2型糖尿病患者血清瘦素水平变化分析

目的 观察2型糖尿病(DM2)患者糖耐量实验前后血清瘦素(Leptin)水平的变化.方法 DM2患者50例及正常对照者(NC)35人,行标准餐实验,测定Leptin及血糖(Plasma glucose,PG)及胰岛素(insulin,Ins).结果 与NC组相比,DM2组空腹血糖(FPG)、餐后2h血糖(2hPG)水平显著增高(P＜0.01),空腹胰岛素(Fins)升高(P＜0.05),胰岛素抵抗指数(HOMA-IR)显著增高.与NC组相比,DM2组Leptin水平明显升高(P＜0.05),且女性患者高于男性(P＜0.05),肥胖患者高于非肥胖者.结论 DM2患者空腹Leptin水平明显升高,且女性患者高于男性,肥胖患者高于非肥胖者.     

男性肥胖患者胰岛素抵抗与瘦素抵抗的相关性分析

目的　探讨男性肥胖者瘦素抵抗与胰岛素瘦素抵抗的相关性。方法　 35例肥胖男性和 30例正常对照组均进行葡萄糖耐量试验 ,空腹血清瘦素及胰岛素采用放射免疫法。空腹血糖及餐后 2h血糖采用氧化酶法 ,同时测每例受试者身高、体重 ,计算体重指数 (BMI =体重 /身高2 )。结果　肥胖组空腹血清瘦素(14 92± 10 38pmol/L)与对照组 (6 6 5± 2 73pmol/L)相比差异有显著意义 (P <0 0 1) ,肥胖组空腹血清胰岛素水平 (11 2 6± 3 90mIU/L)与健康对照组 (6 73± 2 4 8mIU/L)相比差异也有显著意义 (P <0 0 1) ,两组空腹血糖差异无显著意义 ;肥胖组内空腹瘦素与胰岛素相关分析显示两者呈显著正相关 (r =0 5 75 ,P <0 0 1)。结论　肥胖患者存在瘦素抵抗及胰岛素抵抗 ,且瘦素抵抗与胰岛素抵抗显著正相关     

瘦素与2型糖尿病的关系

目的　观察瘦素与体重指数、腰围、臀围及糖代谢指标间的相关性,探讨瘦素与2型糖尿病的关系。方法　将6 4例2型糖尿病患者按体重指数分为非肥胖组及肥胖组,并将6 7例正常对照组亦按体重指数分为健康对照组及单纯肥胖组,测定体重指数、腰围、臀围及糖代谢指标、瘦素等,以胰岛素抵抗指数(HOMA- IR)来评价胰岛素的敏感性。应用SPSS10 .0软件统计分析。结果　①2型糖尿病者的血清瘦素水平及HOMA -IR均高于对照组(P <0 .0 5 ) ;肥胖者的瘦素水平及HOMA -IR均高于非肥胖者(P <0 .0 5 ) ;②Logistic多元回归显示:HOMA- IR(OR =10 6 .6 96 )、瘦素(OR =6 .86 3)是2型糖尿病的危险因素。结论　瘦素抵抗与胰岛素抵抗及2型糖尿病的发生相关。     

肥胖与高血压患者血清瘦素水平与胰岛素抵抗的相关性研究

目的探讨肥胖和高血压患者血清瘦素水平与胰岛素抵抗(IR)的关系及在肥胖和高血压发病机制中的作用。方法选择男性合并肥胖或非肥胖的高血压患者和正常血压者,测定血糖、胰岛素、血脂、尿酸(Ur)、胰岛素敏感性指数(ISI)、24h尿蛋白定量和血清瘦素浓度,分析瘦素水平与IR的相关性及与体重指数(BMI)、血压和其它各项指标的关系。结果血清瘦素水平在高血压组高于正常血压组,肥胖者高于非肥胖者。ISI则为正常血压组的非肥胖者高于肥胖者,而无论肥胖与否,正常血压组均高于高血压组。在高血压组中,ISI降低程度肥胖与非肥胖者无显著差异。在合并肥胖的高血压和正常血压组中,血清瘦素水平与ISI呈显著负相关(r=－0.51,P<0.01)和(r="－"0.38,P<0.05)。BMI、腰臀比、ISI是影响两组瘦素水平的最显著因素,影响ISI的因素依次为BMI、SBP、DBP、TG、Ur和瘦素。BMI是影响瘦素水平和ISI的共同因素。多元逐步回归分析发现,BMI与瘦素、ISI、TG密切相关。结论肥胖者血清瘦素水平升高与IR高度相关,并与脂代谢有关。瘦素抵抗在高血压的发生中可能起间接促进作用,但与IR的关联尚待探讨。     

