Hayashi Tomoshige, Boyko Edward J, Leonetti Donna L, McNeely Marguerite J, Newell-Morris Laura, Kahn Steven E, Fujimoto Wilfred Y
Epidemiologic Research and Information Center, Veterans Affairs Puget Sound Health Care System, Seattle, Washington 98108, USA.
Diabetes Care. 2003 Mar;26(3):650-5. doi: 10.2337/diacare.26.3.650.
Greater visceral adiposity, higher insulin resistance, and impaired insulin secretion increase the risk of type 2 diabetes. Whether visceral adiposity increases risk of impaired glucose tolerance (IGT) independent of other adipose depots, insulin resistance, and insulin secretion is not known.
Study subjects included 128 Japanese Americans with normal glucose tolerance at entry. Baseline variables included plasma glucose and insulin measured after an overnight fast and during a 75-g oral glucose tolerance test, fat areas by computed tomography, insulin secretion (incremental insulin response [IIR] [30 min insulin - fasting insulin]/30 min glucose), and insulin resistance index (homeostasis model assessment for insulin resistance [HOMA-IR]).
During the 10- to 11-year follow-up period, we confirmed 57 cases of IGT. Significant predictors of IGT included intra-abdominal fat area (IAFA) (odds ratio [OR] for a 1 SD increase 3.82, 95% CI 1.63-8.94 at a fasting plasma glucose [FPG] level of 4.5 mmol/l), HOMA-IR (2.41, 1.15-5.04), IIR (0.30, 0.13-0.69 at an FPG level of 4.5 mmol/l), the interactions of IAFA by FPG (P = 0.003), and IIR by FPG (P = 0.030) after adjusting for age, sex, FPG, and BMI. The multiple-adjusted OR of IAFA increased and that of IIR decreased as FPG level decreased because of these interactions. Even after adjustment for total fat area, total subcutaneous fat area, or abdominal subcutaneous fat area, all of these associations remained a significant predictor of IGT incidence.
Greater visceral adiposity increases the risk of IGT independent of insulin resistance, insulin secretion, and other adipose depots in Japanese Americans.
内脏脂肪增多、胰岛素抵抗增强以及胰岛素分泌受损会增加2型糖尿病的风险。内脏脂肪增多是否独立于其他脂肪储存部位、胰岛素抵抗和胰岛素分泌而增加糖耐量受损(IGT)的风险尚不清楚。
研究对象包括128名入组时糖耐量正常的日裔美国人。基线变量包括空腹过夜后及75克口服葡萄糖耐量试验期间测得的血浆葡萄糖和胰岛素、通过计算机断层扫描测得的脂肪面积、胰岛素分泌(胰岛素增量反应[IIR][30分钟胰岛素-空腹胰岛素]/30分钟葡萄糖)以及胰岛素抵抗指数(胰岛素抵抗稳态模型评估[HOMA-IR])。
在10至11年的随访期内,我们确诊了57例IGT病例。IGT的显著预测因素包括腹内脂肪面积(IAFA)(在空腹血糖[FPG]水平为4.5毫摩尔/升时,每增加1个标准差的比值比[OR]为3.82,95%置信区间为1.63 - 8.94)、HOMA-IR(2.41,1.15 - 5.04)、IIR(在FPG水平为4.5毫摩尔/升时为0.30,0.13 - 0.69),在调整年龄、性别、FPG和BMI后,IAFA与FPG的相互作用(P = 0.003)以及IIR与FPG的相互作用(P = 0.030)。由于这些相互作用,随着FPG水平降低,IAFA的多因素调整OR升高,IIR的多因素调整OR降低。即使在调整了总脂肪面积、总皮下脂肪面积或腹部皮下脂肪面积后,所有这些关联仍然是IGT发病的显著预测因素。
在内脏脂肪增多的日裔美国人中,内脏脂肪增多独立于胰岛素抵抗、胰岛素分泌和其他脂肪储存部位增加了IGT的风险。