甘油三酯代谢异常与胰岛素抵抗关系的研究进展

高甘油三酯血症以及甘油三酯的异位沉积是引起胰岛素抵抗的危险因素,阐明甘油三酯代谢的调控因素是深入研究胰岛素抵抗相关疾病发病机制、寻找有效治疗方法的基础.

Abstract：

Hypertriglyceridemia, and the ectopic deposition of triglycerides, are the risk factors for insulin resistance. To clarify the mechanism of regulations in triglyceride metabolism is an approach to the elucidation of pathogenesis and effective treatment of insulin resistance-related diseases.     

甘油三酯代谢异常与胰岛素抵抗关系的研究进展

高甘油三酯血症以及甘油三酯的异位沉积是引起胰岛素抵抗的危险因素,阐明甘油三酯代谢的调控因素是深入研究胰岛素抵抗相关疾病发病机制、寻找有效治疗方法的基础.     

肥胖和高血压患者餐后甘油三酯代谢异常与胰岛素抵抗的关系

目的　探讨高血压病与肥胖患者餐后甘油三酯 (TG)代谢异常与胰岛素抵抗的关系。方法　 19例健康人 ,19例单纯肥胖患者 ,2 1例高血压非肥胖患者 ,2 3例高血压合并肥胖患者禁食 12h后 ,进行标准脂肪负荷试验 ,以TG 8h曲线下面积 (TG AUC)和TG峰反应 (TGPR)作为标准脂肪负荷后TG反应水平的指标。以胰岛素敏感性指数 (ISI)及胰岛素曲线下面积 (IS AUC)作为胰岛素敏感性的判定指标。结果　 (1)高血压合并肥胖、高血压非肥胖、单纯肥胖组TG AUC ,TGPR均显著高于正常组 [TG AUC分别为 :(2 4 5 1± 10 6 8)mmol/L、(17 5 8± 7 6 8)mmol/L、(15 2 6± 4 93)比 (8 74± 2 34)mmol/L ,P <0 0 5 ;TGPR分别为 :(5 2 1± 2 2 7)mmol/L、(3 4 6± 1 82 )mmol/L、(3 0 2± 1 0 1)比 (1 5 4±0 5 6 )mmol/L ,P <0 0 5 ],高血压合并肥胖组TG AUC ,TGPR显著高于高血压非肥胖和单纯肥胖组 (P<0 0 1) ,高血压非肥胖组与单纯肥胖组之间无显著性差异。 (2 )高血压合并肥胖、高血压非肥胖、单纯肥胖组ISI(绝对值 ) ,IS AUC均显著高于正常组 ,高血压合并肥胖组IS AUC ,ISI显著高于高血压非肥胖和单纯肥胖组 (P <0 0 1) ,高血压非肥胖组与单纯肥胖组之间无显著性差异。 (3)高血压合并肥胖、高血压非肥胖和肥胖组中具     

甘油三酯-葡萄糖指数与胰岛素抵抗相关代谢性疾病的关系

胰岛素抵抗在2型糖尿病、冠状动脉粥样硬化、非酒精性脂肪性肝病、代谢综合征等代谢紊乱性疾病的发生发展中均起着重要作用。诸多研究已表明,甘油三酯-葡萄糖(triglyceride glucose,TyG)指数可作为评估胰岛素抵抗的代谢指标,与胰岛素抵抗及其相关代谢性疾病之间存在着不同程度的联系。因此,本综述重点阐述TyG指...     

载脂蛋白A5与甘油三酯代谢及胰岛素抵抗的关系

近年来高甘油三酯(HTG)所致的脂毒性已引起广泛关注,其可引起并加重胰岛素抵抗(IR),使胰岛素的生物学效应降低.而载脂蛋白A5(ApoA5)可降低血浆甘油三酯(TG)水平.目前对于ApoA5与TG的关系仍存在争议,ApoA5调节血脂代谢的机制尚未阐明.明确ApoA5与TG代谢及lR的关系可能会对揭示脂代谢、糖尿病的发...     

