroscopy Assessment in Offspring of Type 2 Diabetic Parents[J]. Diabetes,1999,48(8):1600-1606.
[27] Jacob S,Machann J,Rett K.Association of Increased Intramyocellular Lipid Content with Insulin Resistance in Lean Nondiabetic Offspring of Type 2 Diabetic Subjects[J]. Diabetes,1999,48(5):1113-1119.
[28] Kautzky-Willer A, Krssak M, Winzer C, et al. Increased Intramyocellular Lipid Concentration Identifies Impaired Glucose Metabolism in Women with Previous Gestational Diabetes[J]. Diabetes,2003,52(2):244-251.
[29] Anderwald C,Bernroider E,Krssak M,et al.Effects of Insulin Treatment in Type 2 Diabetic Patients on Intracellular Lipid Content in Liver and Skeletal Muscle[J].Diabetes,2002,51(10): 3025-3032.
[30]张磊,金真,刘彦君等.小腿骨骼肌细胞内脂质的磁共振氢谱测定在2型糖尿病评估中的应用.中国临床康复,2004,8(21):4230-4231.