肥胖患者血清Apelin水平与血糖、血脂和胰岛素抵抗的相关性分析

目的探讨肥胖患者血清Apelin水平与血糖、血脂和胰岛素抵抗的相关性。方法选取2016年10月—2017年10月我院收治的肥胖患者64例作为观察组,选择同期健康体检者64例作为对照组。检测血清Apelin水平,同时观察组行口服葡萄糖耐量试验,并检测空腹血糖、餐后2 h血糖、甘油三酯和空腹胰岛素,计算胰岛素抵抗指数;采用Pearson相关分析评估肥胖患者血清Apelin水平与血糖、血脂和胰岛素抵抗的相关性。结果观察组、对照组血清Apelin水平分别为(446.54±45.32)ng/L、(378.42±38.25)ng/L,比较差异有统计学意义(t=9.189,P0.001)。观察组糖耐量正常(normal glucose tolerance, NGT)28例、糖耐量减低(impaired glucose tolerance, IGT)24例和2型糖尿病(type 2 diabetes, T2DM)12例。与NGT组比较,IGT组、T2DM组血清Apelin水平升高,差异有统计学意义(P0.05);与IGT组比较,T2DM组血清Apelin水平显著升高,差异有统计学意义(P0.05)。Pearson相关分析显示,肥胖患者血清Apelin水平与餐后2 h血糖、甘油三酯和胰岛素抵抗指数呈正相关(r=0.842,P0.001;r=0.938,P=0.000;r=0.916,P0.001)。结论肥胖患者血清Apelin水平与血糖、血脂、胰岛素抵抗均呈正相关,表明Apelin在肥胖患者的发生发展中具有一定的作用。     

2型糖尿病患者体质量指数、血脂与胰岛β细胞功能的相关性研究

目的探讨2型糖尿病(T2DM)患者体质量指数(BMI)、血脂与胰岛β细胞功能的相关性。方法选取2018年12月至2019年12月于该院内分泌科门诊就诊的334例T2DM患者作为研究对象,收集年龄、病程等基线资料,计算BMI,检测空腹血糖(FBG)、空腹胰岛素(FINS)、血清三酰甘油(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)及高密度脂蛋白胆固醇(HDL-C),计算胰岛β细胞功能指数(HOMA-β)、胰岛素敏感指数(HOMA-ISI)及胰岛素抵抗指数(HOMA-IR)。结果相关性分析显示,HOMA-IR与BMI呈正相关(P<0.05),HOM A-ISI与HDL-C呈正相关(P<0.05)。根据BMI将患者分为正常组、超重组和肥胖组,3组FBG、HOMA-IR差异有统计学意义(P<0.05);以HDL-C=1.1 mmol/L为界值将患者分为两组,两组年龄、病程、FINS、HOMA-ISI差异有统计学意义(P<0.05)。多元线性回归分析示,BMI是T2DM患者HOMA-IR的独立影响因素(P<0.05);HDL-C是T2DM患者HOMA-ISI的独立影响因素(P<0.05)。结论T2DM患者BMI、HDL-C与胰岛β细胞功能存在一定相关性,对T2DM合并胰岛素抵抗的诊断及指导治疗具有重要参考价值。     

血清补体C1q与2型糖尿病患者血脂紊乱及胰岛素抵抗的相关性研究

目的探讨2型糖尿病(T2DM)患者检测血清中补体C1q的水平与糖尿病血脂紊乱、胰岛素抵抗的相关性。方法选择140例肾功能无异常的T2DM患者(T2DM组)及同期140例健康体检者(对照组),采集血清并采用Olympus Au5400全自动生化分析仪检测C1q、空腹血糖、空腹胰岛素、血脂全套、超敏C反应蛋白(hs-CRP)等。运用SPSS17.0对检测结果进行统计学分析。结果 T2DM患者与对照组比较,C1q、空腹血糖及三酰甘油均升高且差异有统计学意义(P0.05);T2DM患者中胰岛素抵抗指数(HOMA-IR)高值组与低值组比较,C1q、三酰甘油、hs-CRP、空腹血糖及空腹胰岛素均增高且差异有统计学意义(P0.05)。T2DM患者血清中C1q与HOMA-IR、三酰甘油、胆固醇、空腹血糖、磷脂呈正相关(r=0.259、0.371、0.258、0.266、0.291,P0.05);多元Logistic回归分析发现,三酰甘油和空腹血糖是T2DM患者血清C1q的独立影响因素(OR=0.313、0.212,P0.05)。结论 T2DM患者胰岛素抵抗和血脂紊乱加重可能与C1q增高相关。     

