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1.
目的 设计动态脂餐饮食耐量试验,观察高血压患者有关血脂、血糖、胰岛素(INS)、INS敏感指数(ISI)等变化规律。方法 测定67名健康人、54例高血压患者的总胆固醇(TC)、三酰甘油(TG)、载脂蛋白(Apo)A1、ApoB、高密度脂蛋白胆固醇(HDL-C)、血糖、INS及ISI。生化指标测定均采用常规方法,血清INS测定采用微粒子捕捉酶免疫分析(MEIA)方法。结果 67名健康人脂餐饮食后6h生化指标和服糖后2h血糖、INS检测结果与空腹比较差异无显著性。54例高血压患者空腹TG升高,与对照组比较差异有显著性(P〈0.01);空腹HDL-C降低,空腹血糖升高,与对照组比较差异有显著性(P〈0.05)。高血压组脂餐饮食后6hTG升高,服糖后2h血糖明显增高,ISI明显降低,与空腹时比较差异有显著性(P〈0.01),其他指标与空腹时差异无显著性。结论 高血压组处于高血脂状态时间明显比正常对照组延长,并且伴有高INS血症、INS抵抗及ISI降低现象。  相似文献   

2.
目的探讨育龄期多囊卵巢综合征(PCOS)患者的糖代谢异常和胰岛素抵抗。方法选择育龄期PCOS患者168例,分为肥胖PCOS组78例和非肥胖PCOS组90例,正常对照组100例,对比临床表现及检测内分泌激素、空腹血糖、空腹胰岛素、服糖后2h血糖及2h胰岛素。结果育龄期PCOS患者的月经周期、多毛、痤疮、B超提示卵巢增大、卵巢多囊性改变、有不孕史与对照组比较,差异均有显著性(P〈0.05),育龄期PCOS组的血清LH、T与对照组比较,差异有显著性(P〈0.05)。育龄期肥胖P-COS组的空腹血糖、服糖后2h血糖、空腹胰岛素、服糖后2h胰岛素与对照组比较,差异均有显著性(P〈0.05)。结论早期出现月经稀发、BMI升高的患者是否存在PCOS,值得重视。育龄期PCOS患者尤其肥胖型要高度重视糖代谢异常及胰岛素抵抗,以决定是否采取干预措施,避免出现远期并发症而对PCOS患者造成健康威胁。  相似文献   

3.
目的探讨短期胰岛素泵强化治疗对不同病程2型糖尿病患者相关指标的影响。方法 (1)将2012年1月至2013年1月于内分泌科住院的2型糖尿病患者77例,按病程分为三组,A组(病程小于5年)51例,B组(病程5~10年)13例,C组(病程大于10年)13例,均给予短期胰岛素泵强化治疗。比较其置泵前后各组空腹血糖、早餐后血糖、午餐后血糖、晚餐后血糖、基础C肽、1 h C肽、2 h C肽、3 h C肽、基础胰岛素、1 h胰岛素、2 h胰岛素、3 h胰岛素、胰岛素分泌指数(HOMA-β)、胰岛素抵抗指数(HOMA-IR)的变化。(2)分析HOMA-β与所需胰岛素用量、年龄、糖尿病病程、身高、体重、BMI、HbA1c、空腹血糖、早餐后血糖、午餐后血糖、晚餐后血糖、基础C肽、1 h C肽、2 h C肽、3 h C肽、基础胰岛素、1 h胰岛素、2 h胰岛素、3 h胰岛素、TC、TG、HDL-C、LDL-C间的相关性。结果 (1)A组患者经胰岛素泵强化治疗后,空腹血糖及各餐后血糖,HOMA-IR较前明显下降,空腹C肽、餐后1 h、2 h、3 h C肽,餐后1 h、2 h、3 h胰岛素,HOMA-β较前明显增加,差异具有明显统计学意义(P〈0.01);(2)B组患者经胰岛素泵强化治疗后,空腹血糖及各餐后血糖,HOMA-IR明显较前下降,空腹、餐后1 h、2 h、3 h C肽,餐后3 h胰岛素,HOMA-β较前明显增加,差异具有明显统计学意义(P〈0.01);(3)C组患者经胰岛素泵强化治疗后,空腹血糖及各餐后血糖明显较前下降,餐后2 h、3 h C肽分泌较前明显增加,差异具有明显统计学意义(P〈0.01);(4)Pearson相关性分析显示,ΔHOMA-β与体重、BMI、空腹血糖呈正相关(P〈0.05),与年龄呈明显负相关(P〈0.05);(5)多元逐步回归分析显示,ΔHOMA-β与体重、早餐后血糖、晚餐后血糖、HbA1c、尿A/C呈明显正相关,与病程、身高、午餐后血糖呈明显负相关。结论持续性皮下胰岛素输注是目前糖尿病患者控制血糖最理想的方法,且低血糖发生率低,胰岛素用量小,能明显改善2型糖尿病患者胰岛β细胞功能,增加胰岛素敏感性。  相似文献   

