Hjøllund E, Pedersen O, Sørensen N S
Diabetes Care. 1987 May-Jun;10(3):306-12. doi: 10.2337/diacare.10.3.306.
Studies of fat cells from patients with newly diagnosed, untreated non-insulin-dependent diabetes mellitus (NIDDM) have revealed severe abnormalities in insulin action on glucose transport and metabolism. To determine whether these defects can be reversed if good glycemic control is reached by dietary treatment, eight moderately obese NIDDM subjects were studied at diagnosis and again when the patients had been in good glycemic control induced by low-energy dieting for at least 2 mo (absence of glycosuria and fasting plasma glucose less than 7 mM). Average body weight decreased by 8 kg (P less than .05). Fasting plasma glucose decreased from 11.5 +/- 1.2 to 6.9 +/- 0.9 mM, whereas fasting serum insulin concentrations were unchanged. Adipocyte insulin binding at tracer concentration (15 pM, 37 degrees C) was not changed significantly (1.94 +/- 0.52 to 2.05 +/- 0.62% per 30 cm2 surface area/ml). The basal (non-insulin-stimulated) glucose transport (tracer glucose concentration 5 microM) increased from 25 +/- 12 to 44 +/- 14 pmol X 90 min-1 X 10 cm-2 surface area (P less than .02). The maximally insulin-stimulated glucose transport rate increased from 35 +/- 20 to 78 +/- 26 pmol/90 min (P less than .01). The percentage insulin response above basal levels increased from 31 +/- 40 to 89 +/- 58% (P less than .01). The insulin sensitivity (half-maximally stimulating insulin concentrations) was also improved (P less than .05). Glucose conversion rates to total lipids increased 34 +/- 62 and 65 +/- 80% in basal cells and maximally insulin-stimulated cells, respectively (.2 greater than P greater than .1, .1 greater than P greater than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
对新诊断出的未经治疗的非胰岛素依赖型糖尿病(NIDDM)患者的脂肪细胞研究显示,胰岛素在葡萄糖转运和代谢方面的作用存在严重异常。为了确定通过饮食治疗实现良好血糖控制后这些缺陷是否可以逆转,对8名中度肥胖的NIDDM受试者在诊断时进行了研究,并在患者通过低能量饮食诱导至少2个月达到良好血糖控制时(无糖尿且空腹血糖低于7 mM)再次进行研究。平均体重下降了8千克(P<0.05)。空腹血糖从11.5±1.2降至6.9±0.9 mM,而空腹血清胰岛素浓度未变。示踪剂浓度(15 pM,37℃)下脂肪细胞胰岛素结合无显著变化(每30 cm2表面积/毫升从1.94±0.52降至2.05±0.62%)。基础(非胰岛素刺激)葡萄糖转运(示踪剂葡萄糖浓度5 microM)从25±12增加到44±14 pmol×90分钟-1×10 cm-2表面积(P<0.02)。最大胰岛素刺激的葡萄糖转运速率从35±20增加到78±26 pmol/90分钟(P<0.01)。高于基础水平的胰岛素反应百分比从31±40增加到89±58%(P<0.01)。胰岛素敏感性(半最大刺激胰岛素浓度)也有所改善(P<0.05)。基础细胞和最大胰岛素刺激细胞中葡萄糖向总脂质的转化率分别增加了34±62%和65±80%(0.2>P>0.1,0.1>P>0.05)。(摘要截取自250字)