Duke-NUS Medical School, Singapore, Singapore.
Cardiovascular Metabolic Program, Duke-NUS Medical School, Singapore, Singapore.
Obes Surg. 2019 Jan;29(1):149-158. doi: 10.1007/s11695-018-3487-2.
Obesity-induced insulin resistance leads to abnormalities in glucose, lipid, and amino acid metabolism. Our study examined the differences in insulin-mediated glucose, amino acid, and lipid metabolism between morbidly obese subjects with non-obese controls and the associated changes following sleeve gastrectomy (SG).
Non-obese controls and individuals with morbid obesity and scheduled for SG were recruited. Metabolic assessments were performed for all subjects at baseline and at 6 months after SG for eight subjects. The hyperinsulinemic-euglycemic clamp technique together with comprehensive metabolomic profiling was used to quantify insulin-mediated glucose, amino acid, and lipid metabolism.
Eleven morbidly obese non-diabetic subjects scheduled for SG and nine non-obese controls were recruited. Compared to controls, obese subjects had significantly lower glucose uptake (4.4 ± 0.6 vs. 17.3 ± 2.4 mg/kg FFM/min per μU/mL·100) and higher concentration of branched-chain amino acids (BCAAs, 332.5 ± 26.8 vs. 235.3 ± 11.0 μM), non-esterified fatty acid (52.9 ± 9.9 vs. 25.6 ± 6.7 μM), and lipid-related acylcarnitines (intermediate chain 389.8 ± 32.5 vs. 285.9 ± 20.5; long chain 301.7 ± 22.1 vs. 236.0 ± 13.3 nM) during insulin clamp. Body weight significantly reduced at 6 months after bariatric surgery (92.5 ± 6.3 vs. 115.2 ± 6.9 kg), together with improvements in insulin-mediated glucose uptake, and suppression of BCAAs, non-esterified fatty acids, and lipid-related metabolites.
Morbid obesity in Asian individuals was associated with impairment in the regulatory actions of insulin on glucose, amino acid, and lipid metabolism, and these obesity-induced regulatory dysfunctions improved significantly 6 months after SG.
肥胖引起的胰岛素抵抗导致葡萄糖、脂质和氨基酸代谢异常。我们的研究旨在比较病态肥胖患者与非肥胖对照组之间胰岛素介导的葡萄糖、氨基酸和脂质代谢的差异,并观察袖状胃切除术(SG)后的相关变化。
招募了非肥胖对照组和计划接受 SG 的病态肥胖患者。所有受试者在基线时和 SG 后 6 个月时进行代谢评估,其中 8 名受试者进行了 8 次评估。采用高胰岛素-正葡萄糖钳夹技术和全面代谢组学分析,定量检测胰岛素介导的葡萄糖、氨基酸和脂质代谢。
共招募了 11 名计划接受 SG 的病态肥胖非糖尿病患者和 9 名非肥胖对照组。与对照组相比,肥胖组的葡萄糖摄取量明显较低(4.4±0.6 比 17.3±2.4mg/kg 去脂体重/min/μU/mL·100),支链氨基酸(BCAA)、非酯化脂肪酸(NEFA)和脂质相关酰基肉碱的浓度较高(332.5±26.8 比 235.3±11.0μM;52.9±9.9 比 25.6±6.7μM;中间链 389.8±32.5 比 285.9±20.5;长链 301.7±22.1 比 236.0±13.3nM)。SG 后 6 个月,体重显著减轻(92.5±6.3 比 115.2±6.9kg),同时胰岛素介导的葡萄糖摄取增加,BCAA、NEFA 和脂质相关代谢物受到抑制。
亚洲人群的病态肥胖与胰岛素对葡萄糖、氨基酸和脂质代谢的调节作用受损有关,SG 后 6 个月,这些肥胖引起的调节功能障碍显著改善。