硝苯地平对高血压胰岛素敏感性的影响

目的探讨硝苯地平对高血压（ＥＨ）患者胰岛素敏感性的影响。方法应用钙拮抗剂硝苯地平治疗老年ＥＨ患者，治疗前后行口服葡萄糖耐量试验测血糖（ＳＧ）及血胰岛素（ＩＳ）浓度，求出两者曲线下面积（ＡＵＣ），并计算ＩＳ敏感性。结果ＥＨ患者无论有无糖耐量异常，均可见ＩＳ敏感性降低和糖负荷高ＩＳ血症，糖耐量减低组表现更明显。用硝苯地平治疗后，随着血压被降至正常，症状消失，糖耐量减低组空腹及糖负荷后的ＳＧ和ＩＳ水平以及两者ＡＵＣ均较治疗前降低，ＩＳ敏感性增加，糖耐量改善。而糖耐量正常组除糖负荷后１ｈ、２ｈ血ＩＳ水平较前降低外，糖耐量及ＩＳ敏感性无显著变化。结论硝苯地平可改善伴糖耐量减低的ＥＨ患者的糖耐量及ＩＳ抵抗，增强其ＩＳ敏感性     

非肥胖高血压病患者的胰岛素抵抗及西拉普利对其影响

对３０例非肥胖高血压病（ＥＨ）患者、１７例正常血压者（ＮＴ）行口服葡萄糖耐量试验（ＯＧＴＴ）和胰岛素释放试验（ＩＲＴ）．结果显示：ＥＨ组空腹、服糖后２小时血清胰岛素及胰岛素释放曲线下面积（［ＡＵＣ］１）高于ＮＴ组；ＥＨ组空腹、服糖后２小时血糖及葡萄糖耐量曲线下面积（［ＡＵＣ］Ｇ）亦高于ＮＴ组，提示非肥胖ＥＨ患者存在胰岛素抵抗（ＩＲ）。西拉普利（ｃｉｌａｚａｐｒｉｌ）治疗后ＥＨ患者血清胰岛素、［ＡＵＣ］１、血糖及［ＡＵＣ］Ｇ均较治疗前降低，显示有改善ＩＲ的作用。     

卡托普利对高血压高胰岛素血症的干预

通过对４２例原发性高血压患者、２６例正常人测定口服葡萄糖耐量试验前后血糖、血胰岛素及其反应曲线下面积，发现ＥＨ组空腹ＧＳ与对照组之间无统计学差异；空腹ＩＳ和服糖ＥＨ组ＧＳ、ＩＳ及其曲线下面积显著高于对照组，提示ＥＨ患者存在糖耐量降抵、ＩＳ抵抗。ＥＨ组中２１例患者单纯接受卡托普利有效降压４－８周后，ＯＧＴＴ显示糖负荷１ｈ，２ｈ的ＩＳ和ＧＳ水平均显著低于治疗前水平，结果提示卡托普利可以改善ＥＨ患者ＩＲ     

肥胖对高血压病人胰岛素抵抗的影响

目的观察肥胖是否加重高血压病人的胰岛素抵抗。方法口服７５ｇ葡萄糖做葡萄糖耐量试验（ＯＧＴＴ），用己糖激酶法测血糖，放免法测胰岛素和Ｃ肽。结果糖负荷后高血压两组的葡萄糖、胰岛素和Ｃ肽浓度及曲线下面积（ＡＵＣ）高于对照组，而肥胖高血压组（ＯＥＨ）又高于非肥胖高血压组（ＮＯＥＨ）。在２ｈ和３ｈ时ＮＯＥＨ的Ｃ肽／胰岛素摩尔比显著低于对照组，高血压两组间的Ｃ肽／胰岛素摩尔比无显著差异。结论肥胖加重了高血压病人的胰岛素抵抗（ＩＳＲ）。     

