三种脂肪酸饮食对糖耐量正常人群胰岛素敏感性的影响

目的 探讨饱和脂肪酸(SFA)、单不饱和脂肪酸(MUFA)、多不饱和脂肪酸(PU FA)饮食对糖耐量正常人群胰岛素敏感性的影响.方法 20例健康受试者分别接受MUFA(M)饮食、PUFA(P)饮食、SFA(S)饮食干预3d,每组饮食干预后行口服葡萄糖耐量试验(OGTT),空腹血清测定空腹血糖(FPG)、总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白-胆固醇(LDL-C)、高密度脂蛋白-胆固醇(HDL-C)、极低密度脂蛋白-胆固醇( VLDL)、胰岛素(INS)、C肽,其余各时间点血清分别测定血糖、胰岛素、C肽.结果 ①与S组相比,M组和P组的FPG显著降低(P＜0.05),但M组和P组之间无差异(P＞0.05).其余时间点的血糖三组间均无差异(P＞0.05).与S组相比,M组和P组的TC、LDL、apoB显著降低(P＜0.05),但M组和P组之间无差异(P＞0.05).而三组间TG、HDL、VLDL、ApoA均无差异(P＞0.05).②与M组相比,S组和P组的FINS、HOMA-IR、AUCins、WBISI显著升高(P＜0.01),但S组和P组之间无差异(P＞0.05).三组间AUC Glu、HOMA-B、△Ins/△FPG均无差异(P＞0.05).结论 MUFA饮食较PUFA、SFA饮食可以改善胰岛素敏感性.     

不同脂肪酸饮食对Wistar大鼠胰岛素敏感性的影响

目的 探讨饱和脂肪酸(SFA)、单不饱和脂肪酸(MUFA)、多不饱和脂肪酸(PUFA)饮食对大鼠胰岛素敏感性的影响.方法 48只雄性Wistar大鼠随机分为正常对照组、SFA组、MUFA组、PUFA组.正常对照组给基础饲料(脂肪占10.3%);SFA组饲料在基础饲料中添加15%猪油;MUFA组饲料在基础饲料中添加15%茶油;PUFA组饲料在基础饲料中添加15%豆油(脂肪占35.4%).8 w后4组各随机选8只大鼠行高胰岛素-正葡萄糖钳夹实验,同时留取空腹血清测定血脂、胰岛素等指标.结果 实验第8周末,与其他3组相比,正常对照组大鼠进食量有所增加,差异有统计学意义(P>0.05).除外进食量的影响,与SFA组相比,正常对照组、MUFA组、PUFA组血清TC、TG降低,差异有统计学意义(P<0.05),而正常对照组、MUFA、PUFA三组间无统计学意义(P>0.05).与正常对照组、MUFA组相比,SFA、PUFA组FINS、FPG升高,差异有统计学意义(P<0.05),GIR明显下降,差异有统计学意义(P<0.05),但该两组间无统计学差异(P>0.05).与正常对照组相比,MUFA组血清FINS、FPG有升高趋势,差异无统计学意义(P>0.05),GIR下降,差异有统计学意义(P<0.05). 结论 MUFA饮食较PUFA、SFA饮食可以改善胰岛素敏感性.     

糖耐量正常的2型糖尿病一级亲属氧化应激水平与胰岛素敏感性的相关性研究

目的观察2型糖尿病（T2DM）患者及糖耐量正常的T2DM一级亲属（FDRs）体内氧化应激状态,探讨氧化应激与胰岛素敏感性之间的关系。方法检测外周血清丙二醛（MDA）、谷胱甘肽过氧化物酶（GSH—PX）、超氧化物歧化酶（SOD）、8-异前列腺素F2a（8-isoPGF2a）水平,高胰岛素正葡萄糖钳夹技术评估胰岛素敏感性。结果T2DM组、FDRs组较NC组MDA、8-isoPGF2a水平升高（P〈0．05）,而血GSH—PX、SOD水平降低,差异有统计学意义（P〈0．05）;MDA、8iso—PGF2a与葡萄糖输注速率（GIR）呈明显负相关（r=-0．415和-0．443,P〈0．05）,GSH—PX、SOD与GIR呈明显正相关（r=0．327和0．439,P〈0．05）。结论T2DM患者及糖耐量正常的T2DM一级亲属存在氧化应激状态的改变,且与胰岛素敏感性密切相关。     