单纯性肥胖患者血清瘦素与胰岛素、性激素的相关分析

[目的]观察单纯性肥胖患者血清瘦素水平与胰岛素、性激素浓度的父系。[方法]川放射免疫法测定64例肥胖者和65例非肥胖者的血清瘦素水平,并分析血清瘦素水平与年龄,体重指数（BMI）、腰臀比值（WHR）、胰岛素（INS）、睾酮（T、）雌二醇（E2）的相关性。[结果]1．无论肥胖组还是非肥胖组,女性血清瘦素水平显著高于男性（P〈0．01）;同性别比较,肥胖组显著高于非肥胖组（P〈0．01）。2．相关性分析,无论是男性还是女性,血清瘦素与BMI、WHR旱显著正相关,而与年龄无关。3．血清瘦素水平与胰岛素浓度呈正相关,与血糖浓度无关。4．血清瘦素水平与T,男性呈负相关（r=一0．310,P〈0．01）,而女性呈正相关（r=0．360,P〈0．01）;与E2在男性无相关性,女性呈正相关（r=0．323,P〈0．01）。[结论]肥胖者窄腹血清瘦素水平升高,血清高瘦素与高胰岛索血症的相关性提示瘦素可能在2型糖尿病的发病中起一定作用。BMI足影响血清瘦素水平的主要原因之一,而性别间的差异则与性激素有关。     

代谢综合征患者瘦素水平与肥胖及血压的关系

目的:观察代谢综合征(metablic syndrome,MS)患者血清瘦素(Leptin)水平的变化,探讨MS患者血清瘦素水平与肥胖和高血压的关系.方法:选择50例符合下列条件的MS患者(MS组)进入研究,(1)腰围及体质指数异常;(2)血脂异常;(3)糖耐量异常;(4)高血压.另选择与MS组年龄相匹配的正常对照者(对照组)40例, 采用酶联免疫吸附法(ELISA)测定受试者空腹血清瘦素水平,同时测定身高、体重、腰围、血压、血糖、血脂. 结果: MS 组患者血清瘦素水平明显高于对照组(P ＜ 0.01). 结论:血清瘦素水平在MS患者中明显升高, 血清瘦素升高水平与肥胖及血压程度明显相关.     

瘦素抵抗与老年男性肥胖高血压的关系

背景：目前已经了解血清瘦素与肥胖的关系密切，血清瘦素和胰岛素与伴有肥胖的高血压关系如何?目的：研究老年男性肥胖高血压患者血清瘦素和胰岛素水平的变化，探讨瘦素抵抗与老年男性肥胖高血压的关系。设计：以诊断为依据，设立对照的回顾性研究。单位：华中科技大学同济医学院附属协和医院神经内科、核医学科。对象：62例老年男性患者均来自2001—10／2002—06华中科技大学同济医学院附属协和医院的住院和门诊患者，年龄60—82岁。高血压的诊断采用1999年世界卫生组织建议的血压判定标准：收缩压≥140mmHg(1mmHg=0．133kPa)和(或)舒张压390mmHg即诊断为高血压。方法：用放射免疫法测定41例高血压和21例正常血压的老年男性患者血清瘦素和胰岛素的含量。主要观察指标：老年男性肥胖患者和非肥胖者血压、体质量指数、血清瘦素和胰岛素水平。结果：高血压肥胖者较正常血压肥胖者血清瘦素和胰岛素含量分别升高1．8μg／L和2．7mIU／L，差异均有显著性意义(t=2．212，2．395，P&;lt;0．01)。高血压肥胖者较非肥胖者血清瘦素和胰岛素水平分别升高2．7μg／L和4．7mIU／L，差异均有显著性意义(t=3．348，5．113，P均&;lt;0．001)。高血压70岁以上者较高血压60-70岁者血清瘦素水平升高1．7μg／L，差异均有显著性意义(t=2．767，P&;lt;0．05)。结论：老年肥胖高血压患者存在瘦素抵抗和胰岛素抵抗．瘦素与伴肥胖的高血压有密切关系。     

