The increased insulin sensitivity in growth hormone-deficient adults is reduced by growth hormone replacement therapy

BACKGROUND: Growth hormone deficiency is associated with increased morbidity and mortality from cardiovascular diseases, which might be related to changes in glucose and lipid metabolism. DESIGN: To assess the influence of long-term growth hormone replacement therapy (GHRT) on glucose metabolism we examined eight growth hormone-deficient (GHD) adults (seven female/one male; age, 46 +/- 3 years; body mass index, 31 +/- 2 kg m-2) over a period of 18 months in comparison to an adequate control group consisting of eight obese subjects matched for age, sex, and body mass index. We performed frequently sampled intravenous glucose tolerance tests (FSIGT) with minimal model analysis before the study, and after 12 and 18 months. RESULTS: Following GHRT, insulin-like growth factor-1 (IGF-1) increased significantly from a basal level of 75.9 +/- 18.9 to 200.8 +/- 31.0 microg L-1 after 12 months of therapy and remained stable, thereafter. GHRT did not affect fasting blood glucose, basal insulin, cholesterol, blood pressure and body weight. However, at 12 months, HbA1c (6.0 +/- 0.1 vs. 5.6 +/- 0.1% at basal, P < 0.05) and triglyceride (2.3 +/- 0.4 vs. 1.4 +/- 0.3 mmol L-1) significantly increased but returned to pretreatment values at 18 months. Insulin sensitivity was higher in GHD (8.2 +/- 3.1) compared to controls (3. 6 +/- 0.53 x 10-4 min-1/(microU mL-1), P = 0.06) and decreased significantly after 18 months of GHRT to 5.1 +/- 2.6, P < 0.05. Basal insulin secretion was similar to that in the control group and increased significantly after 12 and 18 months, total insulin secretion only after 12 months. SG (glucose effectiveness)was lower in GHD patients (0.0095 +/- 0.001 min-1) compared to controls (0.020 +/- 0.003 min-1, P < 0.05) and increased significantly after 12 and 18 months of GHRT (0.016 +/- 0.002, and 0.015 +/- 0.001 min-1, P < 0. 05), respectively. Hepatic insulin extraction rate was similar in both groups and remained unchanged following GHRT. CONCLUSION: We conclude that long-term GHRT induces a significant decrease of the increased insulin sensitivity in GHD patients to levels observed in body mass index-matched control subjects. This is accompanied by an increase in basal and total insulin secretion as well as in glucose effectiveness as a possible compensatory mechanism.     

Alcohol consumption and insulin resistance in young adults

BACKGROUND: Alcohol may have a cardioprotective effect. One possible mechanism is by reducing insulin resistance, a known cardiovascular risk factor. The aim of this study was to assess the relationship between alcohol consumption, insulin resistance and other parameters determining glucose tolerance in 154 young men and women. SUBJECTS AND METHODS: Subjects completed a questionnaire documenting weekly alcohol consumption. Insulin sensitivity and glucose tolerance were measured using the intravenous glucose tolerance test with minimal model analysis. Height, weight, usual level of exercise, smoking habits and socio-economic status were also recorded. RESULTS: Insulin sensitivity correlated inversely with body mass index (r = - 0.529, P < 0.001) but not with level of physical fitness. Women were significantly less insulin sensitive than men (4.19 and 5.63 104 min-1 pmol-1 L-1, respectively; P < 0.001). Insulin sensitivity correlated positively with alcohol consumption and this trend remained significant allowing for body mass index and gender (beta = 0.17, P < 0.014). First-phase insulin secretion showed a weak but non-significant trend in the opposite direction. Fasting glucose, fasting insulin and glucose tolerance showed no relationships with alcohol consumption. CONCLUSION: These data suggest a close relationship between alcohol consumption and insulin resistance in young adults. Regular alcohol consumption is associated with decreased insulin resistance and this may partly explain the cardioprotective effect of alcohol.     

Effects of burn injury on insulin secretion and on sensitivity to insulin in the rat in vivo.