2型糖尿病患者血清游离脂肪酸水平与胰岛素抵抗的关系

目的探讨2型糖尿病(T2DM)患者血清游离脂肪酸(FFA)水平与胰岛素抵抗(IR)的关系。方法选取106例T2DM患者为观察组,选择106例健康体检者为对照组,比较2组受检者体质量指数(BMI)、空腹血糖(FPG)、FFA、糖化血红蛋白(HbA1c)、总胆固醇(TG)、甘油三酯(TC)及胰岛素抵抗指数(HOMA-IR)水平。根据血糖控制水平将T2DM患者分为控制良好组(n=56)和控制不良组(n=50),比较2组患者FFA及HOMA-IR水平。分析T2DM患者血清FFA与HOMA-IR的相关性。结果观察组BMI、FPG、FFA、HbA1c、TC、TG、HOMA-IR均显著高于对照组(P0.05);血糖控制不良组患者FFA及HOMA-IR水平均显著高于控制良好组(P0.05);相关性分析显示,T2DM患者血清FFA与HOMA-IR水平呈正相关性(r=0.621,P0.05)。结论血清游离脂肪酸水平与2型糖尿病患者胰岛素抵抗程度关系密切,且可以反映患者血糖控制水平。     

2型糖尿病患者血清补体因子H与胰岛素抵抗相关性研究

目的探讨2型糖尿病(T2DM)患者糖脂代谢和胰岛素抵抗的变化情况,分析其与患者血清补体因子H表达之间的相关性。方法选择2015年1月至2016年2月期间T2DM的患者120例为研究对象,根据亚太地区2000年的肥胖标准分为肥胖组(64例)和非肥胖组(56例),另选择同期体检的健康人群60例为对照组。比较各组患者的血清补体因子H表达情况及空腹胰岛素、空腹血糖、血脂水平,计算胰岛素抵抗指数(HOMA-IR),分析各指标与补体因子H表达的相关性。结果肥胖组、非肥胖组、对照组血清补体因子水平分别为(196.38±23.49)mg/L、(184.34±21.48)mg/L和(173.26±18.37)mg/L,肥胖组非肥胖组对照组,组间比较差异有显著的统计学意义(P0.01);T2DM患者血清补体因子H与体质指数(BMI)、空腹胰岛素(FINS)、胰岛素抵抗指数(HOMA-IR)、甘油三酯(TG)、空腹血糖(FBG)水平均呈正相关(r=0.397、0.601、0.333、0.312、0.524,P均0.01),与高密度脂蛋白胆固醇(HDL-C)呈负相关(r=-0.588,P0.01)。结论补体因子H可能参与了肥胖及T2DM的发病过程,临床上有望将补体系统作为T2DM的治疗靶点。     

2型糖尿病患者血清视黄醇结合蛋白4水平的临床意义

目的 检测2型糖尿病(T2DM)患者正常体重组和肥胖组的血清视黄醇结合蛋白4(RBP4)水平,探讨与血脂和胰岛素敏感性等的相关性.方法 以体重指数(BMI)将63例糖尿病患者分成两组:T2DM超重/肥胖组和T2DM正常体重组,均采用HOMA-IR评价各组胰岛素敏感性,测定受试者的BMI、腰臀比(WHR),检测空腹状态下血清RBP4、血糖、糖化血红蛋白(HbAlc)、血浆葡萄糖(FBG)、总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)及低密度脂蛋白胆固醇(LDL-C)和胰岛素水平,并以55例健康体检者作对照.结果 T2DM超重/肥胖组血清RBP4浓度明显高于对照组和T2DM正常体重组,差异均有统计学意义(t分别=3.04、2.77,P均＜0.05);RBP4与HOMA-IR、BMI、WHR、TG明显正相关(r分别=0.33、O.28、0.24、0.32,P均＜0.05);多元线性逐步回归分析发现:HOMA-IR、BMI、TG、性别和年龄是血清RBP4的独立相关因素(r分别=0.33、0.56、0.55、-0.41、0.37,P均＜0.05).结论 血清RBP4与胰岛素抵抗呈正相关,可能与T2DM发病有一定关系.     

