Baynes C, Henderson A D, Hughes C L, Richmond W, Johnston D G, Elkeles R S
Department of Clinical Endocrinology, St Mary's Hospital, London, UK.
J Intern Med. 1991 Mar;229(3):267-73. doi: 10.1111/j.1365-2796.1991.tb00343.x.
Factors contributing to fasting hypertriglyceridaemia were studied in 20 patients with non-insulin-dependent diabetes--nine with normal triglyceride concentrations [fasting triglyceride 0.94 (range 0.58-1.23) mmol l-1] and eleven with mild fasting hypertriglyceridaemia [fasting triglyceride 2.4 (1.82-4.0) mmol l-1]. The patients with hypertriglyceridaemia were more obese [body mass index 29.0 (24.6-33.8) vs. 25.7 (21.9-30.1) kg m-2, P less than 0.05] and demonstrated impaired glucose disposal in response to exogenous insulin at isoglycaemia [insulin sensitivity index, SIp 0.7 (0.27-2.5) vs. 2.4 (0.62-5.1) ml m-2 min per mU l-1, P less than 0.001]. Basal non-esterified fatty acid (NEFA) and glycerol concentrations were higher and were suppressed to a lesser extent during isoglycaemic hyperinsulinaemia. Fasting glucose and apolipoprotein B concentrations were higher in the hypertriglyceridaemic patients, but lipoprotein lipase activities were similar in the two groups. When the effect of obesity was removed (by weight-matching six normotriglyceridaemic with seven hypertriglyceridaemic patients) basal NEFA and glycerol concentrations and the suppression of NEFA in response to insulin remained significantly different between the two groups. We propose that defects in both the glucoregulatory and antilipolytic actions of insulin contribute to mild fasting hypertriglyceridaemia in NIDDM, and that these defects cannot be attributed solely to obesity. These disorders of insulin action may also have important implications for the postprandial metabolism of triglyceride-rich lipoproteins and hence atherogenesis.
对20例非胰岛素依赖型糖尿病患者的空腹高甘油三酯血症相关因素进行了研究,其中9例甘油三酯浓度正常[空腹甘油三酯0.94(范围0.58 - 1.23)mmol/L],11例有轻度空腹高甘油三酯血症[空腹甘油三酯2.4(1.82 - 4.0)mmol/L]。高甘油三酯血症患者更肥胖[体重指数29.0(24.6 - 33.8)对25.7(21.9 - 30.1)kg/m²,P<0.05],并且在等血糖状态下对外源性胰岛素的葡萄糖处置受损[胰岛素敏感性指数,SIp 0.7(0.27 - 2.5)对2.4(0.62 - 5.1)ml/m²·min/(mU/L),P<0.001]。基础非酯化脂肪酸(NEFA)和甘油浓度较高,在等血糖高胰岛素血症期间抑制程度较小。高甘油三酯血症患者的空腹血糖和载脂蛋白B浓度较高,但两组的脂蛋白脂肪酶活性相似。当消除肥胖的影响(通过将6例甘油三酯正常的患者与7例高甘油三酯血症患者进行体重匹配)后,两组之间基础NEFA和甘油浓度以及NEFA对胰岛素反应的抑制仍有显著差异。我们认为胰岛素的葡萄糖调节和抗脂解作用缺陷均导致非胰岛素依赖型糖尿病患者出现轻度空腹高甘油三酯血症,且这些缺陷不能仅归因于肥胖。这些胰岛素作用紊乱也可能对富含甘油三酯脂蛋白的餐后代谢以及动脉粥样硬化形成具有重要意义。