Both insulin resistance and impairment of insulin secretion are know to occur in man after injury. The relative importance of these effects was studied in rats 2 h after a non-lethal 20 percent dorsal scald. No impairment of insulin secretion was found after this injury. Concentrations of both blood glucose and plasma insulin were elevated in scalded rats. Scalded rats responded to intravenous glucose injection (1-0 g/kg) with a further rise in plasma insulin concentration, which remained normal for the prevailing blood glucose concentration. However, marked impairment of glucose tolerance was observed, indicating the presence of insulin resistance. After intravenous insulin injection (1-0 U/kg) the initial rate coefficient for fall of blood glucose concentration was significantly lower (p less than 0-02) in scalded (mean 3-9 percent min.(-1) than in control rats (mean 6-3 percent min.(-1). The minimum in blood glucose concentration after insulin injection was reached at 10 min. in control rats, but not until 60 min. after injection in scalded rats. This difference was due to a delay in compensation for the hypoglycaemia in the scalded rats, since the rate of disappearance of insulin measured by injection of a tracer of 125I-labelled bovine insulin was not decreased after this injury. It was concluded that the impairment of glucose utilization in scalded rats (Heath and Corney, 1973) is due to decreased sensitivity to insulin rather than to suppression of insulin release.     

糖负荷后血尿酸与胰岛素分泌及胰岛素敏感性/抵抗的相关性分析

目的研究不同糖负荷人群血尿酸(SUA)水平与胰岛素分泌及胰岛素抵抗的关系。方法 389例符合要求的研究对象行口服糖耐量试验(OGTT),测量空腹SUA,OGTT 0、30、60、120min血糖(GLU)和胰岛素(INS)水平,按照OGTT结果将研究对象分为糖耐量正常组(NGT组,n=88)、糖尿病前期组(preDM,n=119)、糖尿病组(DM,n=182),计算研究对象的胰岛素分泌指数(IGI)、120min胰岛素分泌指数(AUC INS_(120)/AUC GLU_(120))、胰岛素抵抗指数(HOMA-IR)、及Matsuda指数;将SUA按四分位水平分组,比较各糖负荷组不同SUA水平胰岛素分泌及胰岛素抵抗差异;计算SUA与胰岛素分泌及HOMA-IR的直线回归方程。结果 DM组SUA水平低于PreDM组[(346.66±90.60)mmol/Lvs.(367.36±92.34)mmol/L],但是略高于NGT组(339.34±89.51)mmol/L,差异有统计学意义(P0.01);DM组IGI指数、AUC INS_(120)/AUC GLU_(120)指数随着SUA升高有降低趋势(P0.01),Matsuda指数随着SUA水平升高有降低趋势(P0.05)。SUA与IGI、AUC INS_(120)/AUC GLU_(120)、HOMAIR、Matsuda指数的二元一次方程分别是Y=4.050+0.144 X,Y=2.343+0.206 X,Y=1.288+0.176 X,Y=129.373-0.202 X。结论 SUA与胰岛素分泌及胰岛素敏感性显著相关,DM组胰岛素分泌随着SUA水平升高而升高,胰岛素敏感性随着SUA水平升高而降低。SUA与胰岛素分泌及胰岛素敏感性的二元一次方程可大概评估胰岛素功能。     

Smoking cessation improves insulin sensitivity in healthy middle-aged men

Cigarette smokers have recently been shown to exhibit insulin resistance, dyslipidaemia and markers of the insulin resistance syndrome (IRS). The aim of this study was to examine the effects of smoking cessation on insulin sensitivity and IRS. Forty male, non-obese healthy smokers participated in this open parallel study with 8 weeks of follow-up. Seventeen subjects were able to stop smoking, while 23 subjects continued to smoke and served as a controls group. Anthropometric and metabolic data were measured. Degree of insulin sensitivity was determined with the euglycaemic hyperinsulinaemic clamp technique. Smoking cessation increased insulin sensitivity and improved the lipoprotein profile in spite of a modest increase in body weight. Initial smoking habits correlated positively with the increase in BMI as well as the improvements in the metabolic variables after smoking cessation. These data support the view that smoking causes insulin resistance and IRS, and also demonstrate that the beneficial metabolic effects of smoking cessation override the effects of an accompanying modest increase in body weight.     

