正常糖耐量、糖耐量低减和糖尿病人群中胰岛素抵抗与胰岛素分泌功能研究

流行病学调查表明胰岛素抵抗 (ＩＲ)不仅存在于糖尿病(ＤＭ)患者中 ,在糖耐量低减 (ＩＧＴ)甚至正常糖耐量 (ＮＧＴ)人群中也发现ＩＲ存在。本研究从糖尿病流行病学的角度探讨ＩＲ和胰岛素分泌 (ＩＳ)在ＮＧＴ、ＩＧＴ和ＤＭ 3组人群中的改变。一、对象和方法1.对象 :874例馒头餐后 2ｈ指尖毛细血管血糖超过6 .6 7ｍｍｏｌ/Ｌ者行 75ｇ口服葡萄糖耐量 (ＯＧＴＴ)试验 ,并测定空腹胰岛素 (ＦＩＮＳ)和ＯＧＴＴ 2ｈ胰岛素 (ＰＩＮＳ)。根据 1985年ＷＨＯ糖尿病诊断标准 ,将所有受试者分为 3组 :ＮＧＴ 35 1例 ,年龄 (44 .0± 14 .7)岁 ;ＩＧＴ…     

正常糖耐量人群中血压与胰岛素抵抗及胰岛素分泌关系研究

目的研究血压与胰岛素敏感性和胰岛B细胞功能之间的关系。方法采用多阶段分层整群随机抽样方法对江苏省内人群进行研究,根据口服葡萄糖耐量试验结果选取18岁以上正常糖耐量人群952例,根据血压不同,分为正常血压组、正常高值组、1级高血压组、2级高血压组、3级高血压组。胰岛素敏感性采用ISIM及1/HOMA-IR评价;胰岛B细胞功能采用HOMA-β、InsAUC30/GluAUC30和InsAUC120/GluAUC120评估。结果同正常血压组相比,正常高值组和1、2、3级高血压组的1/HOMA-IR分别下降11.1%、14.8%、24.1%、33.3%(P<0.001),ISIM分别下降10.3%、15.5%、27.6%、37.1%(P<0.001);InsAUC30/GluAUC30指数分别升高11.1%、41.3%、42.9%、101.2%(P<0.001),InsAUC120/GluAUC120分别升高13.2%、46.5%、54.2%、96.9%(P<0.001);5组间的HOMA-β有上升趋势,但差异无统计学意义。处置指数DI(包括基础时相DI0、早时相DI30、总时相DI120)在5组别间均没有明显变化。结论正常糖耐量人群中,随着血压升高,胰岛素敏感性逐渐下降,出现胰岛素抵抗,胰岛素分泌逐渐上升,尚未出现胰岛分泌功能的缺陷。     

中国新诊断2型糖尿病患者胰岛素分泌和胰岛素抵抗特点调查

胰岛素抵抗与胰岛素分泌缺陷是2型糖尿病的主要病理生理学缺陷。绝大多数的欧美2型糖尿病患者均肥胖，而肥胖所致的胰岛素抵抗被认为是导致该人群发生2型糖尿病的最主要因素。但是亚洲2型糖尿病患者中，肥胖者还不到半数。胰岛素抵抗抑或胰岛素分泌功能缺陷是亚洲糖尿病患者早期发病的主要因素尚不明了。本文调查了解中国新诊断的2型糖尿病人群胰岛素抵抗和胰岛素分泌功能的状况并观察格列齐特（达美康缓释片）强化治疗对其的影响。     

