CORRELATIONS BETWEEN FATTY-ACID AND GLUCOSE-METABOLISM - POTENTIAL EXPLANATION OF INSULIN-RESISTANCE OF PUBERTY

CORRELATIONS BETWEEN FATTY-ACID AND GLUCOSE-METABOLISM - POTENTIAL EXPLANATION OF INSULIN-RESISTANCE OF PUBERTY
复制标题

DOI:
10.2337/diabetes.43.7.908
复制
发表时间:
1994-07-01
期刊:
影响因子:
7.7
通讯作者:
KALHAN, SC
KALHAN, SC
中科院分区:
医学1区
文献类型:
--
作者:
ARSLANIAN, SA;KALHAN, SC

文献摘要

被引文献

相似文献

青春期期间已记录了体内对胰岛素对葡萄糖摄取作用的抵抗。为了检验兰德尔等人提出的葡萄糖-脂肪酸循环的假设。 (Randle PJ,Garland PB,Hales CN,Nemsholme EA:葡萄糖脂肪酸循环:其在胰岛素敏感性和糖尿病代谢紊乱中的作用。Lancet 1:785-789,1963)可能是造成这种现象的原因,我们研究了九名青春期前(Tanner I)、九名青春期(Tanner II-IV)和五名年轻成年健康受试者。在基础状态期间和逐步高胰岛素(10和40 mU.m(-2).min(-1))-正常血糖钳夹期间用[d-5]甘油示踪剂测量脂肪分解速率。在钳夹过程中测量胰岛素刺激的葡萄糖处理率(R(d)),而葡萄糖和脂肪氧化则通过使用间接呼吸量热法测量。青春期前和青春期受试者之间的基础甘油出现率(R(a);脂肪分解)和脂肪氧化相似,但当数据以每公斤体重或每公斤去脂质量表示时高于成人(FI?lI;甘油R(a):2.5 +/- 0.2、2.6 +/- 0.2 vs. 1.6 +/- 0.2 mu mol . min(-1) . kg FFM(-1),P < 0.05;脂肪氧化:4.4 +/- 0.6、4.8 +/- 0.3 vs. 3.2 +/- 0.6 mu mol . kg FFM(-1),P < 0.05)。然而,当以全身表示时,青春期受试者的甘油 R(a) 和脂肪氧化仅高于青春期前和成年受试者。基线时胰岛素样生长因子 I (IGF-I) 水平与全身脂肪分解(r = 0.52,P = 0.006)和总脂质氧化(r = 0.44,P = 0.016)相关。在低速胰岛素钳夹期间,青春期受试者的甘油 R(a) 和脂肪氧化高于成年受试者(1.5 +/- 0.2 对比 0.9 +/- 0.1 mu mol . min(-1) . kg FFM(-1),P = 0.04,3.7 +/- 0.4 对比 2.2 +/- 0.4 mu mol . min(-1) . kg FFM(-1),P =分别为 0.03)。在高速率胰岛素钳夹期间,青春期 (1.7 +/- 0.3) 的脂肪氧化显着高于青春期前 (0.7 +/- 0.2) 与成年受试者 (0.4 +/- 0.2 mu mol . min kg FFM(-1)),并且 IGF-I 水平与全身脂质氧化呈正相关 (r = 0.72,P ( 0.001)。与青春期前和成年受试者相比,青春期受试者的 R(d) 显着较低(总 R(d)、
In vivo resistance to the action of insulin on gludose uptake has been documented during puberty. To test the hypothesis that the glucose-fatty acid cycle, as proposed by Randle et al. (Randle PJ, Garland PB, Hales CN, Nemsholme EA: The glucose fatty-acid cycle: its role in insulin sensitivity and the metabolic disturbances of diabetes mellitus. Lancet 1:785-789, 1963), may be responsible for this phenomenon, we studied nine prepubertal (Tanner I), nine pubertal (Tanner II-IV), and five young adult healthy subjects. The rate of lipolysis was measured with [d-5]glycerol tracer during basal state and during a stepwise hyperinsulinemic (10 and 40 mU . m(-2) . min(-1))-euglycemic clamp. The rates of insulin-stimulated glucose disposal (R(d)) were measured during the clamp, whereas glucose and fat oxidation were measured by using indirect respiratory calorimetry. Basal glycerol rate of appearance (R(a); Lipolysis) and fat oxidation were similar between prepubertal and pubertal subjects but higher than adults when the data were expressed per kilogram body weight or per kilogram fat-free mass (FI?lI; glycerol R(a): 2.5 +/- 0.2, 2.6 +/- 0.2 vs. 1.6 +/- 0.2 mu mol . min(-1) . kg FFM(-1), P < 0.05; fat oxidation: 4.4 +/- 0.6, 4.8 +/- 0.3 vs. 3.2 +/- 0.6 mu mol . min(-1) . kg FFM(-1), P < 0.05). However, when expressed for total body, glycerol R(a) and fat oxidation mere higher in pubertal versus prepubertal and adult subjects. Insulin-like growth factor I (IGF-I) levels correlated with total-body lipolysis (r = 0.52, P = 0.006) and with total lipid oxidation (r = 0.44, P = 0.016) at baseline. During the low-rate insulin clamp, glycerol R(a) and fat oxidation were higher in pubertal versus adult subjects (1.5 +/- 0.2 vs. 0.9 +/- 0.1 mu mol . min(-1) . kg FFM(-1), P = 0.04, and 3.7 +/- 0.4 vs. 2.2 +/- 0.4 mu mol . min kg FFM(-1), P = 0.03, respectively). During the high-rate insulin clamp, fat oxidation was significantly higher in pubertal (1.7 +/- 0.3) versus prepubertal (0.7 +/- 0.2) versus adult subjects (0.4 +/- 0.2 mu mol . min kg FFM(-1)), and IGF-I levels correlated positively with total-body lipid oxidation (r = 0.72, P ( 0.001). Insulin-stimulated total and nonoxidative R(d) were significantly lower in pubertal subjects compared with prepubertal and adult subjects (total R(d),