Variability of HOMA and QUICKI insulin sensitivity indices

Assessment of insulin sensitivity based on a single measurement of insulin and glucose, is both easy to understand and simple to perform. The tests most often used are HOMA and QUICKI. The aim of this study was to assess the biological variability of estimates of insulin sensitivity using HOMA and QUICKI indices. After a 12-h fast, blood was sampled for insulin and glucose determination. Sampling lasted for 90?min with an intersample interval of 2?min. A total of 56 subjects were included in the study, and in nine subjects sampling was done before and after weight reduction, so total number of analyzed series was 65. To compute the reference value of the insulin sensitivity index, averages of all 46 insulin and glucose samples were used. We also computed point estimates (single value estimates) of the insulin sensitivity index based on the different number of insulin/glucose samples (1–45 consecutive samples). To compute the variability of point estimates a bootstrapping procedure was used using 1000 resamples for each series and for each number of samples used to average insulin and glucose. Using a single insulin/glucose sample HOMA variability was 26.18?±?4.31%, and QUICKI variability was 3.30?±?0.54%. For 10 samples variability was 11.99?±?2.22% and 1.62?±?0.31% respectively. Biological variability of insulin sensitivity indices is significant, and it can be reduced by increasing the number of samples. Oscillations of insulin concentration in plasma are the major cause of variability of insulin sensitivity indices.     

Insulin receptor binding to monocytes and erythrocytes during normal human pregnancy

In normal human pregnancy glucose tolerance deteriorates gradually in spite of a steady increase in plasma insulin levels. To see whether this change in insulin resistance is accompanied by changes in insulin receptor binding, insulin binding to monocytes and erythrocytes was measured serially during pregnancy and again post-partum in fifteen normal women. Insulin binding to monocytes increased from week 12 to week 24 of gestation (P less than 0.001) and it decreased from week 32 to week 36 (P less than 0.05). After delivery a new increase in insulin binding to monocytes was seen (P less than 0.05). Insulin binding to erythrocytes increased from week 30-32 to week 36 (P less than 0.05), decreased from week 36 to delivery (P less than 0.01) and decreased further post-partum (P less than 0.001). Insulin receptor binding was not significantly correlated to plasma insulin, estradiol, estriol, progesterone or cortisol. The insulin receptor binding to monocytes, but not to erythrocytes, paralleled the insulin resistance found in human pregnancy.     

Peripheral and hepatic insulin sensitivity in healthy elderly human subjects

Insulin resistance has been reported in normal ageing but discrepancies between such studies may be related to compounding factors such as body composition and exercise patterns. We employed a two-step hyperinsulinaemic euglycaemic clamp to assess peripheral and hepatic tissue insulin sensitivity and glucose recycling in 13 elderly (E) and 14 young (Y) healthy subjects controlling for the above factors. There was no difference in basal hepatic glucose production (E: 2.36 +/- 0.06, Y: 2.47 +/- 0.1 mg kg-1 min-1; P = 0.4). At step 1 (insulin infusion 15 mU kg-1 h-1) glucose turnover was similar (E: 2.65 +/- 0.13, Y: 2.88 +/- 0.22 mg kg-1 min-1; P = 0.4) but hepatic glucose production was lower in the elderly group (0.20 +/- 0.16 vs 0.64 +/- 0.10 mg kg-1 min-1; P = 0.03). At step 2 (insulin infusion 50 mU kg-1 h-1) glucose turnover was similar (E: 7.60 +/- 0.24, Y: 8.05 +/- 0.34 mg kg-1 min-1; P = 0.3) and hepatic glucose production was equal but negative (E: -1.35 +/- 0.18, Y: -1.34 +/- 0.22 mg kg-1 min-1; P = 0.9). Glucose recycling did not differ between the groups at any stage. Similar serum insulin levels were achieved in both groups at each step. Decreased glucose tolerance was confirmed in E with a higher 2 h blood glucose after an OGTT (5.3 +/- 0.4 vs 4.1 +/- 0.3 mmol l-1; P = 0.03) but incremental insulin response was similar (E: 3236 +/- 289, Y: 3586 +/- 463 mU l-1 min-1; P = 0.5). We conclude that changes in hepatic tissue insulin sensitivity do not cause the deterioration in glucose tolerance observed with age. A small reduction in both peripheral tissue insulin sensitivity and late insulin secretion may be responsible.     