高糖、高饱和脂肪酸及高不饱和脂肪酸饮食对老年大鼠胰岛素抵抗的影响

目的 探讨不同类型高脂肪酸及高糖饮食对老年大鼠胰岛素抵抗（IR）的影响。方法 用高不饱和脂肪酸（HUFA），高饱和脂肪酸（HSFA），高糖（HS）饲料饲养大鼠24w，观察体重（BW）、总胆固醇（TC）、甘油三酯（TG）、空腹血糖（FBG）、空腹胰岛素（FINS）、游离脂肪酸（FFA）的变化，并以正常血糖高胰岛素钳夹技术的葡萄糖输注率（GIR）对大鼠IR进行评价。结果 12w和24w GIR在不同实验组间出现显著差异（均P〈0.01），HSFA组GIR最低，24w时HUFA组、HSFA组、HS组及对照组（NC组）GIR与0w相比分别下降51.6％、52.1％、34.2％、26.4％。各实验组BW、TG、TC、FFA、FBG、FINS与NC组相比有不同程度升高，经多元回归分析，GIR与FFA、TG呈显著负相关（均P〈0.01）。结论 HUFA、HSFA和HS饮食长期摄入均可诱导大鼠IR；TG及FFA的升高与IR的形成有明显相关；随月龄增长大鼠的GIR有显著下降趋势，但饮食结构的影响更重要。     

检测人群胰岛素敏感性的一项新指数

引入一个新的胰岛素敏感性指数－－空腹血浆胰岛素与血糖乘积的倒数。该指数经美国两个种族共３２０例研究的材料证实与胰岛素钳技术测定的胰岛素敏感性指数胰岛素介导的葡萄糖代谢率（Ｍ）高度显著相关（ｒ＞０．７，Ｐ＝０．０００１）。以这一新指数分析８７４命名 国人（正常人２０１例，ＩＧＴ３０７例，新诊断ＤＭ ３６６例）的胰岛素敏感性结果与用Ｃｌａｍｐ技术测定的美国人的胰岛素敏感性极为相似：假定正常糖耐量组的胰     

非胰岛素依赖型糖尿病和糖耐量低减患者的胰岛素敏感性及其…

为评价糖耐量异常者的胰岛素敏感性改变及其有关因素，对５７２例非胰岛素依赖型糖尿病，６４７例糖耐量低减和５４３名正常对照者进行了研究。结果显示，空腹血浆胰岛素水平和高胰素血症的百分率，在ＮＩＤＤＭ组〉ＩＧＴ组〉正常对照组。胰岛素敏感性指数从大到小的排列顺序为：正常对照组，ＩＧＴ组，新诊断糖尿病组和原诊断糖尿病组。     

糖耐量正常的日本人的β—细胞功能损害与胰岛素敏感性

作者旨在研究2型糖尿病患者应用吡格列酮(Pioglitazone)对血糖控制、胰岛素敏感性和胰岛素分泌的剂量.反应效应。方法 共58例采用饮食疗法的2型糖尿病患者,年龄(54±1)岁,男34例,女24例,体重指数(BMI)(31.5±0.6)kg·m-2,随机分为安慰剂组(11例)和吡格列酮7.5(13例)、15(12例)、30(11例)、45(11例),mg/d组,用药26周,用药前和用药26周后行口服葡萄糖(75 g)耐量试验(OGTT)。     