2型糖尿病合并阻塞性睡眠呼吸暂停低通气综合征患者血清抵抗素水平变化及其意义

目的 探讨2型糖尿病(T2DM)合并阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血清抵抗素水平变化及其在发病中的作用.方法 T2DM患者65例(T2DM组),根据是否合并OSAHS分为T2DM未合并OSAHS组35例,T2DM合并OSAHS组30例,并设正常对照组30名.测定血清抵抗素浓度,同时检测空腹血糖、空腹胰岛素、糖化血红蛋白、血脂等相关指标,计算体质量指数、腰臀比及稳态模型评价的胰岛素抵抗指数.结果 (1)与正常对照组血清抵抗素浓度(9.06±0.85) μg/L比较,T2DM组(12.54±1.74) μg/L显著升高,差异有统计学意义(t=2.547,P＜0.01);体质量指数、腰臀比、胰岛素抵抗指数、空腹胰岛素、空腹血糖、糖化血红蛋白和甘油三酯显著升高(P＜0.01),收缩压、低密度脂蛋白胆固醇及总胆固醇升高,差异有统计学意义(P＜0.05),高密度脂蛋白胆固醇显著降低(P＜0.01).(2)与T2DM未合并OSAHS组比较,T2DM合并OSAHS组血清抵抗素浓度[(13.84±1.31)μg/L与(11.43±1.21)μg/L]显著升高,差异有统计学意义(t=2.613,P＜0.01).糖化血红蛋白和甘油三酯显著升高(P＜0.05),高密度脂蛋白胆固醇降低(P＜0.05).抵抗素与低密度脂蛋白胆固醇、总胆固醇及空腹胰岛素呈正相关(r =0.343、0.315、0.298,P均＜0.05);与体质量指数、腰臀比、胰岛素抵抗指数、甘油三酯及空腹血糖呈显著正相关(r=0.615、0.587、0.517、0.435、0.453,P均＜0.01;与高密度脂蛋白胆固醇呈负相关(r=-0.436,P＜0.01).结论 血清抵抗素可能与T2DM发生相关,而且血清抵抗素可能不是通过进一步引起肥胖来增加T2DM患者发生OSAHS的患病风险,有可能通过其他途径,如影响炎症因子的表达来增加OSAHS的患病风险.     

代谢综合征患者血清抵抗素和瘦素与2型糖尿病相关性研究

目的探讨代谢综合征(metabolic syndrome,MS)患者血清抵抗素、瘦素与2型糖尿病(type 2diabetes mellitus,T2DM)的关系。方法选取T2DM并MS患者29例(T2DM+MS组)、非T2DM的MS患者28例(单纯MS组)、体检健康者30例(对照组),采用放射免疫方法检测血清抵抗素、瘦素水平,同时检测身高、体质量、血压、空腹血糖、血脂、血尿酸、胰岛素,并计算体质指数和胰岛素抵抗指数。结果 T2DM+MS组、单纯MS组与对照组空腹血糖、收缩压、舒张压、高密度脂蛋白胆固醇、三酰甘油、瘦素、胰岛素水平和胰岛素抵抗指数比较差异均有统计学意义(P<0.05);T2DM+MS组与单纯MS组空腹血糖、收缩压、瘦素和胰岛素水平比较差异有统计学意义(P<0.05);抵抗素水平升高与体质量指数、血尿酸、收缩压和胰岛素抵抗指数相关;瘦素水平升高与体质量指数、空腹血糖、胰岛素和胰岛素抵抗指数相关。结论血清瘦素和抵抗素水平与MS密切相关,高血清瘦素水平在MS和T2DM形成及发展中起重要作用。     