38例高血压病患者血脂与胰岛素抵抗

对３８例高血压病（ＥＨ）患者及２４例正常人空腹血清胰岛素（Ｉｎｓ）、Ｃ肽（ＣＰ）、血糖（ＳＧ）、甘油三酯（ＴＧ）、总胆固醇（ＴＣ）、高密度脂蛋白胆固醇（ＨＤＬ－Ｃ）及载脂蛋白（Ａｐｏ）含量进行测定，并推算胰岛素敏感指数（ＩＳＩ）。结果ＥＨ组Ｉｎｓ、ＣＰ升高，但ＩＳＩ显著降低，表明ＥＨ患者存在胰岛素抵抗（ＩＲ）。同时伴有ＴＧ、ＴＣ、ＡｐｏＢ１００、脂蛋白（ａ）［ＬＰ（ａ）］升高，ＨＤＬ－Ｃ、ＡｐｏＡＩ降低。相关分析表明，ＥＨ患者Ｉｎｓ与ＴＧ、ＡｐｏＢ１００、ＬＰ（ａ）呈显著正相关，与ＨＤＬ－Ｃ、ＡｐｏＡＩ呈显著负相关。ＩＳＩ与ＴＧ、ＡｐｏＢ１００呈显著负相关，提示ＥＨ患者ＩＲ可能是影响脂代谢的重要因素之一。     

氨氯地平对胰岛素抵抗的影响

３８例高血压病患者用氨氯地平（ａｍｌｏｄｉｐｉｎｅ）治疗，剂量５～１０ｍｇ／ｄ，疗程４周。结果除血压明显下降外，空腹及糖负荷后的血胰岛素水平，血胰岛素／葡萄糖比值（Ｉ／Ｇ）以及曲线下面积（［ＡＵＣ］Ｉ，［ＡＵＣ］Ｉ／Ｇ）在治疗后都有下降。空腹及糖负荷后的血糖水平以及曲线下面积（［ＡＵＣ］Ｇ）在治疗前后无明显差异。表明氨氯地平有改善高血压病患者胰岛素抵抗的作用。     

高血压病与冠心病胰岛素抵抗的比较

检测３５例高血压病（ＥＨ）、３１例冠心病（ＣＨＤ）、２６例对照组糖耐量中胰岛素（ＩＳ）、Ｃ肽（ＣＰ）水平及克分子比值等，结果ＥＨ、ＣＨＤ均存在胰岛素抵抗（ＩＲ）和高胰岛素血症（ＨＩＳ）。但各有特点，ＣＨＤ表现服糖后１小时血糖明显升高，胰岛分泌明显增高，糖耐量异常明显多于ＥＨ（Ｐ＜０．０５）；ＥＨ表现空腹胰岛分泌明显增多，空腹ＩＳ明显高于ＣＨＤ（Ｐ＜０．０５）。ＥＨ服糖后ＩＳ清除明显减少，ＣＨＤ无此现象，特别是１小时ＩＳ清除明显低于ＣＨＤ（Ｐ＜０．０５），提示ＩＳ清除减少可能为ＥＨ所特有。     

老年高血压患者血压昼夜节律与胰岛素抵抗

目的为了探讨高血压病患者２４ｈ血压昼夜节律变化与糖、胰岛素（ＩＳ）代谢的关系。方法４６例老年高血压病患者，按昼夜血压节律不同，分为杓型组（ＤＧ）与非杓型组（ＮＤＧ），行葡萄糖耐量试验和ＩＳ释放试验。结果ＤＧ与ＮＤＧ２组各时相血糖、血糖面积及空腹ＩＳ水平无显著性差异（Ｐ＞００５）；而ＮＤＧ在糖负荷后的６０ｍｉｎ、１２０ｍｉｎＩＳ水平和ＩＳ释放指数（ＩＲＩ）以及ＩＳ面积（ＩＡＵＣ）明显高于ＤＧ（Ｐ＜００１、００５、００１、０００１、００１）；ＤＧ的ＩＳ敏感指数（ＩＳＳＩ）明显大于ＮＤＧ（Ｐ＜００１）；夜间平均血压下降率与ＩＡＵＣ、１２０ｍｉｎＩＲＩ及６０ｍｉｎＩＳ水平呈显著负相关（γ＝－０５９８、－０５１１和－０４８６，Ｐ＜００１、００１和００５），与１２０ｍｉｎＩＳＳＩ呈显著正相关（γ＝０４６２，Ｐ＜００１）。结论老年高血压节律异常者有更显著的胰岛素抵抗及高胰岛素血症。     