Beta-cell function and insulin sensitivity contribute to the shape of plasma glucose curve during an oral glucose tolerance test in non-diabetic individuals

To clarify whether beta-cell function and/or insulin resistance contributes to the shape of plasma glucose curve during an oral glucose tolerance test (OGTT), we investigated 583 Japanese subjects with normal glucose tolerance (NGT, n = 306) or impaired glucose tolerance (IGT, n = 277). Each subject was subdivided into three shapes of plasma glucose curve as follows: monophasic pattern (M type), biphasic pattern (B type) and two peaks (T type). Homeostasis model assessment of insulin resistance, quantitative insulin sensitivity check index and insulinogenic index were assessed by plasma glucose and insulin concentrations obtained at fasting or during an OGTT. There was a greater proportion of M type in the IGT group (M = 80.9%, B = 15.5% and T = 3.6%), whereas the prevalence of B and T types was much higher in the NGT group (M = 66.6%, B = 26.5% and T = 6.9%). There were significant differences in the proportions of shape types between the NGT and IGT groups (p = 0.0006). Among the NGT category, insulin sensitivity was significantly higher in the B type than in the M type, and beta-cell function adjusted for insulin resistance was significantly higher in the B and T types than in the M type. Among the IGT category, no significant differences were seen among the three shape types with respect to insulin sensitivity, but the beta-cell function adjusted for insulin resistance was significantly lower in the M type than in the B and T types. In conclusion, both impaired insulin secretion and insulin resistance may contribute to the underlying mechanisms of the shape of plasma glucose curve in Japanese subjects.     

单纯性肥胖成人血清高敏C反应蛋白、血脂水平与胰岛素抵抗的相关性研究

目的 探讨单纯性肥胖成人血清高敏C反应蛋白(hs-CRP)、血脂水平与胰岛素抵抗(IR)的关系.方法 选择单纯性肥胖成人99例[按体质量指数(BMI)分为i度肥胖组46例,ii度肥胖组38例,iii度肥胖组15例],单纯性超重成人56例及健康成人80例.测定所有入选对象的身高、体质量、腰围、臀围、空腹血糖(FBG)、空腹胰岛素(FIN)、血脂、hs-CRP水平,并计算胰岛素抵抗指数(HOMA-IR)、BMI及腰臀比(WHR).结果 hs-CRP、HOMA-IR、FBG、FIN、TG、TC、LDL-C、脂肪肝发生率随着BMI的升高呈逐渐升高趋势,HDL-C则呈现逐渐降低趋势.血清hs-CRP与BMI、WHR、FIN、HOMA-IR、TG呈显著正相关(P＜0.05～P<0.01),与HDL-C呈显著负相关(P<0.01),多元逐步回归分析提示,BMI、HOMA-IR、HDL-C是影响hs-CRP的独立危险因素.结论 单纯性肥胖成人存在IR,炎性因子hs-CRP的过量表达参与并加重单纯性肥胖成人IR、血脂紊乱的发生和发展.     