4.
目的探讨2型糖尿病(T2DM)合并危重症患者血糖监测的意义及血糖控制对危重症患者的意义。方法选择T2DM并内科危重症患者76例,随机分为对照组和治疗组。对照组采用胰岛素皮下注射控制血糖,治疗组采用胰岛素泵控制血糖水平。人选后分别检测两组对象空腹血糖、三餐后血糖、血清内脂素、空腹C肽、糖化血红蛋白及餐后2hC肽并计算病死率。结果治疗组胰岛素用量较对照组有显著性下降(P〈0.05),治疗组血糖控制良好者较对照组有显著性升高(P〈0.05),对照组血糖控制差者较治疗组有显著性升高(P〈0.01)。治疗组低血糖发生率及内脂素水平较对照组有显著性下降(P〈0.05)。治疗后治疗组血糖波动及病死率较对照组有显著性下降(P〈0.05)。结论采用胰岛素泵治疗可积极的控制血糖并降低血糖波动,可以减少T2DM合并危重症患者病死率。  相似文献   

5.
目的探讨血清内脂素及氧化应激状态评价在妊娠糖尿病患者病情评估中的意义。方法选择妊娠糖尿病患者68例为糖尿病组,对照组选择非糖尿病孕妇60例。人选后分别检测两组对象血清内脂素、空腹血糖、胰岛素抵抗指数、丙二醛、过氧化氢酶、超氧化物歧化酶、谷胱甘肽并计算体重指数。结果糖尿病组空腹血糖、胰岛素抵抗指数,内脂素较非糖尿病组差异有统计学意义(P〈0.05)。糖尿病组的MDA、CAT较非糖尿病组有显著性增高(P〈0.05),糖尿病组SOD水平较非糖尿病组有极显著性下降(P〈0.01),GSH较非糖尿病组有显著性下降(P〈0.05)。空腹血糖与内脂素、MDA呈显著正相关(P〈0.05),空腹血糖与SOD、GSH呈显著负相关(P〈0.05);胰岛素抵抗指数与内脂素、MDA呈显著正相关(P〈0.05),胰岛素抵抗指数与SOD、GSH呈显著负相关(P〈0.05)。结论血清内脂素及氧化应激状态评价可有效反映妊娠糖尿病患者病情严重程度,对判断病情进展具有重要意义。  相似文献   

6.
[目的]探讨2型糖尿病患者血清同型半胱氨酸水平与胰岛素抵抗、胰岛B细胞分泌功能的相关性。[方法]用循环酶法测定49例2型糖尿病患者的血清同型半胱氨酸水平,葡萄糖氧化酶法测定血糖水平,放射免疫法测定C肽、胰岛素水平并与36例正常对照组作比较。[结果]2型糖尿病患者血清同型半胱氨酸水平明显高于正常对照组(P〈0.01),与空腹胰岛素、胰岛素抵抗指数HOMA—IR呈明显负相关(r=-0.362,-0.532;P〈0.05),与空腹血糖、空腹C肽、胰岛β细胞分泌功能指数HO-MA-β无明显相关(r=-0.298,-0.131,0.056;P〉0.05)。[结论]胰岛素缺乏可能是2型糖尿病患者血清同型半胱氨酸水平升高的一个重要相关因素。检测2型糖尿病患者血清同型半胱氨酸水平对于了解患者病情,指导临床治疗具有一定的意义。  相似文献   

7.
目的探讨诺和锐30强化治疗对初诊2型糖尿病患者血糖及胰岛功能的影响。方法对40例初诊2型糖尿病患者进行2周的诺和锐30治疗,分析治疗前后空腹血糖(FPG)及餐后2h血糖(2hPG)、糖化血红蛋白(HbAlc)、静脉葡萄糖耐量试验第一时项胰岛素及C肽分泌和胰岛素及C肽曲线下面积、胰岛素抵抗指数、胰岛素分泌指数、胰岛素敏感指数、空腹胰岛素(FINS)与FPG比值。结果诺和锐30治疗后,FPG、2hPG、HbAlc、胰岛素抵抗指数均较治疗前明显下降(P〈0.01);窄腹及第一时项胰岛素和C肽的分泌、胰岛素及C肽曲线下面积、FINS与FPG比值、胰岛素分泌指数、胰岛素敏感指数均较治疗前明显升高(P〈0.01)。结论诺和锐30强化治疗能显著改善初诊2型糖尿病患者的血糖及胰岛功能。  相似文献   