胰岛素抵抗、胰岛素分泌功能对Ⅱ型糖尿病发生的影响

目的探讨中国非糖尿病人群中胰岛素抵抗、胰岛素分泌功能对糖尿病发生的影响。方法以Ｈｏｍａ模型的胰岛素抵抗指数（ＩＲ）＝ＦＩＮＳ／２２５ｅ－ｌｎＦＰＧ（ＦＩＮＳ为空腹胰岛素，ＦＰＧ为空腹血糖）及β细胞功能指数（ＨＢＣＩ）＝ＦＩＮＳ×２０／（ＦＰＧ－３５），对４０９例非糖尿病者６年随访资料进行糖尿病发病危险因素的比例风险模型分析，再以胰岛素敏感性指数（ＩＡＩ）＝１／（ＦＰＧ×ＦＩＮＳ）、胰岛素分泌功能指数（ＩＳ）＝ＦＩＮＳ／ＦＰＧ这对更简单的指数进行同样分析，并与前者比较。结果以Ｈｏｍａ模型的ＩＲ、ＨＢＣＩ分析显示，排除口服葡萄糖耐量试验２小时血糖、体重指数因素影响后，ＩＲ与糖尿病正相关（Ｐ＜００５），ＨＢＣＩ与糖尿病负相关（Ｐ＜０．０１），生活方式干预有利于减少糖尿病发病危险。与以ＩＡＩ＝１／（ＦＩＮＳ×ＦＰＧ）、ＩＳ＝ＦＩＮＳ／ＦＰＧ分析结果相似。结论（１）胰岛素抵抗及胰岛素分泌功能差是Ⅱ型糖尿病发病危险因素；（２）仅涉及空腹血糖及空腹胰岛素的Ｈｏｍａ模型在流行病研究中可用于评价胰岛素抵抗及β细胞功能，ＩＡＩ＝１／（ＦＰＧ×ＦＩＮＳ）、ＩＳ＝ＦＩＮＳ／ＦＰＧ可在分析中代替Ｈｏｍａ模型     

老年高血压病患者胰岛素抵抗及药物干预的观察

观察了１６例老年高血压病（ＥＨ）患者及１０例健康老年人口服葡萄糖耐量试验（ＯＧＴＴ）的血糖、胰岛素和Ｃ－肽浓度变化。结果显示，ＥＨ组空腹及ＯＧＴＴ后胰岛素、Ｃ－肽及胰岛素／血糖比值明显高于对照组，Ｃ－肽／胰岛素比值明显降低，糖耐量明显下降。老年ＥＨ组经伊拉地平治疗６周后，空腹及ＯＧＴＴ后胰岛素，Ｃ－肽和胰岛素／血糖比值较治疗前上明显下降，Ｃ－肽／胰岛素比值升高，糖耐量改善，但仍未完全恢复正常。提示老年ＥＨ患者存在胰岛素抵抗（ＩＲ），伊拉地平能在一定程度上改善ＥＨ患者的ＩＲ。     

卡托普利对高血压高胰岛素血症的干预

通过对42例原发性高血压患者（EH）、26例正常人测定口服葡萄糖耐量试验（OGTT）前后血糖（GS）、血胰岛素（IS）及其反应曲线下面积，发现EH组空腹GS与对照组之间无统计学差异；空腹IS和服糖后EH组GS、IS及其曲线下面积显著高于对照组，提示EH患者存在糖耐量降低、IS抵抗（IR）。EH组中21例患者单纯接受卡托普利有效降压4～8周后，OGTT显示糖负荷1h、2h的IS和GS水平均显著低于治疗前水平，结果提示卡托普利可以改善EH患者IR。     

A close association between insulin resistance and dehydroepiandrosterone sulfate in subjects with essential hypertension

To examine the serum levels of dehydroepiandrosterone sulfate (DHEAS) and its relation with insulin resistance and the other risk factors in essential hypertension, serum DHEAS and insulin sensitivity were assessed in 35 male hypertensive and 17 male healthy control subjects aged 50-59 years. Fasting plasma insulin and the area under curve of plasma insulin were determined during a 75 g oral glucose tolerance test. Insulin sensitivity was measured by the steady state plasma glucose method. Fasting plasma insulin and the area under curve of plasma insulin were significantly higher in the hypertensive group than in control group. Steady state plasma glucose was significantly higher in hypertensive subjects indicating insulin resistance compared with control subjects. On the other hand, fasting serum DHEAS levels were significantly lower in the hypertensive group than in the control group. Fasting serum DHEAS levels were inversely correlated with steady state plasma glucose significantly (p=0.0008), indicating a close association between DHEAS levels and insulin resistance. Fasting serum DHEAS was inversely correlated with systolic blood pressure and fasting plasma insulin. In multiple regression analysis of hypertensive subjects, steady state plasma glucose was the strongest determinant of the fasting serum level of DHEAS, followed by systolic blood pressure and fasting plasma insulin. These 3 factors accounted for 51.6% of the variation in DHEAS. In nonobese and nondiabetic essential hypertension, serum DHEAS was lower and insulin resistance was the most significant independent determinant of reduced serum DHEAS, followed by systolic blood pressure and fasting plasma insulin.     