慢性阻塞性肺疾病患者胰岛素抵抗的研究

目的 探讨慢性阻塞性肺疾病(COPD)与胰岛素抵抗(IR)的相关性及发生机制.方法 对80例COPD急性加重期患者(急性加重期组),34例稳定期患者(稳定期组)和26名健康体检者(正常对照组)进行肺功能、空腹血糖(FBG)、空腹胰岛素(FINS)、空腹血清C肽(FCP)、C-反应蛋白(CRP)、甘油三脂(TG)、总胆固醇(TC)、尿微量白蛋白(MALB)测定,并计算IR指数(HOMA-IRI).结果 与正常对照组比较,急性加重期组、稳定期组的CRP、TG、MALB、FCP、FBG、FINS、HOMA-IRI、IR发生率升高(P＜0.01);随着COPD病情加重,FCP、FBG、FINS、HOMAIRI、IR发生率也随之增高(P＜0.01或＜0.05).结论 COPD患者存在IR,发生IR的风险与病情严重程度有潜在关系.     

HCV treatment with direct acting antivirals improves the insulin sensitivity

ABSTRACT

Background: There is strong link between hepatitis C virus (HCV) infection and the insulin resistance panel. Homeostatic model assessment (HOMA) β is an indirect measurement of insulin secretion from pancreatic β cells, while HOMA-S accounts for insulin sensitivity.

Aim: We examined the impact of HCV treatment with direct acting antivirals (DAAs) on HOMA-β and HOMA-S results.

Methods: HOMA-IR, HOMA-β, and HOMA-S were calculated before and 12 weeks after treatment in 511 treatment eligible patients with HCV. Five DAA treatment protocols were used. Values before and after treatment were compared.

Results: The mean age of patients was 50.63 years with a 3.2:1 male: female ratio. A total of 29.7% of patients were treatment experienced and 24.7% had diabetes. HCV sustained virological response (SVR) was achieved in 91% of patients. Unlike non-responders, SVR patients showed significantly decreased post-treatment HOMA-Β. Delta HOMA-Β was comparable between groups. HOMA-S increased significantly in patients with SVR compared to in non-responders, as did delta HOMA-S. HOMA-S and HOMA-β improved significantly under 5 and 2 DAA protocols, respectively. The treatment status did not affect the HOMA-β and S dynamics during treatment.

Conclusions: Insulin sensitivity improved markedly in patients who achieved HCV SVR.     

Influence of family history of hypertension on insulin sensitivity in lean and obese hypertensive subjects

We evaluated the influence of family history of hypertension on insulin sensitivity in lean and obese hypertensive subjects (H): 40 lean [body mass index (BMI)  25 kg m⁻²] H with normotensive parents (F−), 50 lean H with one or two parents hypertensive (F+), 30 obese HF− (BMI  30 kg m⁻²) and 35 obese HF+. The four groups were comparable in terms of age, sex and ambulatory blood pressure values. We evaluated glucose, insulin and C-peptide before and 30, 60, 90 and 120 min after an oral glucose load, insulin sensitivity index (ISI, fasting glucose/insulin ratio), fasting insulin/C-peptide ratio (I/Cp). Glucose, fasting and during test, and I/Cp were similar among the four groups; insulin and C-peptide, fasting and stimulated, were significantly higher and ISI lower in obese H than in lean H; at similar BMI, insulin and C-peptide were significantly higher in F+ than in F−. Insulin directly correlated with night-time blood pressure only in lean HF−. The correlation between insulin and BMI was significantly closer in F− than in F+. In conclusion, family history of hypertension appears to play a relevant role in insulin sensitivity in hypertensive subjects also in the presence of obesity.     

高血压病患者认知功能与胰岛素抵抗的相关性研究

目的 探讨高血压病患者认知功能损害与胰岛素抵抗的关系.方法 我院就诊的高血压病患者180例,根据国际通用的简易智力状况量表(mini mental state examination,MMSE)进行认知功能评定,将患者分为两组:认知功能障碍者41例作为病例组,认知功能正常者139例作为对照组.采集一般临床资料,测量血压、身高、体质量,测定总胆固醇,甘油三酯,空腹血糖,空腹胰岛素等指标,用胰岛素抵抗指数(IRI)作为胰岛素敏感性评价指标.结果 单因素分析结果显示:年龄、文化程度、饮酒史、IRI、舒张压5个因素在病例组和对照组之间的差异有统计学意义(均P＜O.05);对180例患者进行Logistic多因素回归分析显示,与认知功能下降有关的指标是:年龄,文化程度和IRI,OR值分别为1.11(95%CI:1.05-1.16,P＜O.05)、10.42(95%CI:2.37-45.78,P＜O.05)、2.14(95%CI:1.06-4.30,P＜O.05).结论 高血压病人群除文化程度和年龄因素外,胰岛素抵抗与认知功能降低密切相关,且胰岛素抵抗独立于其他危险因素,与认知功能障碍的发生有关.胰岛素抵抗是高血压病患者认知功能障碍重要的危险因素.     