8.
目的观察胰岛素泵强化治疗2周对不同病程2型糖尿病患者胰岛β细胞功能及胰岛素抵抗改善的差异。方法选择不同病程的2型糖尿病患者共90例,根据病程长短分为新诊断糖尿病组(A组)、病程1~5年糖尿病组(B组)、病程5年以上糖尿病组(C组),各组30例。对3组患者进行2周胰岛素泵强化治疗,以空腹血糖〈6.1 mmol·L-1,餐后2 h血糖〈8.0 mmol·L-1为治疗目标,治疗前后行标准馒头餐试验,检测3组患者空腹及餐后2 h的血糖、胰岛素、C肽,用稳态模型计算治疗前后的胰岛β细胞功能指数(Homa-β),胰岛素抵抗指数(Homa-IR)。结果 A组和B组治疗后Homaβ-、空腹C肽均较治疗前升高,差异有统计学意义(P〈0.05),而C组治疗后Homaβ-、空腹C肽较治疗前亦升高,但差异无统计学意义(P〉0.05);A组的Homaβ-治疗前后的差值与B组比较,差异有统计学意义(P〈0.05);强化治疗前后各组Homa-IR差异均有统计学意义(P〈0.05)。结论胰岛素强化治疗能改善病程较短的2型糖尿病患者的胰岛β细胞功能,新诊断的2型糖尿病患者获益更大。理想的血糖控制都能使胰岛素抵抗得到改善。  相似文献   

9.
胰岛素强化治疗初诊2型糖尿病   总被引:1,自引:0,他引:1  
谭素玲 《临床医学》2009,29(1):47-49
目的探讨早期胰岛素强化治疗对初诊2型糖尿病的疗效。方法分析我院2006年1月至2007年12月短期应用胰岛素治疗初诊2型糖尿病患者36例,以同期口服药物治疗的初诊2型糖尿病患者40例为对照。初诊时空腹血糖(FBG)〉11.1mmo]/L,分别观察治疗2个月后各纽空腹血糖(FBG)、餐后2h血糖(PBG)、糖化血红蛋白(HbA1c)、胰岛素水平、C肽水平变化情况。结果经短期胰岛素强化治疗后,FBG、PBG、HbA1c显著下降,空腹及餐后2h胰岛素水平、C肽水平,比对照组明显增高,差异有统计学意义(P〈0.01)。结论初诊2型糖尿病患者早期胰岛素强化治疗比口服药物治疗能更有效地控制血糖水平,降低高糖毒性,减轻胰岛素抵抗,使胰岛β细胞功能恢复,可能对延缓糖尿病自然病程的进程,预防糖尿病慢性并发症有积极的意义。  相似文献   

10.
中青年原发性高血压代谢状态研究   总被引:1,自引:0,他引:1  
目的研究中青年原发性高血压患者血糖、血脂、血尿酸等代谢状态。方法对69例(研究组)中青年原发性高血压患者检测空腹血糖(FBG)、餐后2h血糖(2hPG)、空腹胰岛素(FINS)、餐后2h胰岛素(2bINS),进行口服糖耐量试验(OGTT)、胰岛素释放试验,检测血脂、血尿酸(UA),评估患者的代谢状态。并与正常对照组(41例)比较。结果研究组患者FPG、2hPG、FINS与对照组比较差异有统计学意义(P〈0.01、P〈0.05、P〈0.05);血总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、UA与对照组比较差异有统计学意义(均P〈0.01)。OGTT后2hPG7.8-11.1mmol/L的患者占19%。结论中青年原发性高血压部分患者在FPG正常时可能已经出现OGTT减低、空腹胰岛素水平升高,存在胰岛素抵抗;建议早做OGTT,对同时出现血脂、UA代谢紊乱者,应进行早期干预。  相似文献   