The impact of treatment on insulin release and relative peripheral resistance during the oral glucose tolerance test. A study of noninsulin-dependent diabetes mellitus and glucose intolerance

Using 75 g oral glucose tolerance tests (OGTTs), insulin release and relative peripheral resistance were studied in two groups of subjects before and after treatment; ten mostly obese subjects with glucose intolerance (GI), who had improved glucose tolerance after six months of diet and exercise with weight reduction; nine nonobese patients with noninsulin-dependent diabetes mellitus (NIDDM), who received a daily dose of 5 mg glipizide for three months. Total insulin release was measured as the total area under the insulin curve during the OGTT. The insulin response to glucose was expressed as the ratio of the incremental area under the insulin curve to that of the glucose curve above fasting levels (delta AUCI/delta AUCG), during the first 30 minutes and the latter part of the test. The glucose uptake rate (M) was measured as the difference between the glucose load and the increase of glucose in the glucose space after compared to before the OGTT. The relative peripheral resistance (rel-R) against glucose-uptake-promoting factors was expressed as 1/M. The main effects of therapy in the GI-group appeared to be a decrease of the mean rel-R value and a decrease of the mean total insulin release. This implies a mainly peripheral action of therapy at receptor and/or postreceptor levels. The mean [delta AUCI/delta AUCG]0-30 value was unchanged and the mean [delta AUCI/delta AUCG]30-120 value was only slightly increased at follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)     

Perinatal 'programming' of insulin resistance in childhood: critical impact of neonatal insulin and low birth weight in a risk population.

AIM: Low birth weight may predispose to later insulin resistance and hyperinsulinaemia, but the pathophysiological mechanisms are unclear. The perinatal endocrine situation may play an important role, but has been little studied. Children of mothers with diabetes during pregnancy are an important risk population for later insulin resistance and hyperinsulinaemia. We therefore examined relationships between birth weight, insulin and insulin resistance at birth, and insulin secretion and insulin resistance in infancy in these children. METHODS: We studied 104 infants of mothers with Type 1 diabetes mellitus during pregnancy. Oral glucose tolerance tests (area under the curve of glucose, AUCG) with determination of insulin (area under the curve of insulin, AUCI) were performed at 1-5 years of age. Using correlation and regression analysis, birth data were related to insulin secretion (AUCI) and stimulated insulin/glucose ratio (AUCI/AUCG) in childhood. RESULTS: Children with an AUCI in the highest tertile of distribution had the lowest birth weights. Birth weight was negatively correlated to AUCI in childhood (P = 0.03). Insulin/glucose ratio at birth was raised in infants with an AUCI in the upper tertile, accompanied by a positive correlation between insulin/glucose ratio at birth and AUCI (P = 0.02). Insulin and insulin/glucose ratio at birth were both positively correlated to AUCI/AUCG (P = 0.04 and P = 0.02 respectively), while the correlation between birth weight and AUCI/AUCG was not significant (P = 0.12). In a stepwise regression analysis, insulin/glucose ratio contributed as much as birth weight to AUCI in childhood. Birth weight, however, was significantly negatively related to AUCI/AUCG only when the insulin/glucose ratio at birth was included in the regression model. CONCLUSIONS: Insulin and insulin resistance at birth show a positive relation to insulin secretion and insulin resistance in later life, in addition to the influence of a low birth weight, but independent of it. Perinatal and neonatal insulin, known to be of critical importance for long-term outcome, should be evaluated in future studies on the 'small baby syndrome'.     