非胰岛素依赖型糖尿病和糖耐量低减患者的胰岛素敏感性及其相关因素研究

为评价糖耐量异常者的胰岛素敏感性改变及其有关因素，对５７２例非胰岛素依赖型糖尿病（ＮＩＤＤＭ）、６４７例糖耐量低减（ＩＧＴ）和５４３名正常对照者进行了研究。结果显示，空腹血浆胰岛素（ＦＩｎｓ）水平和高胰岛素血症的百分率，在ＮＩＤＤＭ组＞ＩＧＴ组＞正常对照组（Ｐ＜０．０１）。胰岛素敏感性指数（ＩＳＩ）［－ｌｎ（ＦＩｎｓ×空腹血糖）］从大到小的排列顺序为：正常对照组、ＩＧＴ组，新诊断糖尿病组和原诊断糖尿病组（Ｐ＜０．０１）。各组肥胖者的ＩＳＩ小于非肥胖者（Ｐ＜０．０１）。单因素相关性分析显示，各组ＩＳＩ与体重指数（ＢＭＩ）呈负相关，与高密度脂蛋白胆固醇呈正相关。糖尿病组和ＩＧＴ组的ＩＳＩ与血压也呈负相关。多元逐步回归分析显示，ＩＳＩ与ＢＭＩ呈负相关，部分与血压、血脂也有相关性。提示糖耐量异常者伴有高胰岛素血症和胰岛素抵抗，ＩＳＩ与血管病变的危险因素有相关性。     

不同糖耐量个体血清瘦素水平与特异胰岛素、胰岛素原及胰岛素敏感性的关系探讨

目的　研究不同糖耐量人群空腹瘦素水平与特异胰岛素、胰岛素原及胰岛素敏感性之间的关系。方法　用放射免疫法测量 5 4例正常糖耐量 (NGT)、33例糖耐量低减 (IGT)、4 7例新发 2型糖尿病 (DM )的空腹瘦素水平、口服葡萄糖耐量试验 (OGTT) 0、1/2、1、2h的特异胰岛素 (SI)和胰岛素原 (PI)。结果　 (1)多元逐步回归分析显示 ,性别、体重指数 (BMI)、胰岛素敏感性指数是影响空腹瘦素水平最重要的因素 (校正的R2 分别为 0 .2 5 1、0 .4 19、0 .4 38,P值分别为 <0 .0 0 1、<0 .0 0 1、<0 .0 5 ) ;空腹血清瘦素水平与OGTT各时间点PI、SI、PI/SI值无相关性。 (2 )在校正性别、BMI等影响因素后 ,空腹血清瘦素水平在不同糖耐量组差异无显著性 ;DM组OGTT各时间点PI/SI值明显高于IGT组和NGT组 (P <0 .0 1) ;胰岛素敏感性 (ISI)为NGT组 >IGT组 >DM组 (P <0 .0 0 1)。结论　在测定特异胰岛素、胰岛素原时 ,血清瘦素水平除了与性别、BMI相关外 ,尚与胰岛素敏感性 (按SI水平计算 )相关 ;不同糖耐量状态对血清瘦素水平无明显影响 ;DM组存在胰岛素不敏感、PI/SI失调     

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     

The effects of fatty acids on apolipoprotein B secretion by human hepatoma cells (HEP G2)

