Department of Research and Evaluation, Kaiser Permanente Southern California, Pasadena, CA
Division of Endocrinology and Diabetes, Department of Medicine, Keck School of Medicine of the University of Southern California, Los Angeles, CA.
Diabetes Care. 2018 Dec;41(12):2544-2551. doi: 10.2337/dc18-1662. Epub 2018 Oct 3.
Type 2 diabetes (T2D) results from progressive loss of β-cell function. The BetaFat study compared gastric banding and metformin for their impact on β-cell function in adults with moderate obesity and impaired glucose tolerance (IGT) or recently diagnosed, mild T2D.
Eighty-eight people aged 21-65 years, BMI 30-40 kg/m, with IGT or diabetes known for <1 year, were randomized to gastric banding or metformin for 2 years. Hyperglycemic clamps (11.1 mmol/L) followed by arginine injection at maximally potentiating glycemia (>25 mmol/L) were performed at baseline, 12 months, and 24 months to measure steady-state C-peptide (SSCP) and acute C-peptide response to arginine at maximum glycemic potentiation (ACPRmax) and insulin sensitivity (M/I).
At 24 months, the band group lost 10.7 kg; the metformin group lost 1.7 kg ( < 0.01). Insulin sensitivity increased 45% in the band group and 25% in the metformin group ( = 0.30 between groups). SSCP adjusted for insulin sensitivity fell slightly but not significantly in each group ( = 0.34 between groups). ACPRmax adjusted for insulin sensitivity fell significantly in the metformin group ( = 0.002) but not in the band group ( = 0.25 between groups). HbA fell at 12 and 24 months in the band group ( < 0.004) but only at 12 months ( < 0.01) in the metformin group ( > 0.14 between groups). Normoglycemia was present in 22% and 15% of band and metformin groups, respectively, at 24 months ( = 0.66 between groups).
Gastric banding and metformin had similar effects to preserve β-cell function and stabilize or improve glycemia over a 2-year period in moderately obese adults with IGT or recently diagnosed, mild T2D.
2 型糖尿病(T2D)是由于β细胞功能进行性丧失引起的。BetaFat 研究比较了胃束带术和二甲双胍对中重度肥胖伴糖耐量受损(IGT)或新近诊断的轻度 T2D 成人β细胞功能的影响。
88 名年龄在 21-65 岁、BMI 为 30-40kg/m2 的患者,IGT 或糖尿病病史<1 年,随机分为胃束带术组或二甲双胍组,治疗 2 年。在基线、12 个月和 24 个月时,进行高血糖钳夹(11.1mmol/L),随后在最大血糖增强时(>25mmol/L)给予精氨酸注射,以测量稳态 C 肽(SSCP)和急性 C 肽对最大血糖增强(ACPRmax)和胰岛素敏感性(M/I)的反应。
24 个月时,束带组体重减轻 10.7kg;二甲双胍组体重减轻 1.7kg(<0.01)。束带组胰岛素敏感性增加 45%,二甲双胍组增加 25%(组间差异=0.30)。两组 SSCP 均略有下降,但无统计学意义(组间差异=0.34)。调整胰岛素敏感性后,二甲双胍组 ACPRmax 显著下降(=0.002),但束带组无显著变化(组间差异=0.25)。在束带组,HbA 在 12 个月和 24 个月时下降(<0.004),而在二甲双胍组仅在 12 个月时下降(<0.01)(组间差异>0.14)。在 24 个月时,束带组和二甲双胍组的正常血糖分别为 22%和 15%(组间差异=0.66)。
在中重度肥胖伴 IGT 或新近诊断的轻度 T2D 成人中,胃束带术和二甲双胍在 2 年内对β细胞功能具有相似的保护作用,并稳定或改善血糖水平。