内源性高甘油三酯血症存在胰岛素抵抗

为探讨内源性高甘油三酯血症是否存在胰岛素抵抗，本文对５３例内源性高甘油三酯血症患者及３３例年龄及性别相匹配的正常人的耐糖试验，胰岛素分泌试验，空腹血脂及血浆载脂蛋白进行了分析，结果发现，内源性高甘油三酯血症患者口服１００ｇ葡萄糖后血糖及血浆胰岛素水平明显增加，服糖后２ｈ血糖大于７．２２ｍｍｏｌ／Ｌ，服糖后３ｈ血浆胰岛素仍未恢复至空腹水平，且血浆胰岛素面积和葡萄糖面积，血浆胰岛素面积与葡萄糖面积的百     

血浆胆固醇,甘油三酯水平与胰岛素抵抗的关联

目前对于胰岛素抵抗综合征（X综合征）与脂类代谢紊乱关系的认识尚存争议：某些文献中将高胆固醇血症、高甘油三酯血症均包括于此综合征之中，但一些文献则将高胆固醇血症排除在外，认为高甘油三酯及低HDL－C两者才是该综合征的特征［1－4］。我们分析新疆地区1994年糖尿病普查中做葡萄糖耐量试验（OGTT）的1028例临床资料，探讨血浆总胆固醇及甘油三酯水平是否均与胰岛素抵抗相关，现报道如下。对象和方法全部1028例均为新疆地区1994年万人糖尿病普查中早餐（馒头100g）后2小时血糖（强生公司快速血糖仪测手指血）≥6．67mmol／L者，各…     

胰岛素抵抗、糖及脂质代谢异常与高血压

虽然经过数十年的广泛研究,高血压(HT)的病因及其治疗仍未完善解决。有充分资料证实HT,糖尿病与肥胖常同时并存,且随年龄增加。三者又常伴高胰岛素血症(Hyperinsulinemia,HIS),胰岛素抵抗(Insulin resistance,ISR),糖及脂质代谢异常(包括糖耐受不良,高甘油三酯血症(HTC),高VLDL及LDL,低HDL),并有更高心血管病危险。近二十余年,大规模降压治疗明显降低了卒中发生率,但对冠心病影响不大,可能的解释是其它因素而非血压本身是更重要的冠心病危险因素,或由于降压药物;使某些危险因素如血糖,脂质障碍等增     

内源性高甘油三酯血症存在胰岛素抵抗

为探讨内源性高甘油三酯血症是否存在胰岛素抵抗，本文对５３例内源性高甘油三酯血症患者及３３例年龄及性别相匹配的正常人的耐糖试验、胰岛素分泌试验、空腹血脂及血浆载脂蛋白进行了分析。结果发现，内源性高甘油三酯血症患者口服１００ｇ葡萄糖后血糖及血浆胰岛素水平明显增加，服糖后２ｈ血糖大于７．２２ｍｍｏｌ／Ｌ，服糖后３ｈ血浆胰岛素仍未恢复至空腹水平；且血浆胰岛素面积和葡萄糖面积、血浆胰岛素面积与葡萄糖面积的百分比及胰岛素抵抗指数均明显高于正常对照组，说明内源性高甘油三酯血症患者存在胰岛素抵抗，出现高胰岛素血症及葡萄糖耐量降低。     

非酒精性脂肪与胰岛素抵抗及糖代谢异常的关系

目的 探讨非酒精性脂肪肝（脂肪肝）与胰素抵抗及糖代谢异常之间的关系。方法 对４８例脂肪肝患者做胰岛素释放试验和葡萄糖耐量试验,计算胰岛素曲线下面积,血糖曲线下面积和胰岛素敏感性指标（血糖曲线下面积／胰岛素曲线下面积）,并以不嗜酒的正常人作为对照组。结果 脂肪肝组口服葡萄糖６０ｍｉｎ,１２０ｍｉｎ,１８０ｍｉｎ后胰岛素水平高于对照组且高峰后移;除１８０ｍｉｎ外脂肪肝组的各时点的血糖水平显著高于对照级     

Hyperinsulinemia negatively affects the association between insulin resistance and blood pressure

Background and aimsAlthough hyperinsulinemia and insulin resistance (IR) together cause metabolic diseases, the available evidence fails to link hyperinsulinemia with blood pressure (BP) elevation. To further understand the role of hyperinsulinemia in the pathophysiology of hypertension, we conducted this study to investigate the moderating effect of fasting insulin (FINS) on the association between IR and BP.Methods and resultsThe health screening data of 72,076 individuals were analyzed for this moderation analysis. IR was indicated by the homeostatic model assessment of insulin resistance (HOMA-IR), triglyceride-glucose index (TyG), and triglyceride to high-density lipoprotein cholesterol ratio (TG/HDLc). In the adjusted model, three IR indicators were considered independent variables; FINS was used as a moderator, and systolic BP (SBP) and diastolic BP (DBP) were used as dependent variables. The regression coefficient of the interaction term between the three IR indicators and FINS was significantly negative in all moderation models. Simple slope tests and the Johnson–Neymann technique also indicated that FINS negatively moderated the association between IR and BP.ConclusionsThis moderation analysis showed that FINS negatively mediated the association between IR and BP, suggesting that hyperinsulinemia may buffer, not reinforce, the effect of IR on hypertension.     