We have investigated the effect of fatty acids on the rate of apolipoprotein B (apo B) secretion by human hepatoma cells (Hep G2). When Hep G2 cells were maintained in tissue culture flasks oleic acid up to 0.4 mM increased apo B secretion in a dose-dependent manner, whereas increases in triacylglycerol (TG) were smaller and dose dependency was less evident. In the absence of oleic acid, apo B accumulating in the tissue culture medium was predominantly in lipoproteins of higher density than very low density lipoproteins (VLDL). However, when the rate of secretion was stimulated with oleic acid the apo B-containing lipoproteins became lower in density. We postulated that there was a high rate of lipolysis of newly secreted VLDL by Hep G2 cells, which would account both for the relatively smaller effect of oleic acid on TG as opposed to apo B accumulating in the culture medium and the predominance of apo B in lipoproteins of a higher density than VLDL, which became less evident when VLDL secretory rates were stimulated by oleic acid. To test this hypothesis, cultured Hep G2 cells were transferred to columns containing Cytodex beads, permitting their continuous perfusion with culture medium so that newly secreted VLDL did not remain in contact with the cells. Apo B recovered from the perfusate was largely in VLDL range lipoproteins and the TG measured in the perfusate indicated that the true secretory rate of TG-rich lipoproteins was substantially higher than had been reflected by TG accumulating in culture medium left in contact with cells. Apo B measured in the culture medium of Hep G2 cells may thus be a better reflection of VLDL secretion, even though it is contained in higher density lipoproteins due to removal of TG by lipolysis. The effects of saturated fatty acids (SFA), monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA) on apo B (apo B) secretion by Hep G2 cells maintained in tissue culture flasks were next investigated. SFA (0.4 mM), with the exception of stearic acid (C18:0), increased apo B secretion. Lauric acid (C12:0) increased apo B secretion by 32%, myristic acid (C14:0) by 41% (P<0.005), palmitic acid (C16:0) by 154% (P<0.025), and arachidic acid (C20:0) by 186% (P<0.005). The effect of MUFA (0.4 mM) was to increase apo B secretion, oleic acid (C18:1) by 239% ((P<0.0005) and palmitoleic acid (C16: 1) by 125% (P<0.005). Of the PUFA investigated, linolenic acid (C18:3) (0.4 mM) did not have any significant effect on apo B secretion, whereas linoleic acid (C18:2) (0.4mM) arachidonic acid (C20:4) (0.1 mM) and eicosapentaenoic acid (C20:5) (0.1 mM) caused significant increases of 164, 171 and 171%, respectively (P<0.005). The fatty acids studied increased intracellular TG and cholesteryl ester concentrations to varying extents. The increase in intracellular TG produced by the different fatty acids correlated with the rate of apo B secretion (r=0.6; P<0.05). In this human hepatoma cell line, with the exception of the saturated fatty acids, the rate of secretion of apo B-containing lipoproteins does not follow the same pattern as changes in circulating low density lipoprotein (LDL) concentrations reported with dietary manipulation in man. If our findings reflect the in vivo situation, we suggest that whilst the dietary effects of SFA on serum LDL may in part be determined by the hepatic apo B secretory rate, the effects of MUFA and PUFA must be largely mediated through a catabolic effect rather than an effect on hepatic secretion. The marked increase in apo B secretion with the more highly polyunsaturated fatty acids, such as eicosapentaenoic acid, may also explain why they do not lower circulating LDL, despite reports of their apparently favourable effect on LDL-receptor mediated clearance.     

Serum saturated fatty acids containing triacylglycerols are better markers of insulin resistance than total serum triacylglycerol concentrations

Aims/hypothesis

The weak relationship between insulin resistance and total serum triacylglycerols (TGs) could be in part due to heterogeneity of TG molecules and their distribution within different lipoproteins. We determined concentrations of individual TGs and the fatty acid composition of serum and major lipoprotein particles and analysed how changes in different TGs and fatty acid composition are related to features of insulin resistance and abdominal obesity.

Methods

We performed lipidomic analyses of all major lipoprotein fractions using two analytical platforms in 16 individuals, who exhibited a broad range of insulin sensitivity.

Results

We identified 45 different TGs in serum. Serum TGs containing saturated and monounsaturated fatty acids were positively, while TGs containing essential linoleic acid (18:2 n?6) were negatively correlated with HOMA-IR. Specific serum TGs that correlated positively with HOMA-IR were also significantly positively related to HOMA-IR when measured in very-low-density lipoproteins (VLDLs), intermediate-density lipoproteins (IDLs) and LDL, but not in HDL subfraction 2 (HDL₂) or 3 (HDL₃). Analyses of proportions of esterified fatty acids within lipoproteins revealed that palmitic acid (16:0) was positively related to HOMA-IR when measured in VLDL, IDL and LDL, but not in HDL₂ or HDL₃. Monounsaturated palmitoleic (16:1 n?7) and oleic (18:1 n?9) acids were positively related to HOMA-IR when measured in HDL₂ and HDL₃, but not in VLDL, IDL or LDL. Linoleic acid was negatively related to HOMA-IR in all lipoproteins.

