EFFECTS OF PUBERTY AND DIABETES ON METABOLISM OF INSULIN-SENSITIVE FUELS
EFFECTS OF PUBERTY AND DIABETES ON METABOLISM OF INSULIN-SENSITIVE FUELS
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DOI：
10.1152/ajpendo.1994.266.6.e885
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发表时间：
1994-06-01
影响因子：
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通讯作者：
TAMBORLANE, WV
中科院分区：
文献类型：
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作者：
CAPRIO, S;CLINE, G;TAMBORLANE, WV
在正常青春期，胰岛素刺激葡萄糖代谢的能力降低；这些变化在患有胰岛素依赖型糖尿病(IDDM)的青少年中被夸大了。由于青春期和IDDM对胰岛素其他作用的影响尚未确定，我们研究了8名健康青少年和9名IDDM(HBA(1)14+/-2%)青少年和6名健康青年对照组正常血糖高胰岛素血症(20mU·m(2)·min(-1))3h的亮氨酸动力学(使用[1-C-13]亮氨酸)和脂肪代谢。IDDM受试者接受隔夜小剂量胰岛素输注以使空腹血糖正常化。研究期间的基础和稳态胰岛素值(接近240 PM)在所有三组中都是相似的。与成人相比，健康青少年的胰岛素刺激的葡萄糖代谢减少了40%(P<；0.05)，而控制不佳的IDDM患者的胰岛素刺激的葡萄糖代谢减少了40%(P<；0.05与正常青少年相比)。尽管三组基础血糖和血脂氧化率(用间接热法测定)相似，但当输入胰岛素时，只有两组非糖尿病组的葡萄糖氧化增加，而脂质氧化减少。同样，胰岛素只在非糖尿病患者中显著降低了血浆游离脂肪酸水平。基础亮氨酸流量(蛋白质降解指数)在健康对照组中相似，但在IDDM青少年中显着增加。尽管夹闭期间血浆胰岛素有类似的增加，但IDDM青少年的亮氨酸流量仍然高于健康对照组。与非糖尿病组相比，IDDM受试者的基础亮氨酸氧化率也升高，在胰岛素输注期间下降幅度较小。结论：青春期胰岛素抵抗对糖代谢具有选择性，对氨基酸/蛋白质代谢有一定的抑制作用。另一方面，在患有IDDM的青少年中，青春期和糖尿病控制不佳的综合影响会产生更深层次的全身性代谢缺陷，包括蛋白质分解。
Insulin's ability to stimulate glucose metabolism is reduced during normal puberty; these changes are exaggerated in adolescents with insulin-dependent diabetes mellitus (IDDM). Because the effects of puberty and IDDM on the other actions of insulin have not been established, we studied leucine kinetics (using [1-C-13]leucine) and fat metabolism during euglycemic hyperinsulinemia (20 mU.m(2).min(-1)) for 3 h in eight healthy and nine IDDM (HbA(1) 14 +/- 2%) adolescents and six healthy young adult controls. IDDM subjects received overnight low-dose insulin infusion to normalize fasting glucose. Basal and steady-state insulin values (similar to 240 pM) during the study were similar in all three groups. Insulin-stimulated glucose metabolism was reduced by 40% in healthy adolescents vs. adults (P < 0.05) and by an additional 40% in poorly controlled IDDM (P < 0.05 vs. normal adolescents). Although basal glucose and lipid oxidation rates (mea sured by indirect calorimetry) were similar in all three groups, when insulin was infused, glucose oxidation increased and lipid oxidation decreased only in the two nondiabetic groups. Similarly, insulin significantly reduced plasma free fatty acid levels only in the nondiabetics. Basal leucine flux (an index of protein degradation) was similar in healthy controls but was markedly increased in IDDM adolescents. Despite similar increments in plasma insulin during the clamp, leucine flux remained higher in IDDM adolescents than in healthy controls. Basal leucine oxidation rates were also increased in IDDM subjects compared with nondiabetic groups and declined to a lesser extent during insulin infusion. We conclude that insulin resistance of puberty is selective for glucose metabolism, sparing amino acid/protein metabolism. On the other hand, in adolescents with IDDM, the combined effects of puberty and poorly controlled diabetes produce more profound generalized metabolic defects that include proteolysis.