空腹血糖异常人群胰岛素分泌功能及胰岛素抵抗状态的探讨

目的　探讨空腹血糖异常人群的胰岛素分泌及胰岛素抵抗状态。　方法　选择包钢糖尿病普查中复查口服葡萄糖耐量试验 (OGTT) 3985例 ,分为 6组 :正常糖耐量 (NGT)组 2 5 88例 ,异常空腹血糖 (IFG)组 2 72例 ,糖耐量减低 (IGT)组 4 4 9例 ,空腹血糖异常伴糖耐量减低 (IFG/ IGT)组116例 ,新诊断糖尿病 (DM1)组 338例 ,已知糖尿病 (DM2 )组 2 2 2例。测腰围、体重指数、血压、血脂及血浆胰岛素 ,应用稳态模式胰岛素抵抗指数 (HOMA- IR)作为胰岛素抵抗指标 ,稳态模式胰岛 β细胞功能指数 (HBCI)及胰岛素分泌指数 (IS)作为胰岛素分泌指标 ,并对 6组患者的这些指标及临床特征 ,进行对比分析。　结果　与 NGT组比较 ,IFG组 HOMA- IR(1.4 6± 0 .6 0 ,1.0 6± 0 .6 4 ,t=- 6 .716 ,P<0 .0 0 1)、空腹胰岛素 (FINS) (17.90± 10 .0 6 ,15 .79± 10 .94 ,t=- 2 .0 71,P=0 .0 39)增高 ,HB-CI(4.6 5± 0 .6 0 ,5 .2 7± 0 .76 ,t=3.399,P<0 .0 0 1)及 IS(0 .86± 0 .6 0 ,0 .99± 0 .6 2 ,t=2 .36 6 ,p=0 .0 18)降低 ;IGT组 HOMA- IR(1.39± 0 .5 8,t=4 .6 98) ,FINS(2 1.2 7± 15 .39,t=4 .4 93)、2 - h胰岛素(6 0 .84± 37.86 ,t=8.4 82 )、HBCI(5 .4 7± 0 .79,t=2 .6 98)、IS(1.2 5± 0 .6 1,t=4 .0 34,P值均 <0     

早期营养不良对大鼠成年后胰岛素抵抗和糖耐量异常的影响

目的　探讨早期营养不良大鼠成年后胰岛素敏感性和糖代谢变化。　方法　建立早期营养不良大鼠动物模型 ;给予孕期 14d大鼠半量饲料饲养至哺乳期结束 ,造成其子鼠早期营养不良 ;对成年子鼠行腹腔内注射葡萄糖耐量试验和高胰岛素 正常血糖钳夹术。　结果　早期营养不良组(试验组 )子鼠与对照组子鼠比较 ,糖耐量试验各时间点血糖升高 (P <0 0 1) ;试验组子鼠稳态葡萄糖输注速率值 (2 8± 5 )mg·kg-1·min-1较对照组子鼠 (4 0± 7)mg·kg-1·min-1显著降低 (P =0 0 0 2 )。　结论　早期营养不良致大鼠成年后糖耐量受损 (IGT)和胰岛素抵抗 (IR)。     

非酒精性脂肪肝与胰岛素抵抗和糖耐量异常的关系

目的探讨胰岛素抵抗和糖耐量异常与非酒精性脂肪肝（NAFLD）的关系,分析影响NAFLD的因素。方法比较71例糖耐量异常伴有脂肪肝患者和59例糖耐量异常不伴有脂肪肝患者的体质量指数（BMI）、腰臀比（WHR）、总胆固醇（TC）、甘油三酯（TG）、血尿酸、丙氨酸氨基转移酶、仪谷氨酰转移酶、糖化血红蛋白和HOMA-IR水平。结果Logistic回归分析表明,HOMA．IR、TC、TG、WHR是NAFLD形成的独立危险因素。结论肥胖、高TG和胰岛素抵抗是糖耐量异常合并NAFLD的重要因素。     

多次取样的静脉糖耐量试验中胰岛素分泌率的测定和计算

目的 在体内C－肽动力学二室模型及标准参数法基础上,计算多次取样的静脉糖耐量试验（FSIVGTT）中胰岛素分泌率（ISR）。方法 15例糖耐量正常者及11例2型糖尿病者均行口服糖耐量试验（OGTT）及FSIVGTT。所有标本用己糖激酶法测定葡萄糖,用放免法测定胰岛素（INS）、C－肽,根据自编计算机程序,计算各时点ISR。结果 FSIVGTT中,对照组INS、C－肽浓度高峰出现于4min时,无明显第二分泌峰;2型糖尿病组只有5例0－4min时有小的分泌峰,曲线高峰于60－80min。对照组ISR曲线第一分泌峰于2min,较INS及C－肽曲线提前（P＝0.000),22min时出现第二个明显的分泌峰;11例2型糖尿病者的ISR曲线均在2－4min（中位数2min）出现了小的分泌峰。结论 在用血INS及C－肽浓度作为评价β肽浓度作为评价β细胞功能的指标时,应考虑其体内分布、清除过程的影响;对2型糖尿病组,ISR曲线能较好地反映其第一时相INS分泌,在对照组,则对反映第二时相分泌较为敏感。     