胰岛素抵抗对老年男性肥胖高血压的影响

目的分析胰岛素抵抗与老年肥胖高血压的关系。方法用放射免疫法测定40例高血压和22例正常血压的老年男性患者血清胰岛素的含量。结果在高血压和肥胖分组中空腹血糖变化无显著性差异。非肥胖组高血压与正常血压者血清胰岛素的水平变化无显著性。肥胖组高血压者较正常血压者血清胰岛素含量平均升高2.7mIU/L(P<0.01)。高血压组中肥胖者较非肥胖者血清胰岛素水平平均升高4.7mIU/L(P<0.001)。胰岛素敏感指数在肥胖高血压组、肥胖非高血压组、非肥胖高血压组、非肥胖非高血压组中依次递减。结论老年肥胖高血压存在胰岛素抵抗,胰岛素与肥胖高血压有密切关系。     

多囊卵巢综合征患者血清肿瘤坏死因子-α，C反应蛋白水平的改变及与胰岛素抵抗相关性研究

目的 探讨多囊卵巢综合征(PCOS)患者血清肿瘤坏死因子-a(TNF-a),C反应蛋白(CRP)的改变及与胰岛素抵抗的相关性.方法 按体重指数(BMI≥25 kg/m2或<25 kg/m2)分别将PCOS患者56例、对照组54例分为PCOS肥胖组(32例)、PCOS非肥胖组(24例)和对照肥胖组(28例)、对照非肥胖组(26例)4组.用ELISA法测定4组的TNF-a,散射比浊法测定CRP,葡萄糖氧化酶法测定空腹血糖(FPG)、化学发光法测定空腹胰岛素(FIN)水平,并计算胰岛素抵抗指数(HOMA-IR).结果 ①PCOS组TNF-a水平类似于对照组(P>0.05),但肥胖者高于同组非肥胖者(P<0.01).②PCOS组CRP水平高于对照组(P<0.01),且肥胖者明显高于非肥胖者(P<0.01).③TNF-a及CRP水平分别与BMI,HOMA-IR水平呈明显正相关(P<0.01).结论 PCOS组CRP水平升高,且以肥胖者明显,而PCOS组肥胖者TNF-a明显升高,TNF-a及CRP水平与PCOS患者胰岛素抵抗密切相关.     

2型糖尿病患者血清瘦素水平与胰岛功能的关系

目的 :测定 2型糖尿病患者血清激素的水平 ,探讨血清瘦素水平与胰岛功能的关系。方法 :免疫放射法测定 60例 2型糖尿病患者 ,3 0例正常对照组的血清瘦素、胰岛素、C肽水平 ,分析其相关性。结果 :血清瘦素水平与胰岛素、C肽、BMI、TG显著相关 (P <0 0 1) ,肥胖者瘦素明显升高 (P <0 0 1)。结论 :2型糖尿病患者血清瘦素水平与胰岛素、C肽水平密切相关 ,提示瘦素可能在 2型糖尿病的发病中起一定作用。     

Nocturnal rise of leptin in lean, obese, and non-insulin-dependent diabetes mellitus subjects.