2型糖尿病非酒精性脂肪性肝病与胰岛素抵抗的相关性分析

目的探讨在2型糖尿病(T2DM)合并非酒精性脂肪性肝病与胰岛素抵抗的关系。方法将195例2型糖尿病患者分为单纯糖尿病组(A组)83例,合并非酒精性脂肪肝组(B组)60例及合并非酒精性脂肪性肝炎组(C组)52例,分别测定身高、体质量,抽空腹血检查总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、谷丙转氨酶(ALT)、谷草转氨酶(AST)、谷氨酰转肽酶(GGT)、糖化血红蛋白(HbA1C)、空腹血糖(FBG)及空腹胰岛素(FINS)等。计算体质量指数(BMI)及胰岛素抵抗指数(HOMA-IR)。结果 BMI、TG、TC、LDL-C、ALT、AST、GGT、FINS、HOMA-IR水平显示:B组均明显高于A组(P<0.05),C组均明显高于B组(P<0.05)。而HDL-C水平显示:B组均明显低于A组(P<0.05),C组均明显低于B组(P<0.05)。3组间HbA1C、FBG及年龄比较,差异无统计学意义。相关分析显示:HOMA-IR与BMI、TG、TC、LDL-C呈显著正相关(P<0.01),与HDL-C呈显著负相关(P<0.01)。结论胰岛素抵抗是T2DM合并非酒精性脂肪性肝病的危险因素,并且与BMI、TG、TC、LDL-C、HDL-C水平具有相关性。     

胰岛素抵抗与子宫内膜癌发生的关系研究

目的 探讨胰岛素抵抗与子宫内膜癌发生的关系.方法 收集68例子宫内膜癌(EC)患者及68例健康对照者标本,分别对其空腹血糖(FG)、空腹胰岛素水平(FIN)进行检测,对两组病例FG、FIN、胰岛素敏感指数(ISI)及体质指数(BMI)进行比较,分析胰岛素抵抗(IR)与EC患者生育特征的关系.结果 两组FG、FIN、BMI及ISI差异均有统计学意义(t分别=2.86、-9.31、10.16、11.09,P均＜0.05).EC组IR阳性率(60.02%),显著高于对照组(17.65%).EC患者IR的发生与BMI、有无生育史及排卵障碍相关(χ2分别=5.43、5.12,P均＜0.05).结论 对代谢指征的良好控制可能为今后提高子宫内膜癌预后的研究提供新的方向.     

糖尿病前期个体血脂比值与胰岛素抵抗相关性的研究

目的比较空腹血糖受损(IFG)、糖耐量减低(IGT)及IFG IGT个体的血脂比值,并对其与胰岛素抵抗(IR)的相关性进行分析。方法将221例37~65岁非糖尿病个体根据口服葡萄糖耐量试验(OGTT)分为4组,即正常糖耐量(NGT)、单纯IFG、单纯IGT和IFG IGT组;比较各组间空腹血脂及血脂比值的差异,并对其与IR的相关性进行统计学分析。结果IGT组比IFG组甘油三酯(TG)(1.92±0.98 vs 1.49±0.79)mmol/L、TG/高密度脂蛋白胆固醇(HDL-C)比值升高(2.27±0.68 vs 1.61±0.45),HDL-C下降(1.14±0.25 vs 1.35±0.23)mmol/L,差异有统计学意义(均P<0.01),IFG组与NGT组以及IGT组与IFG IGT组间的上述指标差异无统计学意义(P>0.05);各组间总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)和极低密度脂蛋白胆固醇(VLDL-C)水平差异无统计学意义(P>0.05);直线相关分析显示,TG和TG/HDL-C比值与IR呈正相关(r值分别为-0.395、-0.361,均P<0.01)。结论在糖调节受损和NGT人群中,TG/HDL-C比值与IR呈正相关。     