11.
This study was designed to explore the short-term effect of glipizide on insulin secretion and metabolism. Plasma insulin and C-peptide levels in the fasting state and after a 100-g oral glucose load were measured in 17 obese newly diagnosed type II (non-insulin-dependent) diabetic subjects before and after 1 mo of treatment with glipizide (15 mg/day). Plasma glucose levels decreased significantly after treatment with glipizide. Plasma insulin and C-peptide concentrations in the fasting state did not change after glipizide treatment. Also, postglucose plasma insulin levels did not change after glipizide, whereas postglucose plasma C-peptide concentrations significantly increased. A significant relationship was found between the increase in C-peptide plasma levels and the decrease in glycemic profile after glucose load following glipizide treatment. The relation between plasma C-peptide and insulin incremental areas after the oral glucose load significantly increased after treatment. These results suggest that in obese type II diabetic patients, 1 mo of treatment with glipizide potentiates the beta-cell response to oral glucose load and increases insulin metabolism, probably within the liver.  相似文献   

12.
目的 探讨2型糖尿病患者血糖控制与肝功能异常的相关性.方法 选择该院内分泌科门诊和住院已经确诊的2型糖尿病患者156例,检测其糖化血红蛋白(HbA1c)、空腹血糖(FPG)、餐后2 h血糖(2 hPG)、空腹C肽(FCP)、餐后2 h C肽(2 hCP)和肝功能,并对检测结果进行比较及统计学处理,对伴肝功能损害情况进行分析.结果 2型糖尿病患者肝损害发生率37.82%;B组(HbA1c>9%)患者的血糖水平、肝功能异常率显著高于A组(HbA1c≤9%),P<0.01;而B组(HbA1c>9%)C肽水平均明显低于A组(HbA1c≤9%).结论 HbA1c可反映糖尿病控制好坏与否,较好地控制血糖是改善2型糖尿病患者肝损害的主要措施.  相似文献   

13.
1. Danazol elevates plasma insulin, plasma glucagon and serum low-density lipoprotein concentrations and reduces the serum high-density lipoprotein concentration. 2. Associations between these disturbances were studied in 17 women receiving danazol therapy for endometriosis. Eleven women underwent intravenous glucose tolerance tests with measurement of plasma glucose, insulin, C-peptide and glucagon concentrations and modelling analysis of intravenous glucose tolerance test concentration profiles. Six women underwent glucagon sensitivity tests. Serum concentrations of lipids and lipoproteins were measured in all cases. 3. Danazol reduced the fasting plasma glucose and insulin concentrations, but markedly raised the fasting plasma glucagon concentration. The insulin and C-peptide responses to the intravenous glucose tolerance test were increased twofold and the net decrement in glucagon concentration was increased tenfold. The glucose response to the intravenous glucose tolerance test was unaffected. Insulin sensitivity was reduced by 55%. Both first-phase plasma insulin responsiveness and net first-phase pancreatic insulin secretion were increased; insulin half-life was prolonged. The glucose response to the glucagon sensitivity test was reduced on treatment. The calculated low-density lipoprotein cholesterol level rose by 20%, whereas high-density lipoprotein cholesterol level fell by 47%. None of these changes in serum lipoprotein levels correlated with changes in insulin metabolism. In general, metabolic changes normalized after 3 months. 4. Danazol increases the sensitivity of pancreatic insulin and glucagon secretion to glucose. Danazol-induced insulin and glucagon resistance could be due to receptor down-regulation resulting from hypersecretion of insulin and glucagon.  相似文献   

14.
Since C-peptide/immunoreactive insulin (IRI) molar ratios may reflect hepatic extraction of insulin, we measured simultaneous serum glucose, IRI, and C-peptide levels during fasting and 30, 60, 90, 120, and 180 min after 75 g of oral glucose in 10 hyperthyroid patients and 10 age- and weight-matched controls. Mean fasting serum glucose and IRI levels were significantly higher in the hyperthyroid versus control subjects (glucose: 4.9 +/- 0.3 mmol/L versus 4.36 +/- 0.11 mmol/L, P less than 0.01; IRI: 0.10 +/- 0.02 pmol/ml versus 0.05 +/- 0.01 pmol/ml; P less than 0.025). After glucose, mean serum glucose levels were significantly higher in the hyperthyroid versus control subjects at all times studied except for 180 min (P less than 0.01). Mean IRI levels were significantly higher at all times studied including 180 min (P less than 0.01). Mean fasting C-peptide levels were significantly greater in the hyperthyroid patients compared with the controls (1.2 +/- 0.25 pmol/ml versus 0.62 +/- 0.09 pmol/ml; P less than 0.025). After oral glucose, mean C-peptide levels were significantly higher (P less than 0.025) in the hyperthyroid compared with control subjects at 30-60 min but not at 90-180 min. Molar ratios of C-peptide/IRI were significantly lower (P less than 0.05) in the hyperthyroid versus control subjects at all times studied except fasting. In summary, glucose intolerance and hyperinsulinism occur in hyperthyroidism. In addition, C-peptide/IRI molar ratios are reduced after oral glucose ingestion.  相似文献   