We studied 24-h profiles of circulating leptin levels using a sensitive and specific RIA in lean controls and obese subjects with or without non-insulin-dependent diabetes mellitus (NIDDM) during normal routine activity. Serum leptin levels were significantly higher in obese (41.7 +/- 9.0 ng/ml; n = 11) and obese NIDDM (30.8 +/- 6.7; n = 9) subjects compared with those in lean controls (12.0 +/- 4.4, n = 6). In all the three groups, serum leptin levels were highest between midnight and early morning hours and lowest around noon to midafternoon. The nocturnal rise in leptin levels was significant when data were analyzed by ANOVA (lean: F = 3.17, P < 0.0001, n = 4; obese: F = 2.02, P < 0.005, n = 11; and obese NIDDM: F = 4.9, P < 0.0001, n = 5). The average circadian amplitude between acrophase and nadir was 75.6% in lean, 51.7%, in obese and 60.7% in obese NIDDM groups, respectively. No significant correlations (P > 0.05) were observed between circulating levels of leptin and either insulin or glucose levels in any of the 20 subjects studied for 24-h profiles. The nocturnal rise in leptin observed in the present study resembles those reported for prolactin, thyroid-stimulating hormone, and free fatty acids. We speculate that the nocturnal rise in leptin could have an effect in suppressing appetite during the night while sleeping.     

Serum leptin levels in type 1 diabetic and obese children: relation to insulin levels

OBJECTIVES: To compare serum leptin levels in type 1 diabetic and obese children. DESIGN AND METHODS: We studied serum leptin levels in 35 type 1 diabetic, 32 obese, and 35 healthy children. Seven of 35 were new-onset diabetics with ketoacidosis. C-peptide (CPE) levels were used for estimating insulin secretion. RESULTS: Serum leptin levels were lower in diabetics than in controls (p<0.001). Obese children had higher leptin and CPE levels than diabetics and controls. In new-onset diabetics, 1 month insulin treatment did not cause any change in leptin levels (p>0.05). Leptin was correlated positively with body mass index and CPE (p<0.001) and inversely with glucose (p = 0.001) and HbA1c (p<0.05) in the combined group. HbA1c and gender were the independent predictors of leptin in diabetic children (p<0.01). CONCLUSIONS: Low serum leptin levels in type 1 diabetic children may be due to chronic insulin deficiency related with their metabolic control. Leptin and insulin may have complementary roles in maintaining a stable body weight.     

Elevation of plasma leptin concentrations in obese hyperinsulinaemic hypothyroidism before and after treatment

BACKGROUND: Plasma leptin is considered to play a role in maintenance of energy balance and body weight by neuroendocrine mechanisms. Thyroid hormones are permissive for adrenergic activation, which in turn has been shown to decrease leptin expression. This study was therefore designed to test the hypothesis that hyperthyroidism results in lower leptin concentrations, whereas hypothyroidism leads to higher plasma leptin concentrations. In addition, the effects of normalization of thyroid function on plasma leptin were investigated. MATERIALS AND METHODS: Fasting plasma leptin concentrations and body fat mass (total body electrical conductivity) were measured in patients with overt hypothyroidism and hyperthyroidism before and after successful treatment. Plasma leptin, glucose, insulin and free fatty acid concentrations were monitored during an oral glucose tolerance test (OGTT 75 g). RESULTS: Fasting plasma leptin concentrations were similar in lean patients, independently of their thyroid function (hyperthyroid 12.5 +/- 2 ng mL-1, hypothyroid 10.2 +/- ng mL-1, euthyroid 12.7 +/- 3 ng mL-1). In obese hypothyroid patients, plasma leptin was threefold higher (P < 0.0005) than in lean hypothyroid patients, twofold higher (P < 0.005) than in obese hyperthyroid patients matched for fat mass and 30% increased (P < 0.01) compared with obese euthyroid subjects. There were no differences between fasting and post-prandial (OGTT) leptin concentrations in any group. Normalization of thyroid function did not affect plasma leptin, which remained elevated (P < 0.005) in formerly obese hypothyroid patients. Plasma leptin was not associated with serum thyroid hormones but highly correlated with body mass index and body fat mass in all patients (r = 0.85, P < 0.001). Plasma leptin correlated with plasma insulin concentration only in hyperthyroid patients (P < 0.01, r = 0.64), who presented with blunted stimulation of insulin release and higher plasma glucose (P < 0.05) than hypothyroid subjects. CONCLUSION: The results indicate that (a) the correlation of leptin with body fat mass is preserved in thyroid dysfunction, (b) plasma leptin is markedly increased in obese hypothyroid hyperinsulinaemic patients and (c) plasma leptin is not affected by oral glucose loading.     

