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减肥手术后,血清胆汁酸以及血浆肠促胰岛素和血清高分子量脂联素水平会升高。

Serum bile acid along with plasma incretins and serum high-molecular weight adiponectin levels are increased after bariatric surgery.

作者信息

Nakatani Hiroshi, Kasama Kazunori, Oshiro Takashi, Watanabe Mitsuhiro, Hirose Hiroshi, Itoh Hiroshi

机构信息

Department of Internal Medicine, Keio University School of Medicine, Tokyo 160-8582, Japan.

出版信息

Metabolism. 2009 Oct;58(10):1400-7. doi: 10.1016/j.metabol.2009.05.006. Epub 2009 Jul 1.

Abstract

Bariatric surgery has been shown to improve glucose tolerance, although the mechanism has not been fully elucidated. Animal studies have suggested important roles of bile acid (BA) as a regulator of energy homeostasis and glucose metabolism. However, little is known about its role in humans. We investigated the longitudinal changes of BA, incretins, and adipokines after significant weight reduction in 34 Japanese adults with morbid obesity who underwent laparoscopic bariatric surgery. In subjects who underwent malabsorptive or restrictive surgery, body mass index had markedly decreased from 43.0 +/- 6.5 (SD) to 37.8 +/- 5.7 kg/m(2) and from 45.3 +/- 11.2 to 41.5 +/- 10.5 kg/m(2), respectively, at 1 month after surgery. Glycated hemoglobin decreased from 6.1% +/- 1.5% to 5.2% +/- 0.4% and from 6.2% +/- 1.3% to 5.4% +/- 0.7%, and total BA level increased from 3.1 +/- 3.5 to 7.2 +/- 5.3 mumol/L and from 3.2 +/- 2.6 to 9.4 +/- 10.0 mumol/L, respectively. At baseline, serum concentration of primary BA was positively correlated with plasma gastric inhibitory polypeptide level (r = 0.548, P = .001); and change in primary BA level was positively correlated with changes in plasma gastric inhibitory polypeptide (r = 0.626, P = .001) and serum immunoreactive insulin level (r = 0.592, P = .002) at 1 month after surgery. Furthermore, plasma glucagon-like peptide-1 and serum high-molecular weight adiponectin levels increased in both surgeries. These hormonal changes might explain the mechanism(s) of improved glucose tolerance after bariatric surgery in morbidly obese subjects.

摘要

减肥手术已被证明可改善糖耐量,但其机制尚未完全阐明。动物研究表明,胆汁酸(BA)作为能量稳态和葡萄糖代谢的调节因子具有重要作用。然而,其在人类中的作用却知之甚少。我们调查了34名接受腹腔镜减肥手术的日本病态肥胖成年人在体重显著减轻后BA、肠促胰岛素和脂肪因子的纵向变化。在接受吸收不良或限制性手术的受试者中,术后1个月时,体重指数分别从43.0±6.5(标准差)显著降至37.8±5.7kg/m²,以及从45.3±11.2降至41.5±10.5kg/m²。糖化血红蛋白分别从6.1%±1.5%降至5.2%±0.4%,以及从6.2%±1.3%降至5.4%±0.7%,总BA水平分别从3.1±3.5升至7.2±5.3μmol/L,以及从3.2±2.6升至9.4±10.0μmol/L。基线时,初级BA的血清浓度与血浆胃抑制多肽水平呈正相关(r = 0.548,P = 0.001);术后1个月时,初级BA水平的变化与血浆胃抑制多肽的变化呈正相关(r = 0.626,P = 0.001),与血清免疫反应性胰岛素水平也呈正相关(r = 0.592,P = 0.002)。此外,两种手术中血浆胰高血糖素样肽-1和血清高分子量脂联素水平均升高。这些激素变化可能解释了病态肥胖受试者减肥手术后糖耐量改善的机制。

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