多囊卵巢综合征及2型糖尿病患者血清Apelin水平及相关因素分析

目的测定多囊卵巢综合征(PCOS)及2型糖尿病(T2DM)患者的血清Apelin水平,探讨其与肥胖、性激素、代谢指标及胰岛素抵抗的相关性。方法 24例PCOS患者、26例T2DM和22例正常糖调节(NGR)者按体重指数(BMI)≥25kg/m2或<25kg/m2又各自分为超重(over weight,OW)与正常体重(normal weight,NW)亚组,采用放射免疫法检测空腹血清Apelin水平,空腹血糖(FPG)、空腹胰岛素(FINS)、性激素水平,计算BMI,并以稳态模型方法计算胰岛素抵抗指数(HOMA-IR)。结果 PCOS组患者血清Apelin水平高于NGR组[(247.8±47.5)ng/Lvs.(220.2±42.3)ng/L,P<0.05],T2DM组患者血清Apelin水平明显高于NGR组[(249.5±55.2)ng/Lvs.(220.2±42.3)ng/L,P<0.05],血清Apelin水平在PCOS组及T2DM组间比较,差异无统计学意义。在PCOS组、T2DM及NGR组中,OW亚组Apelin水平高于相应NW亚组。空腹血清Apelin水平与BMI、FPG、FINS、HOMA-IR、TG及TC呈正相关(r值分别为0.612、0.356、0.407、0.411、0.349、0.334,P<0.05)。结论血清Apelin水平变化与BMI、胰岛素抵抗及血脂有关,并可能在PCOS及T2DM的发生发展中起一定的作用。     

初诊2型糖尿病患者前列环素与胰岛素抵抗的相关分析

目的分析初诊2型糖尿病(T2DM)患者血浆前列环素(PGI2)水平变化及其与胰岛素抵抗(IR)的相关性。方法选择初诊T2DM患者60例及健康对照组60例,测定体质量、身高、血脂、空腹血糖(FPG)、餐后2h血糖(2hPG)、空腹胰岛素(FINS)、餐后2h胰岛素(2hINS),计算胰岛素抵抗指数(HOMA-IR),测定血浆PGI2的稳定代谢产物6-酮-前列腺素F1α(6-keto-PGF1α)浓度,并作相关性分析。结果 T2DM组体质量指数(BMI)、三酰甘油(TG)、总胆固醇(TC)、FPG、2hPG、FINS、2hINS、HOMA-IR均高于健康对照组,差异有统计学意义(P0.05);T2DM组血浆6-keto-PGF1α水平较健康对照组明显下降(P0.01);血浆6-keto-PGF1α水平与HOMA-IR呈负相关(r=-0.82,P0.01)。结论 T2DM患者存在IR,血浆PGI2的代谢终末产物6-keto-PGF1α水平与IR密切相关。     

Patterns of glucose and lipid abnormalities in black NIDDM subjects.

OBJECTIVE: We had previously shown two variants among black non-insulin-dependent diabetic (NIDDM) subjects in a normoglycemic remission: one with insulin resistance and the other with normal insulin sensitivity. This study examined whether these two variants exist in the ordinary hyperglycemic black NIDDM population. Research Design and Methods: Fifty-two black NIDDM subjects were assessed for insulin-stimulated glucose disposal (euglycemic clamp), glycemic control (fasting plasma glucose and HbA1c), and fasting lipid profiles. RESULTS: The distribution of glucose disposal in 30 black NIDDM subjects (body mass index; BMI less than 30 kg/m2) was bimodal, which indicated two populations. Eighteen of 30 subjects (BMI 26.4 +/- 0.5 kg/m2) had insulin resistance (glucose disposal 3.21 +/- 0.24 mg.kg-1.min-1). Twelve of 30 subjects (BMI 24.83 +/- 1.1 kg/m2) had normal insulin sensitivity (glucose disposal 7.19 +/- 0.46 mg.kg-1.min-1). Twenty-one of the remaining 22 subjects (BMI 33.4 +/- 0.7 kg/m2) were insulin resistant (glucose disposal 2.88 +/- 0.21 mg.kg-1.min-1). Fasting serum triglyceride levels were lowest in the insulin-sensitive population (0.91 +/- 0.07 mM) and different from the insulin-resistant population, BMI less than 30 and greater than 30 kg/m2, (1.20 +/- 0.10 mM, P less than 0.05 and 1.42 +/- 0.17 mM, P less than 0.025, respectively). Fasting serum low-density lipoprotein cholesterol levels were not significantly different among the groups, although it did increase with insulin resistance and increasing obesity. Total serum cholesterol levels and glycemic control were similar for all three groups. Serum high-density lipoprotein cholesterol levels were higher in women compared with men. CONCLUSIONS: In the hyperglycemic black NIDDM population, two variants exist: one with insulin resistance and one with normal insulin sensitivity. This insulin-sensitive variant represents 40% of subjects with a BMI less than 30 kg/m2. Moreover, the insulin-sensitive group has a lower risk profile for cardiovascular disease.     