15.
The goal of this study was to investigate whether treatment with bezafibrate improves glucose tolerance in non-insulin-dependent diabetes mellitus (NIDDM). The study included 37 NIDDM patients with HbA1 concentrations greater than 8.5% and normal kidney and liver function who were being treated with diet alone or diet together with a sulfonylurea drug. One patient withdrew because of constipation. At randomization and after 3 mo of treatment, patients were given a standard mixed-test-meal tolerance test (MTT; 500 cal) after an overnight fast, and plasma glucose, insulin, C-peptide, metabolite, nonesterified fatty acid (NEFA), and triglyceride concentrations were measured at 15- to 30-min intervals. Serum lipid, HbA1, and fructosamine concentrations were measured at monthly intervals. Glucose, NEFA, and triglyceride concentrations were significantly lower throughout the second MTT in bezafibrate patients (P less than 0.01-0.001) but not in the placebo group. Fasting serum insulin and C-peptide levels, but not postprandial concentrations, were reduced only in bezafibrate patients (P less than 0.05). After 3 mo, mean fasting serum triglyceride concentrations fell from 2.2 to 1.4 mM (P less than 0.001), total serum cholesterol concentrations from 6.3 to 5.5 mM (P less than 0.001), and low-density lipoprotein cholesterol concentrations from 4.2 to 3.5 mM (P less than 0.001) in bezafibrate patients. There were no changes in serum lipid concentrations in the placebo group. Treatment of patients with moderately controlled NIDDM with bezafibrate improves glucose tolerance and the serum lipid profile. Bezafibrate treatment may be a useful adjunct to hypoglycemic therapy in patients with NIDDM.  相似文献   

16.
It has been postulated that glucose regulation is secondary to maintenance of normal basal insulin secretion. Serum glucose, insulin, and C-peptide levels were measured at fasting in 209 consecutive non-insulin-dependent diabetic patients and after glucose stimulation in 193 patients. The basal serum insulin C-peptide levels were not significantly different in control subjects (mean 22 +/- 8.8 microU/ml) and in patients with varying severity of diabetes (mean 24 +/- 9.6 microU/ml) except in the most severely diabetic group [fasting serum glucose greater than 350 mg/dl (19.4 mmol/L), mean 19 +/- 7 microU/ml]. In 39 patients who developed ketonuria without acidosis during follow-up, the mean basal serum insulin was 22 microU/ml during the episode of ketonuria, 21 microU/ml during the glucose tolerance test, and 25 microU/ml after glucose stimulation (statistically nonsignificant differences). Our data suggest that hyperglycemia compensates for beta-cell impairment so that basal insulin secretion usually stays above the threshold for ketoacidosis unless there is marked beta-cell impairment. Patients who fail to increase insulin in response to nutrient challenge are at risk of developing ketosis.  相似文献   

17.
【目的】探讨辛伐他汀治疗对2型糖尿病(T2DM)合并肾病患者的糖代谢影响。【方法】选取本医院60名T2DM合并肾病患者进行辛伐他汀治疗3个月。比较治疗前后空腹血糖(FBG)、C肽、糖化血红蛋白(HbA1c),C反应蛋白(CRP)、空腹胰岛素(FINs)水平、胰岛素敏感指数(ISI)、胰岛素/葡萄糖比率(IGR)、HOMA—IR、脂联素(ANP)以及游离脂肪酸水平等变化,以评价辛伐他汀对T2DM病合并肾病患者的治疗效果。【结果】在辛伐他汀治疗3个月后的葡萄糖耐量试验(0GTT)中,各时点血糖水平较治疗前均显著下降(P〈0.05),而胰岛素与C肽在0min和30rain时较治疗前显著下降(P〈0.05)。在辛伐他汀治疗后,对比治疗前,FBG、HbA1c、CRP、血糖曲线下面积(AUC)、胰岛素AUC、FINS、ISI、游离脂肪酸(FFA)以及HO-MA—IR均显著下降(P〈0.05),尿白蛋白排泄率(UAER)也明显下降(P〈0.01),但是C肽AUC(P〈0.05)以及APN(P〈0.01)均显著上升,而IGR及校正胰岛素反应(CIR)无显著变化(P〉0.05)。【结论】辛伐他汀治疗可以显著降低血糖,提高患者对胰岛素的敏感性,改善胰岛素抵抗,从而改善T2DM合并肾病患者的糖代谢。  相似文献   