代谢性高血压的临床特点研究

检测62例高血压病(EH)中单纯EH(EH-1,n=23),伴高胰岛素血症(HIS)和糖耐量异常(IGT)的EH(EH-2,n=15)、伴HIS的EH(EH-3,n=21)和对照组(NS,n-24)糖耐量中血糖(SG)、胰岛素(IS)、C肽(CP)及其克分子比值、IS敏感性指数(ISI)等,发现:①服糖后1小时、2小时SG各时间点的IS、CP及其面积,EH-2、EH-3组明显高于EH-1和NS组(P<0.05);②ISI、服糖后CP/IS比值,EH-2、EH-3组明显低于EH-1和NS组(P<0.05);③EH-2和EH-3两组(即代谢性高血压,MH)中肥胖者50%与EH 1组中肥胖者39.13%无明显统计学差异(P>0.05);④甘油三酯、尿酸、高密度脂蛋白、体重指数等在MH与EH-1组之间未见明显差异(P>0.05).提示,EH中存在一类MH,按其临床特点包括EH-2、EH-3两组;EH中肥胖与MH之间似无直接联系;MH似无明显的高甘油三酯、高尿酸、低HDL-C和肥胖等典型表现,临床主要应按有否HIS及其ISI值来判断是否MH.     

2型糖尿病患者内生肌酐清除率与胰岛β细胞功能相关

目的 探讨2型糖尿病患者的胰岛β细胞分泌功能及胰岛素敏感性与内生肌酐清除率(creatinine clearance rate,Ccr,ml·min-1·1.73-1 m-2)的相关性.方法 432例2型糖尿病患者按Ccr水平分为4组:肾功能正常组(90≤Ccr＜130,123例)、肾小球高滤过组(Ccr≥130,80例),肾功能轻度下降组(60≤Ccr＜90,145例)和肾功能中重度下降组(Ccr＜60,84例).进行口服葡萄糖耐量试验及胰岛素释放试验,用稳态模型评估的胰岛素抵抗指数(HOMA-IR)、胰岛素曲线下面积(AUCI)和葡萄糖曲线下面积(AUCG)的比值(AUCI/AUCG)来评价胰岛素抵抗;用胰岛素敏感指数(ISI)及Matsuda ISI来反映胰岛素敏感性;以稳态模型评估的β细胞功能指数(HOMA-β)、早期胰岛素分泌功能指数(△I30/△G30)、第二时相胰岛素分泌功能指数(胰岛素曲线下面积)及葡萄糖处置指数(disposal index,DI)评价胰岛β细胞分泌功能;比较各组间各指标的差异,并对Ccr与胰岛素抵抗相关指标进行相关性分析.结果 (1)与肾功能正常组相比,肾功能轻度下降、肾功能中重度下降组HOMA-IR明显升高,ISI、Matsuda ISI明显下降(P＜0.01);肾功能中重度下降组AUCI/AUCG明显高于其他3组(P＜0.05).(2)肾功能中重度下降组AUCI明显高于其他3组(P＜0.05);肾功能轻度下降、肾功能中重度下降组DI明显低于肾功能正常组(P＜0.05).(3)Ccr与糖尿病病程、收缩压、舒张压、AUCI、HOMA-IR、AUCI/AUCG呈负相关(P＜0.05),与ISI、Matsuda ISI呈正相关(P＜0.01);多元逐步回归分析结果显示Ccr与收缩压、病程、AUCI/AUCG呈负相关(P＜0.05).结论 在2型糖尿病中,Ccr与胰岛素抵抗负相关,随着Ccr的下降,胰岛素抵抗逐渐加重,胰岛素抵抗可能是肾功能下降的独立危险因素.     

The patterns of glucose tolerance and insulin resistance among rural Chinese twin children, adolescents, and young adults

Pubertal insulin resistance (IR) is well recognized; but little data are available for glucose and insulin pattern from a large, unselected lean population. This report describes the age- and sex-specific distributions of glucose tolerance and IR in a rural Chinese twin population. This report includes 4488 subjects aged 6 to 24 years. The primary variables of interest are fasting plasma glucose, 2-hour postload plasma glucose (2-h PG), fasting serum insulin, 2-hour postload insulin, and the homeostatic model assessment for IR. Age- and sex-specific patterns for the primary variables are described using smoothing plot, arithmetic or geometric mean, and percentiles. There is an increase in fasting plasma glucose, 2-h PG, and IR during puberty (10-19 years) and a return to prepuberty level by the age of 20 years. Insulin resistance peaks at around the age of 14 years in girls and 16 years in boys. Two-hour postload plasma glucose and 2-hour postload insulin are higher in girls than in boys from early puberty, and the sex differences are more pronounced afterward. Moreover, the prevalence of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) increases after puberty and is higher in girls than in boys. In this community-based, nonobese rural Chinese twin population, we observed sex-specific remarkable pubertal surge of IR and modest increase in plasma glucose as well as increasing prevalence of IFG and IGT with age. Notably, females had higher 2-h PG and higher prevalence of IFG and IGT. Our study underscored that adolescence (even more so in females) is a critical period for developing IR and prediabetes.     