Increased visceral fat and serum levels of triglyceride are associated with insulin resistance in Japanese metabolically obese,normal weight subjects with normal glucose tolerance

OBJECTIVE: The purpose of this study was to investigate the association between visceral adiposity or triglyceride (TG) metabolism and insulin resistance in metabolically obese, normal weight (MONW) Japanese individuals with normal glucose tolerance. RESEARCH DESIGN AND METHODS: We evaluated body fat areas, lipid profiles, and the glucose infusion rate (GIR) during a euglycemic-hyperinsulinemic clamp study in 20 MONW subjects (BMI <25 kg/m(2)and visceral fat areas 100 cm(2)) with normal glucose tolerance. Body fat areas were measured by computed tomography scans. Control data were obtained from 20 normal subjects (BMI <25 kg/m(2) and visceral fat areas <100 cm(2)). RESULTS: MONW subjects showed a significant increase in fasting serum levels of TG (P < 0.01) and a decrease in GIR (P < 0.01) compared with normal subjects. There were significant correlations between visceral fat areas (r = -0.563, P < 0.01) or serum levels of TG (r = -0.474, P < 0.05) and GIR in MONW subjects. Multiple regression analyses showed that visceral fat areas (F = 7.702, P < 0.02) and serum levels of TG (F = 7.114, P < 0.05) were significantly associated with GIR in all (MONW and normal) subjects. CONCLUSIONS: Increased visceral fat and serum levels of TG are associated with insulin resistance in Japanese MONW subjects with normal glucose tolerance. Excess visceral fat and elevated TG levels may play important roles in the development of insulin resistance in Japanese MONW subjects with normal glucose tolerance.     

Adiponectin and insulin resistance in obesity-related diseases

The relationship between insulin resistance and serum adiponectin levels in 400 subjects with different obesity-related diseases was studied. Lean subjects with body mass index (BMI) < 25 kg/m(2) were placed in one group and the other five groups of overweight/obese subjects with BMI >or= 25 kg/m(2) were grouped according to disease profile. The homeostasis model assessment insulin resistance (HOMA-IR) index and adiponectin levels were similar in the lean, metabolically normal (MNO) and hypertensive groups, but were different when the dyslipidaemic group was compared with the lean and MNO groups. The type 2 diabetic (DMO) and hypertensive, type 2 diabetic (DMHTO) groups were significantly different from other groups with respect to HOMA-IR index and adiponectin levels. Adiponectin levels were lower in the DMHTO than the DMO group. In multiple regression analysis, adiponectin levels correlated with group categorization independently of age, sex, BMI and HOMA-IR. Hypoadiponectinaemia may play a role in the development of complications of obesity.     