18.
目的 2型糖尿病(T2DM)患者血清游离脂肪酸(FFA)水平的变化及与糖代谢、胰岛素抵抗各指标间的相关性,并探讨影响T2DM的危险因素。方法通过口服糖耐量试验(OGTT)筛选105例未经药物治疗的T2DM患者和66名健康人(正常对照组),分别测定其血浆葡萄糖(PG)和胰岛素(Ins)水平,计算胰岛素抵抗指数(HOMA-IR)和胰岛素分泌指数(HOMA-IS),同时检测空腹血清FFA。对血清FFA浓度与性别、年龄、体重、体重指数(BMI)、0~3 h PG和Ins以及HOMA-IR、HOMA-IS进行相关性分析。以T2DM是否发病为因变量Y(T2DM组=1,正常对照组=0),性别、年龄、体重、BMI、HOMA-IR、HOMA-IS和FFA为自变量,做Logistic回归分析。结果 T2DM组HOMA-IR、HOMA-IS和血清FFA水平与正常对照组比较差异均有统计学意义(P<0.01、P<0.001)。相关分析发现,空腹血清FFA与0 h PG、0.5 h PG、1 h PG、2 h PG、3 h PG、3 h Ins、HOMA-IR呈弱正相关(r分别为0.340、0.281、0.282、0.307、0.302、0.193、0.225,P均<0.05)。Logistic回归分析显示血清FFA是T2DM的重要风险因素[OR=14.05,95%可信区间(CI):1.87~105.55]。结论血清FFA水平升高可能影响机体糖动态平衡,与胰岛素抵抗和T2DM发病密切相关。  相似文献   

19.
摘要 目的: 观察抗脂益肝汤联合二甲双胍对非酒精性脂肪肝(NAFLD)胰岛素、瘦素抵抗的影响。方法: 按不同治疗方法将123例诊断为NAFLD的患者随机分成4组:抗脂益肝汤联合二甲双胍治疗组(33例)、二甲双胍治疗组(30例)、抗脂益肝汤治疗组(32例)、安慰剂组(28例),各组均同时予饮食控制和运动处方,疗程为6月。治疗前后检测肝功能、血脂水平、空腹血糖、空腹血胰岛素、血清瘦素水平,计算BMI、胰岛素抵抗指数(采用稳态模式评估法计算胰岛素抵抗指数),比较治疗前后各指标的变化。结果: 4组患者治疗后肝功能、血脂紊乱均明显改善,差异显著(P<0.05或P<0.01);联合治疗组、二甲双胍治疗组、抗脂益肝汤组胰岛素、瘦素抵抗均明显改善,差异显著,以联合治疗组改善最显著(P<0.05或P<0.01),安慰剂组无明显改善,用药期间4组患者均未出现显著的不良反应。结论: 抗脂益肝汤联合二甲双胍能明显改善NAFLD患者肝功能、促进脂质代谢、改善胰岛素及瘦素抵抗。  相似文献   

20.
目的 研究甲状腺机能亢进症(简称甲亢)和血糖代谢的关系.方法 选取52例甲亢患者和38例糖尿病患者分别使用电化学发光免疫分析仪检测血清甲状腺激素(TH,包括FT3、T3、FT4、T4和sTSH)、胰岛素(INS)和C-肽(CP)水平以及全自动生化分析仪检测空腹血糖水平,并同时测定了口服葡萄糖耐量试验后3h的血糖水平并与60名正常对照组进行了比较性分析.结果 甲亢组血清FT3、T3、FT4和T4水平较正常对照组明显增高(P<0.01),糖尿病组亦然(P<0.01),而sTSH水平明显降低(P<0.01).口服葡萄糖耐量试验表明:甲亢组空腹血糖明显高于正常对照组(P<0.01),而低于糖尿病组;口服糖后3h,正常对照组恢复至正常水平,甲亢组和糖尿病组糖耐量降低;甲亢组和糖尿病组空腹INS和CP水平较正常对照组明显增高,INS释放功能欠佳,甲亢组和糖尿病组CP释放试验呈现分离现象.结论 甲亢具有糖代谢紊乱、糖耐量明显降低、且合并糖尿病,是一种临床代谢综合症.  相似文献   

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