Acute insulin administration does not affect plasma leptin levels in lean or obese subjects

Abstract. Whether leptin levels are related to insulin sensitivity or subject to acute regulation by insulin is not known. In 12 obese [body mass index (BMI) = 34.0 ±1.5 kg m^-2] and 12 lean (BMI = 22.2 ±0.6 kg m^-2) non-diabetic subjects, plasma leptin concentrations were measured in the fasting state and during 2 hours of euglycaemic hyperinsulinaemia (˜600 pmol L^-2). Fasting plasma leptin was significantly higher in obese (26.6 ±3.2) than in lean subjects (6.4 ±1.2 ng mL^-1, P = 0.0001), and in women (21.1 ±3.3) than in men (7.3 = 2.3 ng mL^-1, P = 0.01). In univariate analysis, fasting plasma leptin was strongly related to all anthropometric measures (body weight, fat mass, percent fat mass, waist and hip circumferences). In multiple regression, per cent adiposity, hip circumference and duration of obesity explained 90% of the variability in fasting leptin concentrations. Fasting and stimulated (OGTT) insulin levels, insulin sensitivity (22.6 ±1.9 vs 36.7 ±2.0 μmol min^-1 kg^-1 in lean and obese subjects, respectively, P < 0.0001), glucose area, and serum triglycerides were positively related to fasting plasma leptin concentrations; none of these associations, however, was statistically significant after adjusting for BMI. During the clamp, plasma leptin concentrations remained constant in both lean and obese subjects. We conclude that neither insulin levels nor sensitivity relate to leptin levels independently of fat mass, and that leptin is not subject to acute (2 hours) regulation by insulin in lean or obese humans.     

Mechanisms of insulin resistance in human obesity: evidence for receptor and postreceptor defects.

To assess the mechanisms of the insulin resistance in human obesity, we have determined, using a modification of the euglycemic glucose clamp technique, the shape of the in vivo insulin-glucose disposal dose-response curves in 7 control and 13 obese human subjects. Each subject had at least three euglycemic studies performed at insulin infusion rates of 15, 40, 120, 240, or 1,200 mU/M2/min. The glucose disposal rate was decreased in all obese subjects compared with controls (101 +/- 16 vs. 186 +/- 16 mg/M2/min) during the 40 mU/M2/min insulin infusion. The mean dose-response curve for the obese subjects was displaced to the right, i.e., the half-maximally effective insulin concentration was 270 +/- 27 microU/ml for the obese compared with 130 +/- 10 microU/ml for controls. In nine of the obese subjects, the dose-response curves were shifted to the right, and maximal glucose disposal rates (at a maximally effective insulin concentration) were markedly decreased, indicating both a receptor and a postreceptor defect. On the other hand, four obese patients had right-shifted dose-response curves but reached normal maximal glucose disposal rates, consistent with decreased insulin receptors as the only abnormality. When the individual data were analyzed, it was found that the lease hyperinsulinemic, least insulin-resistant patients displayed only the receptor defect, whereas those with the greatest hyperinsulinemia exhibited the largest post-receptor defect, suggesting a continuous spectrum of defects as one advances from mild to severe insulin resistance. When insulin's ability to suppress hepatic glucose output was assessed, hyperinsulinemia produced total suppresssion in all subjects. The dose-response curve for the obese subjects was shifted to the right, indicating a defect in insulin receptors. Insulin binding to isolated adipocytes obtained from the obese subjects was decreased, and a highly significant inverse linear relationship was demonstrated between insulin binding and the serum insulin concentration required for halfmaximal stimulation of glucose disposal. In conclusion: (a) decreased cellular insulin receptors contribute to the insulin resistance associated with human obesity in all subjects; (b) in the least hyperinsulinemic, insulin-resistant patients, decreased insulin receptors are the sole defect, whereas in the more hyperinsulinemic, insulin-resistant patients, the insulin resistance is the result of a combination of receptor and postreceptor abnormalities; (c) all obese patients were insensitive to insulin's suppressive effects on hepatic glucose output; this was entirely the result of decreased insulin receptors; no postreceptor defect in this insulin effect was demonstrated.     