胰岛素抵抗是糖耐量正常人群糖耐量恶化的重要危险因素

目的 探讨胰岛素抵抗和胰岛素分泌对糖在耐量正常人群糖耐量恶化的影响。方法 以口服葡萄糖耐量试验（ＯＧＴＴ）做人群普查一,确定糖耐量正常者（ＮＧＴ）（空腹血糖（ＦＰＧ）〈５．８ｍｍｏｌ／Ｌ及２小时血糖（ＰＧ２ｈ〈６．７ｍｍｏｌ／Ｌ＿１２５例,测定血浆胰岛素。６年后随访再以ＯＧＴＴ确定盲人 群糖耐量状态,以稳态模型（Ｈｏｍａ Ｍｏｄｅｌ）公式评估胰岛素抱搞（ＩＲ）、胰岛素分泌功能（ＩＳ）,并分析其对糖     

不同糖耐量者血清游离脂肪酸与胰岛素抵抗的关系

以口服糖耐量试验(OGTT)确定受试者为正常人,糖耐量低减(IGT)和2型糖尿病,并测定空腹和OGTT 2h的游离脂肪酸(FFA)、血糖和胰岛素浓度,计算胰岛素敏感指数(IAI)。2型糖尿病和IGT患者的空腹和OGTT 2 h FFA、血糖和胰岛素浓度均明显高于正常组(均P<0.05),IAI均明显低于正常对照组(均P<0.01)。空腹及OGTT 2 h FFA与IAI之间呈显著负相关(分别为r=-0.38,P<0.01和r=-0.32,P<0.05),体重指数与IAI呈显著负相关(r=-0.39,P<0.05)。上述结果提示脂毒性在2型糖尿病的发病机制中有重要作用。     

糖调节受损个体胰岛β细胞功能和胰岛素抵抗观察

评价152例人选者[正常糖耐量、空腹血糖受损和(或)糖耐量受损]胰岛β细胞功能和胰岛素抵抗.结果 显示空腹血糖受损者主要表现胰岛素早期分泌功能缺陷和基础分泌不足,胰岛素抵抗严重;糖耐量受损者则胰岛素早期和晚期分泌功能显著下降伴轻度胰岛素抵抗.     

Serum bone morphogenetic protein 7, insulin resistance, and insulin secretion in non-diabetic individuals

This study was to explore the relationship of serum BMP7 with insulin secretion and metabolic parameters in non-diabetic individuals. Serum BMP7 concentrations positively correlated with HOMA2-%B (insulin secretion index) and fasting insulin. Our findings suggested that BMP7 may stimulate insulin secretion and improve islet cell function in humans.     

Feedback inhibition of insulin and glucagon secretion by insulin is altered in abdominal obesity with normal or impaired glucose tolerance

We investigated the feedback inhibition of insulin and glucagon secretion during euglycemic-hyperinsulinemic clamp at about 350 pmol/l in 16 patients with abdominal obesity [8 with normal glucose tolerance (oNGT), 8 with impaired glucose tolerance (oIGT)] and 8 normal-weight subjects matched for age, sex and blood pressure. In oNGT and oIGT, fasting plasma C-peptide levels were twice those in the controls (962±51 and 915±85 vs 439±28 pmol/l,P<0.001) and their suppression was lower than in the controls, both in absolute terms (155±19 and 185±17 vs 274±18 pmol/l,P<0.001) and as a percentage decline from basal levels (16±2% and 21±2% vs 63±2%,P<0.001). Fasting plasma glucagon levels were similar in the patients and in the controls, but were less suppressed during clamp in oNGT and oIGT, both in absolute terms (7.0±0.9 and 5.6±0.6 vs 13.2±1.2 pmol/l,P<0.001) and as a percentage change from basal levels (23±3% and 19±2% vs 44±4%,P<0.001). These results suggest that the insulin feedback on B and A cells is impaired in abdominal obesity, and that this defect is of similar degree in oNGT and oIGT. These alterations could be implicated in the pathogenesis of hyperinsulinemia in obesity.     