Lispro Mix25 insulin as premeal therapy in type 2 diabetic patients

OBJECTIVE: Insulin Mix25 is a new premixed insulin analog containing 25% insulin lispro and 75% neutral protamine lispro (NPL) suspension (NPL insulin). The aim of the study was to compare serum glucose and insulin responses after breakfast in type 2 diabetic patients who received Mix25, premixed regular/NPH (30%/70%), or NPH insulin before the meal. RESEARCH DESIGN AND METHODS: We studied 22 type 2 diabetic patients of age 62 +/- 1 years, BMI 30 +/- 1 kg/m2, duration of diabetes 15 +/- 2 years, duration of insulin therapy 6 +/- 1 years, insulin dose 65 +/- 6 U/day, and HbA1c 7.9 +/- 0.2%. Ten healthy individuals (age 56 +/- 1 years, BMI 28 +/- 1 kg/m2) served as control subjects. Each patient (except healthy subjects, who were studied once each) was studied three times in a double-blind, randomized fashion. After an overnight fast, the patients received 36 +/- 4 U of test insulin. Ten minutes after insulin injection, the patients ingested a breakfast meal (512 kcal, 60% carbohydrate, 20% fat, and 20% protein), identical in all studies. Blood samples were taken before and at 10- to 30-min intervals for 240 min after the breakfast meal. RESULTS: The peak rise in serum glucose was lower after Mix25 (76 +/- 7 mg/dl) than after 30/70 (94 +/- 5 mg/dl, P < 0.05) or NPH (113 +/- 4 mg/dl, P < 0.005) insulin. The incremental area under the serum glucose curve was 36% smaller after Mix25 than after 30/70 (P < 0.01) and 56% smaller than after NPH (P < 0.005) insulin. The peak rise in serum insulin concentration was higher after Mix25 (103 +/- 18 mU/l) than after 30/70 (87 +/- 13 mU/l, P < 0.05) or NPH (62 +/- 12 mU/l, P < 0.01) insulin. The incremental area under the serum insulin curve was higher after Mix25 than after 30/70 during the first 2-3 h (P < 0.02), but the difference disappeared by the end of the 4-h follow-up period. After Mix25 injection, there was an inverse correlation between the glucose response to a meal and insulin dose (r = -0.56, P < 0.01) or the incremental area under the serum insulin curve (r = -0.39, P < 0.05). No such correlations were observed with the other insulins. CONCLUSIONS: Because of its faster initial absorption rate, the new premixed insulin analog Mix25 reduces blood glucose response to a breakfast meal in type 2 diabetic patients compared with premixed 30/70 (regular/NPH) or NPH insulin.     

Liver fat content measured by magnetic resonance spectroscopy at 3.0 tesla independently correlates with plasminogen activator inhibitor-1 and body mass index in type 2 diabetic subjects

We measured liver fat content by 3-Tesla magnetic resonance spectroscopy (MRS) in 34 non- to mild obese Japanese subjects with type 2 diabetes, who were not complicated with any liver diseases including clinical fatty liver (liver/spleen ratio of computed tomography [CT] < 0.9) and were not being treated with oral hypoglycemic agents, insulin, or lipid-lowering agents, and analyzed the relationship between liver fat content and body composition and plasma metabolite. The liver fat content is significantly correlated with variables relating to obesity (body mass index [BMI], body weight, fat mass, waist to hip ratio, visceral fat area, subcutaneous fat area, and serum triglyceride), insulin resistance (fasting plasma insulin and homeostasis model assessment of insulin resistance [HOMA-IR]), adipocytokines (serum plasminogen activator inhibitor-1 [PAI-1] and leptin), and serum cholinesterase, but not CT liver/spleen ratio, which is correlated only with fasting plasma glucose, BMI, and HOMA-IR. Multiple regression analysis revealed that the liver fat content is independently associated with serum PAI-1 level (p < 0.001) and BMI (p < 0.05), but not visceral fat area. MRS is a more sensitive method for quantifying liver fat content than CT in type 2 diabetic subjects with non- to mild obesity and without clinical fatty liver.     