Serum Insulin,Insulin Sensitivity,and Erythrocyte Sodium Metabolism in Normotensive and Essential Hypertensive Subjects with and Without Overweight

Increased insulin circulating levels and perturbations of intracellular sodium metabolism have been reported in essential hypertensive patients, leading to postulate their involvement in the pathophysiology of the disease. In-vitro studies have shown that insulin modulates the activity of some transmembrane sodium transporters. The aim of this investigation was to assess in subjects with essential hypertension and/or overweight, the levels of fasting serum insulin, the activity of sodium transporters and their possible relationships. In 18 lean normotensive, 12 overweight normotensive, 18 untreated lean essential hypertensive, and 16 untreated overweight essential hypertensive subjects, we measured the fasting levels of blood glucose and serum insulin, and calculated the glucose/insulin ratio as an index of sensitivity to insulin. In addition, in the red blood cells of these subjects, we evaluated the maximal rate of ouabain-sensitive Na/K pump, furosemide-sensitive outward Na/K cotransport, Na_i/Li_o countertransport, and the constant rate of passive permeabilty to Na. When compared to lean normotensive, overweight normotensive, lean hypertensive, and overweight hypertensive subjects exhibited significantly higher fasting insulin levels, with lower glucose/insulin ratio. No significant difference was found in the activity of Na/K pump, Na/K cotransport, and passive permeability to Na. The Na_i/Li_o exchange was significantly increased in both hypertensive groups. Mean blood pressure correlated positively and independently with body mass index and fasting insulinemia, and inversely with the glucose/insulin ratio. No relationships were found between blood pressure, fasting insulin levels or glucose/insulin ratio and the activity of sodium transport systems. We conclude that hyperinsulinemia and insulin resistance are associated with essential hypertension independently of overweight. These data lend support to the hypothesis that insulin is involved, concurrently with other factors, in the pathogenesis of essential hypertension in both lean and obese subjects.     

Insulin hypersecretion: a distinctive feature between essential and secondary hypertension.

Several studies have demonstrated that patients with hypertension have greater plasma insulin levels than normotensive subjects. The aim of the present study was to clarify if hyperinsulinemia in hypertension is a consequence of either increased pancreatic secretion or decreased hepatic clearance, and to determine whether abnormalities of glucose metabolism are equally present in essential and secondary hypertension. In an observational cross-sectional study, fasting blood glucose, plasma insulin, and plasma C-peptide levels were measured in five patient groups: 34 lean normotensive, 19 overweight normotensive, 25 lean essential hypertensive, 27 overweight essential hypertensive, and 20 secondary hypertensive subjects. The blood glucose/plasma insulin and plasma insulin/plasma C-peptide ratios were calculated as indexes of insulin sensitivity and hepatic insulin clearance, respectively. Subjects with essential hypertension and, to a greater extent, those who were overweight, exhibited significantly higher fasting insulin and C-peptide levels and significantly lower glucose/insulin ratios as compared with lean normotensive subjects. In contrast, no differences were observed between secondary hypertensive and control subjects. Mean blood pressure was significantly and independently correlated to body mass index, plasma insulin and plasma C-peptide levels, and the glucose/insulin ratio. In lean essential hypertensive and secondary hypertensive subjects, the insulin/C-peptide ratios were comparable to controls, indicating normal hepatic insulin clearance. In both overweight groups, a trend to increased insulin/C-peptide ratios was observed. This study shows that in essential hypertensive subjects, hyperinsulinemia is caused by insulin hypersecretion, whereas in overweight subjects, both increased insulin secretion and decreased hepatic insulin clearance might be involved.(ABSTRACT TRUNCATED AT 250 WORDS)