Conclusions/interpretation

Serum concentrations of specific TGs, such as TG(16:0/16:0/18:1) or TG(16:0/18:1/18:0), may be more precise markers of insulin resistance than total serum TG concentrations.

     

Nutrition and physical activity in Asian Indians with non-alcoholic fatty liver: A case control study

AimWe tested the hypothesis that Asian Indians with non-alcoholic fatty liver disease (NAFLD) would have imbalanced diets and lower intensity of physical activity than those without NAFLD.MethodsWe studied dietary intake, intensity of physical activity and anthropometric and metabolic profiles in subjects with NAFLD and in healthy controls. Complete clinical, biochemical, dietary and physical activity profiles were studied for 169 cases and 173 controls in a prospective manner. Bivariate and multivariate analyses were carried out to identify the predictors of NAFLD [odds ratio (OR) and 95% confidence intervals (95%CI)].ResultsThe mean dietary intakes of total energy, carbohydrate, protein, total fat, saturated fat and total cholesterol were significantly higher, while intake of monounsaturated fatty acids and polyunsaturated fatty acids was significantly lower in cases as compared to controls (p < 0.01 for all). Further, mean physical activity in a day (expressed as MET.Minutes) and total energy expenditure were significantly lower in cases than in controls (33.3 ± 3.6 vs.36.2 ± 0.5, p = 0.001 and 2707.6 ± 505.6 vs. 2904.3 ± 690.3, p = 0.02, respectively). On multivariate analysis, percentage dietary total fat intake (OR: 13.4; 95% CI: 4.6–39.3, p = 0.001), homeostatis model assessment for insulin resistance (OR: 6.9; 95% CI: 3.2–14.8, p = 0.001) abdominal obesity (OR: 2.7; 95% CI: 1.5–5.0, p = 0.001) and high serum triglycerides (OR: 2.1; 95%CI: 1.2–3.8, p = 0.007) were associated with an increased risk for development of NAFLD.ConclusionDecrease in intake of total dietary fats and improvement of insulin resistance, abdominal obesity and blood triglycerides should be important measures for management of NAFLD in Asian Indians in north India.     

Relationship of dietary fat to glucose metabolism

The relationship between dietary fat and glucose metabolism has been recognized for at least 60 years. In experimental animals, high fat diets result in impaired glucose tolerance. This impairment is associated with decreased basal and insulin-stimulated glucose metabolism. Impaired insulin binding and/or glucose transporters has been related to changes in the fatty acid composition of the membrane induced by dietary fat modification. In humans, high-fat diets, independent of fatty acid profile, have been reported to result in decreased insulin sensitivity. Saturated fat, relative to monounsaturated and polyunsaturated fat, appears to be more deleterious with respect to fat-induced insulin insensitivity. Some of the adverse effects induced by fat feeding can be ameliorated with omega-3 fatty acid. Epidemiological data in humans suggest that subjects with higher intakes of fat are more prone to develop disturbances in glucose metabolism, type 2 diabetes or impaired glucose tolerance, than subjects with lower intakes of fat. Inconsistencies in the data may be attributable to clustering of high intakes of dietary fat (especially animal fat) with obesity and inactivity. Metabolic studies suggest that higher-fat diets containing a higher proportion of unsaturated fat result in better measures of glucose metabolism than high-carbohydrate diet. Clearly, the area of dietary fat and glucose metabolism has yet to be fully elucidated.     