Heterogeneity in the relationship between ethnicity,BMI, and fasting insulin

OBJECTIVE: To determine whether the association of BMI and fasting insulin is modified by ethnicity. RESEARCH DESIGN AND METHODS: Non-Hispanic black (black), non-Hispanic white (white), and Mexican-American men and women aged 20-80 years from the Third National Health and Nutrition Examination Survey (1988-1994) were included in this study. Linear regression models with an interaction term were used to test whether ethnicity modified the association between BMI and fasting insulin. RESULTS: Fasting insulin was 19, 26, 20, and 19% higher in black women than white women with BMI levels of <22, 22-24, 25-27, and 28-30 kg/m(2), respectively. These differences between black and white women converged at BMI levels >30 kg/m(2). Mexican-American women had fasting insulin levels that were 17, 22, 20, and 16% higher than those of white women at BMI levels of 25-27, 28-30, 31-33, and >34 kg/m(2), respectively, but were not different in individuals with BMI levels <25 kg/m(2). Adjusting for established risk factors did not attenuate these associations in women. Differences in fasting insulin among men were not as apparent. CONCLUSIONS: These findings suggest that the effect of obesity on insulin sensitivity is different for Americans in ethnic minorities. In black subjects, fasting insulin is higher at lean weight when compared with white and Mexican-American subjects. In Mexican-American subjects, fasting insulin is higher in overweight individuals when compared with white and black subjects. These findings are more pronounced in women than in men. This result reinforces the importance of designing prevention programs that are tailored to meet the needs of specific populations. Investigation of possible explanations for these differences seems warranted.     

Insulin action in black Americans with NIDDM.

OBJECTIVE--To assess the influences that obesity and hyperglycemia have on insulin action in black NIDDM patients. RESEARCH DESIGN AND METHODS--Thirty-nine subjects were studied who had normal GHb levels and/or FPG less than 6.4 mM and who had not taken pharmacological agents for 2-91 mo before the study. Insulin action was studied using the euglycemic insulin clamp with a D-[3-3H]glucose infusion. Degree of obesity was assessed with BMI. During carefully monitored follow-up, 9 patients relapsed into a hyperglycemic state, and insulin action was restudied after acute reregulation of their plasma glucose. RESULTS--Insulin action was related to the degree of obesity at the extremes of BMI: 7 of 8 patients (87.5%) with a BMI less than 24.0 kg/m2 were insulin sensitive, and 8 of 9 patients (88.9%) with a BMI greater than 28.5 kg/m2 were insulin resistant. In the midrange BMI (24.0-28.5 kg/m2), patients were equally likely to be insulin resistant or insulin sensitive. A plot of frequency versus glucose disposal in those patients was compatible with a bimodal distribution (P less than 0.025): 12 of 22 patients were normally insulin sensitive (glucose disposal 6.1-9.4 mg.kg-1.min-1), and 10 were insulin resistant (glucose disposal 2.4-4.8 mg.kg-1.min-1). Analysis of this midrange BMI group showed that in the insulin-sensitive group, an inverse relationship existed between BMI and glucose disposal (r = -0.64, P less than 0.05), whereas no such relationship was found in the insulin-resistant group. The clinical characteristics of the midrange BMI group indicated that fasting plasma insulin, total cholesterol, and triglycerides were higher; whereas BMI, age, and FPG were not different in the insulin-resistant compared with the insulin-sensitive group. With the development of hyperglycemia, insulin action in the insulin-sensitive group. With the development of hyperglycemia, insulin action in the insulin-sensitive group was decreased, independent of obesity, whereas it was unchanged in the insulin-resistant group. CONCLUSIONS--Insulin resistance exists in only approximately 50% of black NIDDM patients. The relationship between obesity and insulin resistance is not a simple one. The data can be explained by one of two hypotheses: 1) insulin resistance in black NIDDM patients is an acquired defect related to the development of obesity and is modulated by hyperglycemia, or 2) NIDDM exists as two variants, one with primary insulin resistance and one with normal insulin sensitivity, and that insulin resistance causes central and/or generalized obesity.     

