Î²-cell function is a major contributor to oral glucose tolerance in high-risk relatives of four ethnic groups in the US-猫眼课题宝

DOI：

10.2337/diabetes.51.7.2170

发表时间：

2002-07-01

期刊：

DIABETES

影响因子：

7.7

通讯作者：

中科院分区：

医学1区

文献类型：

作者：

Jensen, CC;Cnop, M;Kahn, SE

2型糖尿病患者的一级亲属患高血糖的风险增加。对531名无糖尿病病史的一级亲属(年龄44.1+/-0.7岁，体重指数29.0+/-0.3 kg/m(2))进行口服葡萄糖耐量试验(OGTT)。新发现的糖尿病占19%(n=100)，空腹血糖受损(IFG)和/或糖耐量受损(IGT)占36%(n=191)。因此，只有45%(n=240)的人糖耐量正常(NGT)。胰岛素抵抗的稳态模型评估(HOMA-IR)用于评估胰岛素敏感性；P细胞功能以OGTT(DeltaI(30)/DeltaG(30))期间前30分钟增量胰岛素与葡萄糖反应的比率来量化。后一项指标还根据胰岛素敏感性进行了调整，因为它调节了β细胞功能([DeltaI(30)/DeltaG(30)]/HOMA-IR)。糖耐量降低与胰岛素抵抗增加(HOMA：NGT12.01+/-0.54pmoL/mmo1；IFG/IGT16.14+/-0.84；糖尿病26.99+/-2.62；P&lt；0.001)和β细胞功能降低(DeltaI(30)/DeltaG(30)：NGT12.01+/-9.7pmoL/mmo1；IFG/IGT 100.4+/-5.4；糖尿病57.5+/-7.3P&lt；0.001)相关。在根据胰岛素敏感性调整这一指标时，也发现了β细胞功能的下降([DeltaI(30)/DeltaG(30)/HOMA-IR)。在所有四个民族(非洲裔美国人，n=55；亚裔美国人，n=66；高加索人，n=217；西班牙裔美国人，n=193)中，IFG/IGT和糖尿病受试者表现出逐渐增加的胰岛素抵抗和降低的β细胞功能。在整个队列中检查胰岛素敏感性和胰岛细胞功能与葡萄糖处置的关系，通过曲线下增量葡萄糖面积(AUCG)来衡量。胰岛素敏感性与AUCG呈线性相关，因此胰岛素抵抗与较差的葡萄糖处置相关(r(2)=0.084，P&lt；0.001)。相反，P细胞功能和AUCG之间存在着强烈的反曲线关系，胰岛素释放较差与葡萄糖处置较差相关[DeltaI(30)/DeltaG(30)]：R(2)=0.29，P&lt；0.001；LOG[(DeltaI(30)/DeltaG(30))/HOMA-IR]：R(2)=0.45，P&lt；0.001。因此，糖代谢异常在2型糖尿病患者的一级亲属中很常见。在所有种族中，胰岛素抵抗和β细胞功能受损都与葡萄糖代谢受损有关，其中β细胞功能似乎在决定葡萄糖处置方面更重要。

First-degree relatives of individuals with type 2 diabetes are at increased risk of developing hyperglycemia. To examine the prevalence and pathogenesis of abnormal glucose homeostasis in these subjects, 531 first-degree relatives with no known history of diabetes (aged 44.1 +/- 0.7 years; BMI 29.0 +/- 0.3 kg/m(2)) underwent an oral glucose tolerance test (OGTT). Newly identified diabetes was found in 19% (n = 100), and impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) was found in 36% (n = 191). Thus, only 45% (n = 240) had normal glucose tolerance (NGT). The homeostasis model assessment of insulin resistance (HOMA-IR) was used to estimate insulin sensitivity; P-cell function was quantified as the ratio of the incremental insulin to glucose responses over the first 30 min during the OGTT (DeltaI(30)/DeltaG(30)). This latter measure was also adjusted for insulin sensitivity as it modulates beta-cell function ([DeltaI(30)/DeltaG(30)]/HOMA-IR). Decreasing glucose tolerance was associated with increasing insulin resistance (HOMA: NGT 12.01 +/- 0.54 pmol/mmol; IFG/IGT 16.14 +/- 0.84; diabetes 26.99 +/- 2.62; P < 0.001) and decreasing beta-cell function (DeltaI(30)/DeltaG(30): NGT 157.7 +/- 9.7 pmol/mmol; IFG/IGT 100.4 +/- 5.4; diabetes 57.5 +/- 7.3; P < 0.001). Decreasing beta-cell function was also identified when adjusting this measure for insulin sensitivity ([DeltaI(30)/DeltaG(30)/HOMA-IR). In all four ethnic groups (African-American, n = 55; Asian-American, n = 66; Caucasian, n = 217; Hispanic-American, n = 193), IFG/IGT and diabetic subjects exhibited progressively increasing insulin resistance and decreasing beta-cell function. The relationships of insulin sensitivity and beta-cell function to glucose disposal, as measured by the incremental glucose area under the curve (AUCg), were examined in the whole cohort. Insulin sensitivity and AUCg were linearly related so that insulin resistance was associated with poorer glucose disposal (r(2) = 0.084, P < 0.001). In contrast, there was a strong inverse curvilinear relationship between P-cell function and AUCg such that poorer insulin release was associated with poorer glucose disposal log[DeltaI(30)/DeltaG(30)]: r(2) = 0.29, P < 0.001; log[(DeltaI(30)/DeltaG(30))/HOMA-IR]: r(2) = 0.45, P < 0.001). Thus, abnormal glucose metabolism is common in first-degree relatives of subjects with type 2 diabetes. Both insulin resistance and impaired beta-cell function are associated with impaired glucose metabolism in all ethnic groups, with beta-cell function seeming to be more important in determining glucose disposal.

Î²-cell function is a major contributor to oral glucose tolerance in high-risk relatives of four ethnic groups in the US

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