Substituting dietary saturated for monounsaturated fat impairs insulin sensitivity in healthy men and women: The KANWU study

Aims/hypothesis. The amount and quality of fat in the diet could be of importance for development of insulin resistance and related metabolic disorders. Our aim was to determine whether a change in dietary fat quality alone could alter insulin action in humans. Methods. The KANWU study included 162 healthy subjects chosen at random to receive a controlled, isoenergetic diet for 3 months containing either a high proportion of saturated (SAFA diet) or monounsaturated (MUFA diet) fatty acids. Within each group there was a second assignment at random to supplements with fish oil (3.6 g n-3 fatty acids/d) or placebo. Results. Insulin sensitivity was significantly impaired on the saturated fatty acid diet (-10 %, p = 0.03) but did not change on the monounsaturated fatty acid diet ( + 2 %, NS) (p = 0.05 for difference between diets). Insulin secretion was not affected. The addition of n-3 fatty acids influenced neither insulin sensitivity nor insulin secretion. The favourable effects of substituting a monounsaturated fatty acid diet for a saturated fatty acid diet on insulin sensitivity were only seen at a total fat intake below median (37E %). Here, insulin sensitivity was 12.5 % lower and 8.8 % higher on the saturated fatty acid diet and monounsaturated fatty acid diet respectively (p = 0.03). Low density lipoprotein cholesterol (LDL) increased on the saturated fatty acid diet ( + 4.1 %, p < 0.01) but decreased on the monounsaturated fatty acid diet (MUFA) (–5.2, p < 0.001), whereas lipoprotein (a) [Lp(a)] increased on a monounsaturated fatty acid diet by 12 % (p < 0.001). Conclusions/interpretation. A change of the proportions of dietary fatty acids, decreasing saturated fatty acid and increasing monounsaturated fatty acid, improves insulin sensitivity but has no effect on insulin secretion. A beneficial impact of the fat quality on insulin sensitivity is not seen in individuals with a high fat intake ( > 37E %). [Diabetologia (2001) 44: 312–319] Received: 21 August 2000 and in revised form: 8 November 2000     

高游离脂肪酸血症所致胰岛素抵抗与氧化应激的关系

研究高游离脂肪酸(FFA)血症所致大鼠机体氧化应激及胰岛素抵抗之间的相互关系,以及其对机体抗氧化能力的影响,探讨胰岛素抵抗的病理生理机制.经研究证实大鼠高FFA血症不仅使组织活性氧簇生成增加[(886±105 vs 427±42)mmol/L,P<0.05],同时损伤机体抗氧化能力,细胞内还原捌谷胱甘肽生成减少[(272±47 vs 561±36)μmol/L,P<0.05],导致氧化应激,从而促进胰岛素抵抗的形成.     

Improvements in glucose tolerance and insulin sensitivity after lifestyle intervention are related to changes in serum fatty acid profile and desaturase activities: the SLIM study

Aims/hypothesis The aim of this study was to investigate whether lifestyle intervention-induced changes in serum fatty acid profile of cholesteryl esters and estimated desaturase activities are related to improvements in insulin sensitivity in subjects at risk of type 2 diabetes. Materials and methods In the Study on Lifestyle Intervention and Impaired Glucose Tolerance Maastricht (SLIM), 97 men and women with IGT were randomised to a combined diet and exercise programme (47 intervention) or a control group (50 control subjects). At baseline and after 1 year the following assessments were made: an OGTT, an exercise test to determine maximal aerobic capacity, anthropometry, and analysis of the serum fatty acid profile of cholesteryl esters. Results The lifestyle programme was effective in reducing the intake of total and saturated fat, increasing physical activity, reducing obesity and improving insulin sensitivity and glucose tolerance. Regression analysis of the total population showed that an increase in the C20:4 n-6/C20:3 n-6 ratio (estimated Δ5-desaturase activity) and reductions in the C18:3 n-6/C18:2 n-6 ratio (estimated Δ6-desaturase activity) and the C16:1 n-7/C16:0 ratio (estimated Δ9-desaturase activity or stearoyl-CoA desaturase-1) were significantly associated with a decrease in homeostasis model assessment for insulin resistance. After adjustment for lifestyle changes (change in percentage body fat, aerobic capacity and saturated fat intake), these associations were partly reduced, but remained statistically significant. Conclusions/interpretation Lifestyle-induced changes in fatty acid profile of cholesteryl esters and desaturase activities were independently related to changes in insulin sensitivity in subjects at risk of type 2 diabetes.     