腹部和大腿皮下脂肪组织抵抗素蛋白的表达

背景:抵抗素是脂肪细胞分泌的一种多肽激素。而中心性肥胖时可引起胰岛素抵抗和导致2型糖尿病。目的:比较正常人腹部和大腿皮下脂肪组织抵抗素蛋白表达的情况,探讨抵抗素在中心性肥胖引起胰岛素抵抗中的作用。设计:对照观察实验。单位:华中科技大学同济医学院附属同济医院内分泌科。对象:选择2003-01/04华中科技大学同济医学院附属同济医院外科住院患者20例,根据留取脂肪组织的部位分腹部皮下脂肪组织组12例和大腿皮下脂肪组织组8例。方法:①所有患者测量血压、身高、体质量,计算体质量指数,体内脂肪百分比(按白种人数据推导的公式):男性=1.2×体质量(kg) 身高-2(m-2) 0.23×年龄-16.2;女性=1.2×体质量(kg) 身高-2(m-2) 0.23×年龄-5.4。②葡萄糖氧化酶法测定空腹血糖。③留取的脂肪组织标本用单去污裂解液提取脂肪组织中的蛋白质,考马斯亮蓝法测定蛋白质浓度,Western-blot测量脂肪组织抵抗素蛋白的表达水平。主要观察指标:两组患者的血压、体质量指数,体内脂肪百分比,空腹血糖,抵抗素蛋白的表达水平。结果:纳入患者20例,均进入结果分析。①两组的空腹血糖、收缩压、舒张压、体质量指数、体内脂肪百分比差异无显著性(P>0.05)。②腹部皮下脂肪组织抵抗素蛋白表达(A)为14942±6076,明显高于大腿皮下脂肪组织组39421±6087,二者比较差异显著(P<0.01)。结论:抵抗素蛋白在腹部皮下脂肪组织的表达高于腿部皮下脂肪组织,此结果对中心性肥胖并引起胰岛素抵抗和2型糖尿病的发生具有参考价值。     

慢性丙型肝炎病毒感染对胰岛素敏感性和血清脂联素水平的影响

目的:探讨在限制代谢因素后丙型肝炎病毒(HCV)感染对胰岛素敏感性和血清脂联素水平的影响.方法:以2009年1月～2010年12月我院收治的非糖尿病慢性HCV感染者35例为研究组,健康受试者35例为对照,两组空腹血糖水平、体重指数(BMI<26 kg/m2)和腹部超声检查均正常.比较两组的胰岛素抵抗指数和血清脂联素水平.结果:研究组的胰岛素抵抗指数和血清脂联素水平无显著性差异(P>0.05).结论:在无代谢紊乱如肥胖、糖尿病和脂肪肝时,单独慢性HCV感染不影响胰岛素敏感性和血清脂联素水平.     

Obesity,Type II diabetes and the beta 2 adrenoceptor gene Gln27Glu polymorphism in the Tongan population

As there is a high prevalence of obesity in Tonga, we aimed to determine the distribution of the beta2 adrenoceptor gene Gln(27)Glu polymorphism and to assess its relevance to obesity and to Type II diabetes, known to be prevalent in that population. A random sample of 1022 individuals from Tonga were genotyped for the Gln(27)Glu polymorphism in the beta 2 adrenoceptor gene. To assess the prevalence of obesity we measured body-mass index (BMI), fat-free mass, percentage fat and waist-to-hip ratio (WHR). To assess glucose metabolism we measured HbA(1c), fasting blood glucose, fasting serum insulin, and 1- and 2-h glucose; we also measured serum lipid and creatinine levels. We found that 84% of the Tongan men and 93% of the women were overweight or obese (BMI > or = 25 kg/m(2)) and 15.1% had Type II diabetes. Genotype frequencies among the 1022 Tongans were: Gln/Gln 90.3% and Gln/Glu 9.6%; we found one Glu/Glu homozygote. The mean BMI (+/-S.D.) for men was not significantly different for those who were homozygous (30.2+/-5.4 kg/m(2)) or heterozygous (30.1+/-5.5 kg/m(2)) for the Gln allele; this was also true for women (33.7+/-6.2 kg/m(2) for homozygous and 34.0+/-5.6 kg/m(2) for heterozygous). The Glu allele was not associated with other measures of obesity or abnormal glucose metabolism in this generally overweight population. There is a unique frequency of the Gln/Glu beta 2 adrenoceptor polymorphism among Tongans. We found no association of the polymorphism with obesity measures or Type II diabetes-related variables in the Tongan population among whom we documented a high prevalence of obesity and Type II diabetes and a low frequency of the Glu allele.