Correlation of plasma leptin and adiponectin with insulin sensitivity and beta-cell function in children - the Taipei Children Heart Study

To investigate the association between plasma leptin and adiponectin and insulin sensitivity in children, 580 school children (294 boys and 286 girls) with mean age of 13.3 years (12-16 years) were randomly selected from the Taipei Children Heart Study. Baseline measurements included body weight, body mass index (BMI), plasma glucose, insulin, proinsulin, leptin and adiponectin levels. Insulin resistance and beta-cell function were assessed using the method of homeostatic model, HOMA-IR and HOMA-beta, respectively. We found that girls had higher levels of plasma leptin, adiponectin and HOMA-beta than boys. There was no significant difference in HOMA-IR between boys and girls. Plasma leptin concentrations were positively correlated with body weight, BMI, insulin and proinsulin concentrations, HOMA-IR and HOMA-beta, whereas plasma adiponectin levels were inversely associated with body weight, BMI and proinsulin levels in both sexes. In girls, adiponectin concentrations were negatively correlated with insulin concentration and HOMA-IR. In multiple regression analyses, plasma leptin was more positively associated with insulin and proinsulin levels, HOMA-IR and HOMA-beta than was adiponectin in boys. This association persisted even after adjusting for body weight, BMI and pubertal status. In conclusion, plasma leptin was more strongly associated with insulin sensitivity and beta-cell function than was adiponectin among children, particularly in boys.     

赖诺普利对高血压病血小板活化和胰岛素抵抗的影响

目的 :探讨赖诺普利对高血压患者血小板活化功能、胰岛素抵抗的干预作用。方法 :对 12 0例高血压患者用赖诺普利治疗 4周 ,治疗前后观察血中血小板颗粒膜蛋白、空腹血糖、空腹胰岛素、计算胰岛素敏感指数并与 60例正常人对照。结果 :赖诺普利有效降低高血压患者血压 ( P <0 0 5 )。并且显著降低空腹血糖、胰岛素、血小板颗粒膜蛋白 ,升高胰岛素敏感指数。结论 :高血压病存在胰岛素抵抗、血小板粘附力增强。赖诺普利在有效降压同时 ,可以纠正基础代谢紊乱     

Relationship of insulin clearance and secretion to insulin sensitivity in non-diabetic Mexican Americans

The antecedents of type II diabetes, while still controversial, are thought to involve decreased insulin sensitivity and compensatory hypersecretion of insulin. Mexican Americans have a three-fold excess risk of type II diabetes and non-diabetic Mexican Americans are characterized by hyperinsulinaemia and insulin resistance. Few data exist, however, on whether there are defects in insulin secretion and/or clearance in this population. We examined insulin sensitivity, secretion and clearance using combined insulin and C-peptide measurements analysed by the minimal model technique of Bergman and colleagues in 10 non-obese, normoglycaemic Mexican Americans and 11 age, sex and obesity-matched non-Hispanic whites. Mexican Americans had significantly decreased insulin sensitivity (SI 4.06 s. 7.56, P = 0.017), higher first phase insulin secretion (1.03 nM vs. 0.72 nM) and decreased insulin clearance (0.099 vs. 0.161) than non-Hispanic whites. Thus, normal Mexican Americans have higher rather than lower insulin secretion suggesting that lower insulin sensitivity may be an early defect in this ethnic group. In addition, they have reduced insulin clearance. Moreover, insulin sensitivity and insulin clearance were positively correlated. We thus speculate that decreased insulin clearance may represent a further autoregulatory mechanism in addition to increased insulin secretion to compensate for decreased insulin sensitivity.