Polyunsaturated fatty acids may impair blood glucose control in type 2 diabetic patients.

Fifteen patients with Type 2 diabetes were given two diets rich in either saturated fat or polyunsaturated fat in alternate order over two consecutive 3-week periods on a metabolic ward. Both diets contained the same amount of fat, protein, carbohydrates, dietary fibre, and cholesterol. The proportions of saturated, monounsaturated and polyunsaturated fatty acids in the saturated fat diet were 16, 10, and 5%-energy and in the polyunsaturated fat diet (PUFA) 9, 10, and 12%-energy. The PUFA diet contained a high proportion of n-3 fatty acids. Metabolic control improved significantly in both dietary periods, due to both qualitative dietary changes and a negative energy balance. The serum lipoprotein concentrations decreased on both diets but the serum lipids were significantly lower after the PUFA diet (serum triglycerides -20%, p = 0.001; serum cholesterol -5%, p = 0.03; VLDL-triglycerides -29%, p less than 0.001; and VLDL-cholesterol -31%, p = 0.001) than after the saturated fat diet. Average blood glucose concentrations during the third week were significantly higher fasting (+15%, p less than 0.01), and during the day at 1100 h (+18%, p less than 0.001) and 1500 h (+17%, p = 0.002) on PUFA than on the saturated fat diet. Significantly higher blood glucose levels were also recorded with a standard breakfast, while the sum of the insulin values was lower (-19%, p = 0.01). HbA1c did not differ significantly between the two dietary periods.(ABSTRACT TRUNCATED AT 250 WORDS)     

血清游离脂肪酸水平在不同体重指数及糖耐量个体中与胰岛素敏感性及相关指标的关系

目的　运用Bergman的最小模型技术研究不同体重指数 (BMI)及糖耐量个体血清空腹游离脂肪酸水平与胰岛素敏感性之间的关系。方法　用放射免疫分析法检测 2 6例正常人 (正常BMI及糖耐量 )、39例糖耐量正常单纯性肥胖者、新近诊断的 2 5例糖耐量异常 (IGT)患者及 2 1例 2型糖尿病患者的血清空腹游离脂肪酸 (FFA)水平 ,测定空腹血清甘油三酯 (TG)、血清总胆固醇 (TC)水平 ,并利用Bergman最小模型技术计算胰岛素敏感性指数 (ISI)。结果　 (1)正常对照组血清FFA值显著低于单纯肥胖组、IGT组及 2型糖尿病组 ,但FFA值在后 3组之间差异无显著性。 (2 )正常对照组ISI值显著高于单纯肥胖组、IGT组及 2型糖尿病组 ,但ISI值在后 3组之间差异无显著性。 (3)在校正了BMI因素影响后 ,正常对照组血清FFA值仍显著低于其他各组。 (4 )相关性研究显示 ,血清FFA值与ISI值呈明显负相关 ,与简易胰岛素敏感性指数HOMAIR以及BMI、腰臀围比 (WHR)、TG值呈明显正相关 (r值分别为 - 0 4 5 4、0 2 13、0 2 4 1、0 336、0 4 14 ,P值分别 <0 0 1、<0 0 5、<0 0 5、<0 0 1、<0 0 1) ,而与年龄、性别及TC值无相关性 ;(5 )以FFA为应变量 ,ISI、HOMAIR、BMI、WHR、TG为自变量进行多元逐步回归分析显示 ,ISI、BMI、TG为影响空腹血