High prevalence of abnormal glucose homeostasis secondary to decreased insulin secretion in individuals with hereditary haemochromatosis

Aims/hypothesis The prevalence and mechanisms of diabetes in hereditary haemochromatosis are not known. We therefore measured glucose tolerance, insulin secretory capacity and insulin sensitivity in adults with haemochromatosis.Subjects and methods Subjects recruited from referrals to a haemochromatosis clinic underwent OGTT and frequently sampled IVGTT. A chart review of former clinic patients was also performed.Results The prevalence of diabetes (23%) and IGT (30%) was increased in haemochromatosis compared with matched control subjects (0% diabetes and 14% IGT). Subjects with haemochromatosis and diabetes were overweight (14%) or obese (86%). The prevalence of diabetes, as determined by chart review of fasting glucose values, in subjects who had haemochromatosis and were in the 40–79 years age range was 26%. Overall, patients with haemochromatosis and control subjects had similar values for acute insulin response to glucose and insulin sensitivity. However, patients with haemochromatosis and IGT had a 68% decrease in acute insulin response to glucose (p<0.02) compared with those with NGT. They were not insulin-resistant, exhibiting instead a 62% increase in insulin sensitivity (NS). Haemochromatosis subjects with diabetes exhibited further declines in acute insulin response to glucose, insulin resistance, or both.Conclusions/interpretation Diabetes and IGT are common in haemochromatosis, justifying screening for diabetes and therapeutic phlebotomy. The major abnormality associated with IGT is decreased insulin secretory capacity. Diabetes is usually associated with obesity and concomitant insulin resistance.     

不同血糖水平人群胰岛素敏感性及β细胞功能分布

目的 探讨超生理浓度的血浆葡萄糖对胰岛素分泌功能及外周组织胰岛素敏感性的作用。方法 874例受试者根据FBG、PBG水平,各分成5组。FBG1：6．11mmol/L以下;FBG2：6．11－6．99mmol/L,FBG3:7.0-7.77mol/L;FBG4:7.78-11.10mmol/L;FBG5:11.11mmol/L以上。PBG分5组。PBG1：7.78mmol/L以下：PBG2：7．78－11．10mmol/L;PBG3:11.11-13.88mmol/L;PBG4：13．89－16．66mmol/L;PFG5:16.67mmol/L以上。结果（1）随FBG升高,FINS水平逐渐升高,当FBG＞7．78mmol/L后,FINS水平变化不明显,但未见高浓度FBG抑制胰岛素分泌功能的现象。（2）随PBG升高,PINS水平随之升高,当PBG在7．78－16．67mmol/L范围内时,PINS浓度变化不明显,PBG＞16．67mmol/L后,PINS浓度随PBG升高反而下降。（3）高浓度葡萄糖和抑制外周组织对胰岛素的敏感性,增加IR,并抑制胰岛素分泌功能。相关分析表明,FBG与HOMA－IR显著正相关,与FINS／FBG显著负相关。（4）逐步回归分析表明,FINS水平主要决定于HOMA－IR、FINS／FBG,PINS水平主要决定于FINS／FBG、BMI、TG。结论 血浆葡萄糖对胰岛素分泌及其作用有三个方面影响;（1）低浓度葡萄糖刺激胰岛功能,增加胰岛素分泌;当血浆葡萄糖浓度在7．78－16．67mmol/L范围内时,血浆胰岛素浓度变化不明显;但血浆葡萄糖浓度＞16．67mmol/L后,高浓度葡萄糖抑制胰岛分泌功能,血浆胰岛素浓度反而下降。（2）血浆葡萄糖浓度降低外周组织对胰岛素的敏感性,增加IR。（3）血浆胰岛素最终浓度主要决定于FINS／FBG、HOMA－IR及BMI。     

Decreased insulin action and insulin secretion predict the development of impaired glucose tolerance

Summary The relative importance of insulin resistance and abnormal insulin secretion as risk factors for the development of impaired glucose tolerance (IGT) is controversial. Few prospective data are available on metabolic precursors of IGT. We examined the relation of fasting serum insulin level (as a marker of insulin resistance) and change in insulin/glucose ratio (ΔI ₃₀/ΔG₃₀) over the first 30 min after glucose ingestion (as a marker of insulin secretion) as predictors of the 7-year development of IGT in 839 Mexican Americans and non-Hispanic whites with normal glucose tolerance at baseline from the San Antonio Heart Study. IGT eventually developed in 148 subjects. When modelled separately, fasting serum insulin (odds ratio (OR)=2.60,95 % confidence interval (CI)=1.58,4.28,p<0.005), but not ΔI ₃₀/ΔG₃₀ (OR=0.80, 95 % CI=0.50,1.27,p=0.339) predicted the development of IGT. However, when both variables were included in the same logistic regression model, fasting serum insulin (OR=3.50, 95 % CI=1.97,6.21,p<0.001) and low ΔI ₃₀/ΔG₃₀ (OR=0.48, 95 % CI=0.28,0.82,p=0.008) both predicted IGT. These results were basically unchanged after further adjustment for obesity, body fat distribution and fasting plasma glucose level. We conclude that both decreased insulin secretion (as assessed by low ΔI ₃₀/ΔG₃₀) and increased insulin resistance (as assessed by fasting serum insulin) predict the development of IGT and are thus early precursors of non-insulin-dependent diabetes mellitus; further studies of insulin secretion should take into account the level of basal insulin resistance.     

