应用扩展高胰岛素-正葡萄糖钳夹技术检测肥胖伴糖耐量异常个体的胰岛素敏感性

目的应用扩展高胰岛素-正葡萄糖钳夹技术检测肥胖伴糖耐量异常者的胰岛素敏感性。方法按照WHO1998肥胖及WHO1999糖尿病诊断标准,将52例研究对象分为正常体重-正常糖耐量组、超重/肥胖-正常糖耐量组、超重/肥胖糖耐量减退组及超重/肥胖糖尿病组;将超重/肥胖-正常糖耐量者进一步分为3个亚组:超重亚组、轻度肥胖亚组、中度肥胖亚组。应用核磁共振对所有研究对象进行腹内脂肪测量,以腹腔内脂肪面积100cm2为切割点,将正常糖耐量者分为非腹内型肥胖组(non-VA)及腹内型肥胖组(VA)。以扩展高胰岛素-正葡萄糖钳夹技术检测机体胰岛素敏感性。结果单纯超重/肥胖、超重/肥胖伴糖耐量减退或糖尿病者的葡萄糖消失率分别为(3·25±0·13)、(3·06±0·26)和(3·19±0·44)mg·kg-1·min-1,较正常体重正常糖耐量组的(5·86±0·65)mg·kg-1·min-1显著减少(P<0·05,P<0·01);超重、轻度肥胖及中度肥胖但糖耐量正常亚组的葡萄糖消失率分别为:(3·50±0·19)、(3·03±0·13)和(2·75±0·24)mg·kg-1·min-1,较正常体重正常糖耐量组显著降低(P<0·05,P<0·01)。腹型肥胖组的葡萄糖消失率(2·97±0·12)mg·kg-1·min-1、葡萄糖氧化率(1·47±0·19)mg·kg-1·min-1较非腹型肥胖组的(4·55±0·43)mg·kg-1·min-1和(2·24±0·19)mg·kg-1·min-1显著减少(P<0·05,P<0·01)。体重指数、腰臀比、腰围、腹腔内脂肪面积分别与葡萄糖利用率呈负相关(P<0·05,P<0·01)。体重指数、腹腔内脂肪面积及腹部皮下脂肪面积分别是影响葡萄糖利用率的主要因素。结论超重/肥胖无论伴或不伴糖代谢异常,胰岛素敏感性均显著降低,腹内脂肪增多者胰岛素介导的葡萄糖利用率显著减少,总体脂和腹部脂肪与精确胰岛素敏感性指数呈负相关,总体脂和腹部脂肪是影响机体胰岛素敏感性的主要因素。

Application of extended hyperinsulinemic euglycemic clamp in the assessment of insulin sensitivity in obese individuals with glucose intolerance

OBJECTIVE: To study the changes of insulin sensitivity in individuals with impaired glucose tolerance and diabetes and the relationship between insulin sensitivity and over weight/obesity (OW/OB) . METHODS: Fifty-two individuals were divided into 4 groups according to WHO diagnostic criteria of obesity (1998) and diabetes (1999): normal weight with normal glucose tolerance (NW-NGT) group, OW/OB with normal glucose tolerance (OW/OB-NGT) group, OW/OB with impaired glucose tolerance (OW/OBIGT) group and OW/OB with diabetes mellitus (OW/OB-DM) group. Individuals in OW/OB-NGT group were further classified into 3 subgroups: over weight subgroup, mild obesity subgroup, and mediate obesity subgroup. Abdominal fat area was measured with magnetic resonance imaging. Visceral obesity was defined as intra-abdominal fat area over 100 cm(2). All subjects with NGT were divided into visceral obesity (VA) group and non-visceral obesity ( Non-VA) group. Extended hyperinsulinemic euglycemic clamp was performed to assess the peripheral tissue insulin sensitivity in all subjects. RESULTS: The rates of insulin mediated glucose disappearance (Rd) were (3. 25+/-0. 13) mg x kg (-1) min (-1) in OW/OB-NGT group, (3. 06+/-0. 26) mg x kg(-1) x min(-1) in OW/OB-IGT group, and (3.19+/-0.44) mg x kg(-1) x min (-1) in OW/OB-DM group, which were significantly lower than that in NW-NGT group [ (5. 86+/-0. 65) mg x kg (-1) min (-1) ] (P < 0. 05, P < 0.01). The Rd in over weight subgroup [(3.50+/-0. 19) mg kg(-1) x min(-1) ] , mild obesity subgroup [(3. 03+/-0. 13) mg x kg (-1) min(-1)] , and mediate obesity subgroup [(2. 75 +/-0. 24) mg x kg (-1) min(-1)] were significantly lower than that of NW-NGT group (P <0. 05, P <0. 01). The Rd [ (2. 97+/-0. 12) mg kg(-1) x min(-1) vs (4.55+/-0.43) mg x kg(-1) x min(-1)] and glucose oxidation [(1.47 +/-0. 19) mg x kg(-1) min(-1) vs (2.24 +/-0. 19) mg kg(-1) x min(-1) in VA group were significantly decreased than that in non-VA group (P < 0. 05, P < 0. 01). Body mass index, waist and hip ratio, waist circumference, and intra-abdominal fat area were negatively correlated with Rd, respectively (P < 0. 01). Multiple regression analysis showed that body mass index, intra-abdominal fat area and abdominal subcutaneous fat area were the main risk factors of insulin sensitivity. CONCLUSIONS: Insulin sensitivity decreased in OW/OB individuals with or without hyperglycemia. Insulin sensitivity is lower in subjects with visceral obesity. Total body fat and abdominal fat are the main risk factors of insulin sensitivity.