Meneilly G S, Elliott T, Tessier D, Hards L, Tildesley H
Department of Medicine, University of Sherbrooke, Quebec, Canada.
Diabetes Care. 1996 Dec;19(12):1320-5. doi: 10.2337/diacare.19.12.1320.
We conducted this study to assess the metabolic alterations in elderly patients with NIDDM.
Healthy, lean (n = 15; age, 73 +/- 1 years; BMI, 23.8 +/- 0.5 kg/m2), and obese (n = 10; age, 71 +/- 1 years; BMI, 28.9 +/- 1.2 kg/m2) control subjects and lean (n = 10; age, 75 +/- 2 years; BMI, 24.0 +/- 0.5 kg/m2) and obese (n = 23; age, 73 +/- 1 years; BMI, 29.9 +/- 0.7 kg/m2) NIDDM patients underwent a 3-h glucose tolerance test, a 2-h hyperglycemic glucose clamp study, and a 3-h euglycemic glucose clamp study with tritiated glucose methodology to measure glucose production and disposal rates.
Waist-to-hip ratio (WHR) was greater in both lean and obese NIDDM patients than in control subjects. Insulin responses during the oral glucose tolerance test were similar in obese subjects (control subjects: 417 +/- 64 pmol/l; NIDDM patients: 392 +/- 47 pmol/l) but were reduced in lean NIDDM patients (control subjects: 374 +/- 34 pmol/l; NIDDM patients: 217 +/- 20 pmol/l, P < 0.01). Lean and obese NIDDM patients had absent first-phase insulin responses during the hyperglycemic clamp. Second-phase insulin responses were reduced in lean (P < 0.01 vs. control subjects by analysis of variance) but not obese NIDDM patients. Hepatic glucose output was not increased in lean or obese NIDDM patients. Steady-state (150-180 min) glucose disposal rates were 16% less in lean NIDDM patients (control subjects: 8.93 +/- 0.37 mg.kg LBM (lean body mass)-1.min-1; NIDDM patients: 7.50 +/- 0.28 mg.kg LBM-1.min-1, P < 0.05) and 37% less in obese NIDDM patients (control subjects: 8.17 +/- 0.38 mg.kg LBM-1.min-1; NIDDM patients: 5.03 +/- 0.36 mg.kg LBM-1.min-1, P < 0.001).
Lean elderly NIDDM patients have a profound impairment in glucose-induced insulin release but mild resistance to insulin-mediated glucose disposal. Obese elderly NIDDM patients have adequate circulating insulin, but marked resistance to insulin-mediated glucose disposal. Hepatic glucose output is not increased in elderly NIDDM patients.
我们开展这项研究以评估非胰岛素依赖型糖尿病(NIDDM)老年患者的代谢改变。
健康、体型瘦的(n = 15;年龄,73±1岁;体重指数,23.8±0.5kg/m²)和肥胖的(n = 10;年龄,71±1岁;体重指数,28.9±1.2kg/m²)对照受试者,以及体型瘦的(n = 10;年龄,75±2岁;体重指数,24.0±0.5kg/m²)和肥胖的(n = 23;年龄,73±1岁;体重指数,29.9±0.7kg/m²)NIDDM患者接受了3小时葡萄糖耐量试验、2小时高血糖葡萄糖钳夹研究以及采用氚标记葡萄糖方法的3小时正常血糖葡萄糖钳夹研究,以测量葡萄糖生成和处置率。
体型瘦和肥胖的NIDDM患者的腰臀比(WHR)均高于对照受试者。肥胖受试者口服葡萄糖耐量试验期间的胰岛素反应相似(对照受试者:417±64pmol/l;NIDDM患者:392±47pmol/l),但体型瘦的NIDDM患者的胰岛素反应降低(对照受试者:374±34pmol/l;NIDDM患者:217±20pmol/l,P<0.01)。体型瘦和肥胖的NIDDM患者在高血糖钳夹期间均无第一相胰岛素反应。体型瘦的NIDDM患者第二相胰岛素反应降低(通过方差分析,与对照受试者相比P<0.01),但肥胖的NIDDM患者未降低第二相胰岛素反应。体型瘦或肥胖的NIDDM患者的肝脏葡萄糖输出均未增加。稳态(150 - 180分钟)葡萄糖处置率在体型瘦的NIDDM患者中降低了16%(对照受试者:8.93±外0.37mg·kg去脂体重(瘦体重)-1·min-1;NIDDM患者:7.50±0.28mg·kg去脂体重-1·min-1,P<0.05),在肥胖的NIDDM患者中降低了37%(对照受试者:8.17±0.38mg·kg去脂体重-1·min-1;NIDDM患者:5.03±0.36mg·kg去脂体重-1·min-1,P<0.001)。
体型瘦的老年NIDDM患者在葡萄糖诱导的胰岛素释放方面有严重损害,但对胰岛素介导的葡萄糖处置有轻度抵抗。肥胖的老年NIDDM患者有足够的循环胰岛素,但对胰岛素介导的葡萄糖处置有明显抵抗。老年NIDDM患者的肝脏葡萄糖输出未增加。