非诺贝特对高甘油三酯血症人群胰岛素抵抗和胰岛β细胞分泌功能的影响

目的观察非诺贝特对高甘油三酯(TG)血症人群的胰岛素抵抗和胰岛β细胞分泌功能的影响。方法正常糖耐量、高TG血症(TG≥12．3 mmol/L)患者12例(HTG组),予非诺贝特200 mg/d治疗3个月,于治疗前后应用高葡萄糖钳夹技术评价胰岛素敏感性和胰岛β细胞功能。并与正常糖耐量、正常血脂志愿者12名(NC组)进行比较。结果HTG组胰岛素敏感性指数(ISI)显著低于NC组;第一时相胰岛素分泌(1PH)稍低于NC组;第二时相胰岛素分泌(2PH)和最大胰岛素分泌(INS120-150)均明显高于NC组。HTG组非诺贝特治疗后,ISI较治疗前显著升高(18．35±1．76 vs 9．40±1．76,P＜0．01);1PH变化无统计学意义[(247．7±32．9)mIU/L vs (225．7±36．7)mIU/L,P=0．94];2PH和INS120-150较治疗前降低[分别为(73．2±9．0)mIU/L vs (106．0±11．3)mlU/L,p=0．014;(89．2±8．9)mIU/L vs (141．6±13．8) mIU/L,P=0．005]。结论非诺贝特调脂治疗能显著改善高TG血症人群的胰岛素抵抗及高葡萄糖钳夹试验中的胰岛素分泌。     

Association between vitamin D deficiency and insulin resistance markers in euthyroid non-diabetic individuals

AimTo evaluate the association between vitamin D deficiency and insulin resistance (IR) or hyperinsulinemia after oral glucose tolerance test (OGTT) in euthyroid non-diabetic individuals.Materials and methodsWe carried out an analytical cross-sectional study in euthyroid non-diabetic adults of both sexes, who attended the outpatient service of a private clinic in Lima-Peru during the 2012–2016 period. Participants were categorized in two groups according to their serum vitamin D levels: normal vitamin D levels (serum vitamin D values ≥ 20 ng/dL) and vitamin D deficiency (serum vitamin D values < 20 ng/dL). IR was defined as a Homeostasis Model Assessment (HOMA-IR) value ≥ 3.8 and hyperinsulinemia after OGTT was defined as a serum insulin value ≥ 80μU/mL after 120 min of 75-g glucose intake. We elaborated crude and adjusted Poisson regression models to assess the association between serum vitamin D levels and IR or hyperinsulinemia after OGTT. The reported association measure was the prevalence ratio (PR) with their respective 95% confidence intervals (95%CI).ResultsWe analyzed 204 participants, the average age was 38.5 ± 10.6 (SD) years, 40 (19.6%) were males and the vitamin D median was 25.0 (IQR: 19.0–33.3) ng/dL. The prevalence of vitamin D deficiency, IR and hyperinsulinemia after OGTT was 29.4% (n = 60), 29.9% (n = 61) and 25.0% (n = 51). In the adjusted Poisson regression models, the prevalence of hyperinsulinemia after OGTT was higher among the vitamin D deficient group (aPR=1.75; 95%CI: 1.06–2.90); however, we did not find statistically significant association between vitamin D deficiency and IR (aPR=0.99; 95%CI: 0.61–1.63).ConclusionsWe found an association between vitamin D deficiency and hyperinsulinemia after OGTT in euthyroid people with no T2DM.Our findings are consistent with previous reports; providing evidence that serum vitamin D deficiency could be an IR marker.