糖尿病庆大霉素药代动力学及肾毒性

目的：介绍糖尿病状态庆大霉素药代动力学及肾毒性的研究现状。方法：检索了近十年有关糖尿病庆大霉素动力学及肾毒性的研究文献并结合我们的工作。结果：多数研究得出非预料的结果，即糖尿病可抵御庆大霉素的肾毒性。结论：糖尿病可抵御庆大霉素的肾毒性。其机理有待进一步研究。     

2型糖尿病患者血清抵抗素与血糖、血脂及胰岛素抵抗的关系

目的:探讨2型糖尿病患者血清抵抗素与血糖、血脂及胰岛素抵抗的关系。方法:52例2型糖尿病(T2DM)患者按体质指数(BMI)分为肥胖(BMI≥25kg/m2)(26例)与非肥胖(BMI<25kg/m2)(26例)2组,及17例糖耐量正常的同期健康体检者作为对照组,采用酶联免疫分析法检测空腹血清抵抗素水平;同时行口服葡萄糖耐量(OGTT)和胰岛素释放试验,检测血脂,测量血压、身高、体重、腰围、臀围,计算BMI和腰臀比值(WHR),并以稳态模型(HOMA)计算胰岛素抵抗指数(HOMA-IR)。结果:肥胖T2DM患者血清抵抗素水平(ng/mL)明显高于非肥胖T2DM患者(P<0.01);肥胖T2DM组高于对照组、对照组略高于T2DM非肥胖者,但差异无显著性(P>0.05);女性血清抵抗素水平明显高于男性(P<0.05)。空腹血清抵抗素与BMI、HOMA-IR呈正相关(r=0.403、r=0.337、P<0.001);与FINS及餐后2hINS呈正相关(r=0.652、r=0.428、P<0.001);与甘油三酯呈正相关(r=0.320、P<0.01);与空腹血糖无关而与餐后2h血糖呈负相关(r=-0.303,P<0...     

Effects of jejuno-ileal bypass on serum lipoproteins and glucose tolerance in severely obese patients

Plasma insulin and blood glucose during oral glucose tolerance tests (OGTT) and serial determinations of serum lipoprotein fractions before and after jejuno-ileostomy in twenty severely obese (mean weight 137 kg) patients with a mean age of 29 years revealed statistically significant postoperative decreases in all parameters concomitant with a mean weight loss of 42 kg. Before the operation the patients were hyperinsulinaemic and had elevated blood glucose levels during OGTT though no patient had overt diabetes. Serum triglyceride and total cholesterol levels were normal but HDL cholesterol was significantly lower than in controls. During follow-up at least until body weight had levelled off a mean 19 months post-operative, there were statistically significant reductions in blood glucose and plasma insulin as well as serum total cholesterol and lipoprotein fractions. There was no change in serum triglycerides. The low preoperative HDL levels decreased. In a subgroup of these patients we have earlier shown postoperative increases in arterial tissue cholesterol coincident with the present significant decreases in HDL as well as in LDL cholesterol. Correlations between total cholesterol and lipoprotein cholesterol values in serum and blood glucose and plasma insulin at fast and during OGTT and changes in these parameters demonstrate interrelationships between lipid and carbohydrate metabolism. The bypass procedure most likely reduces the intestinal synthesis of HDL which in turn may increase hepatic cholesterol synthesis. Evidently there is a multifactorial aetiology for the low HDL levels in the severely obese both before and after jejuno-ileostomy.