瘦素与胰岛素抵抗及糖代谢异常的关系

当供给人体的热量多于消耗量而以脂肪形式贮存在体内 ,使人体重量超过标准体重的 2 0 %时称为肥胖。肥胖患者常出现胰岛素抵抗 (ＩＲ) ,血浆胰岛素增高 ,外周组织对胰岛素的敏感性下降。研究表明 ,肥胖是糖代谢异常的重要诱发因素 ,与 2型糖尿病的发生相关。近年来发现 ,肥胖基因的蛋白质产物瘦素 (ｌｅｐｔｉｎ)能调节体重与能量代谢 ,但与ＩＲ及糖代谢异常的关系仍不十分清楚 ,本研究测定 84例受检者血清瘦素含量及其它有关指标 ,探讨瘦素与ＩＲ及糖代谢异常的关系。一、对象和方法1.对象 :84例受检者以往未发现患有糖尿病、甲状腺等内分…     

Evidence for an independent relationship between insulin resistance and fasting plasma HDL-cholesterol, triglyceride and insulin concentrations.

Elevated plasma insulin and triglyceride (TG) and decreased high-density-lipoprotein (HDL)-cholesterol concentrations have been shown to be risk factors for coronary heart disease (CHD). It has been suggested that these metabolic abnormalities are all secondary to resistance to insulin-stimulated glucose uptake. To examine this in more detail, we divided 18 non-diabetic, moderately overweight, sedentary men aged 25-50 years into three groups on the basis of their steady-state plasma glucose levels (SSPG): a low group, (n = 7; SSPG less than 8.3 mmol l-1), a middle group, (n = 6; SSPG 8.3-11.1 mmol l-1), and a high group (n = 5; SSPG greater than 11.1 mmol l-1). The high group had significantly higher fasting (P less than 0.05) and post-oral glucose challenge (P less than 0.01) insulin concentrations, higher fasting TG (P less than 0.05) and lower fasting HDL-cholesterol (P less than 0.05) concentrations than the other two groups. However, there were no statistically significant differences between the groups with regard to body mass index, waist-to-hip ratio or physical endurance capacity as determined by maximal oxygen consumption during a treadmill test. The data suggest that insulin resistance has an effect on the modulation of plasma insulin, TG and HDL-cholesterol concentrations, independent of generalized, abdominal or physical endurance capacity.     

Defective regulation of triglyceride metabolism by insulin in the liver in NIDDM

Summary Insulin administration to healthy subjects inhibits the production of very low density lipoprotein (VLDL)1 (Svedbergs flotation (Sf) rate 60–400) without affecting that of VLDL2 (Sf 20–60) subclass. This study was designed to test whether this hormonal action is impaired in non-insulin-dependent diabetes mellitus (NIDDM). We studied six men with NIDDM (age 53 ± 3 years, body mass index 27.0 ± 1.0 kg/m², plasma triglycerides 1.89 ± 0.22 mmol/l) during an 8.5 h infusion of saline (control) and then in hyperinsulinaemic (serum insulin ∼ 540 pmol/l) conditions during 8.5 h infusions of glucose and insulin to give either hyper- and normoglycaemic conditions. [3-²H]-leucine was used as tracer and kinetic constants derived using a non-steady-state multicompartmental model. Compared to the control study, patients with NIDDM reduced VLDL1 apo B production by only 3 ± 8 % after 8.5 h of hyperinsulinaemia (701 ± 102 vs 672 ± 94 mg/day respectively, NS) in hyperglycaemic conditions and by 9 ± 21 % under normoglycaemic conditions (603 ± 145 mg/day). In contrast, in normal subjects insulin induced a 50 ± 15 % decrement in VLDL1 apo B production (p < 0.05). Direct synthesis of VLDL2 apo B in patients with NIDDM was not markedly affected by insulin. We conclude that a contributory factor to hypertriglyceridaemia in NIDDM is the inability of insulin to inhibit acutely the release of VLDL1 from the liver, despite efficient suppression of serum non-esterfied fatty acids. [Diabetologia (1997) 40: 454–462] Received: 7 October 1996 and in revised form: 24 December 1996