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首页> 外文期刊>Metabolism: Clinical and Experimental >13-cis-Retinoic acid therapy induces insulin resistance, regulates inflammatory parameters, and paradoxically increases serum adiponectin concentration.
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13-cis-Retinoic acid therapy induces insulin resistance, regulates inflammatory parameters, and paradoxically increases serum adiponectin concentration.

机译:13-顺式视黄酸疗法可诱导胰岛素抵抗,调节炎症参数并反常增加血清脂联素的浓度。

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摘要

13-cis-Retinoic acid treatment causes insulin resistance and disturbances in lipid and glucose metabolism. We studied how 13-cis-retinoic acid affects inflammatory factors and adiponectin. A total of 23 healthy patients (age, 24.9 +/- 0.9 years; body mass index, 22.6 +/- 0.7 kg/m(2)) who received 13-cis-retinoic acid treatment of acne participated in the study. The patients were studied before the treatment, after 3 months of therapy, and 1 month after the treatment. Inflammatory parameters were measured, and a 4-hour oral glucose tolerance test was performed at each visit. Treatment with 13-cis-retinoic acid resulted in a significantly elevated serum adiponectin concentration (from 24.9 +/- 2.5 to 29.4 +/- 3.6 mg/L, P < .05), hemoglobin A(1c) (from 5.27% +/- 0.05% to 5.42% +/- 0.06%, P < .01), C-peptide area under the curve (from 314.2 +/- 16.6 to 350.0 +/- 21.0 (nmol . min)/L, P < .05), and triglycerides (from 0.97 +/- 0.06 to 1.29 +/- 0.10 mmol/L, P < .05), whereas high-density lipoprotein cholesterol decreased (from 1.50 +/- 0.07 to 1.38 +/- 0.08 mmol/L, P < .05). The increase in adiponectin during 13-cis-retinoic acid therapy correlated with baseline triglycerides (r = 0.51, P < .02). Many inflammatory markers, which were nonsignificantly elevated during therapy, decreased significantly after cessation of treatment. These were C-reactive protein (median from 1.78 to 1.23 mg/L, P < .05), soluble intercellular adhesion molecule 1 (from 210 +/- 10 to 204 +/- 10 microg/L, P < .02), ceruloplasmin (256 +/- 17 to 231 +/- 17 microg/L, P < .02), and erythrocyte sedimentation rate (from 6.4 +/- 1.3 to 4.7 +/- 0.9 mm/h, P < .02). Interleukin 6 concentration was unaffected by the therapy, but decreased significantly after the treatment (from 2.18 +/- 0.46 to 1.65 +/- 0.43 ng/L, P < .05). In conclusion, although treatment with 13-cis-retinoic acid results in disturbances in glucose and lipid metabolism, paradoxically serum adiponectin concentration increases. 13-cis-Retinoic acid has profound effects on the regulation of inflammatory markers.
机译:13-顺式视黄酸治疗会引起胰岛素抵抗,并破坏脂质和葡萄糖代谢。我们研究了13-顺式视黄酸如何影响炎症因子和脂联素。总共接受了13-顺-视黄酸治疗痤疮的23名健康患者(年龄24.9 +/- 0.9岁;体重指数22.6 +/- 0.7 kg / m(2))参加了该研究。在治疗前,治疗后3个月和治疗后1个月对患者进行了研究。测量炎症参数,并在每次就诊时进行4小时口服葡萄糖耐量测试。用13-顺式视黄酸治疗可显着提高血清脂联素浓度(从24.9 +/- 2.5增至29.4 +/- 3.6 mg / L,P <.05),血红蛋白A(1c)(从5.27%+ / -0.05%至5.42%+/- 0.06%,P <.01),曲线下的C肽面积(从314.2 +/- 16.6到350.0 +/- 21.0(nmol。min)/ L,P <.05 )和甘油三酸酯(从0.97 +/- 0.06降低到1.29 +/- 0.10 mmol / L,P <.05),而高密度脂蛋白胆固醇降低(从1.50 +/- 0.07降低到1.38 +/- 0.08 mmol / L ,P <.05)。 13-顺-视黄酸治疗期间脂联素的增加与基线甘油三酸酯相关(r = 0.51,P <.02)。在治疗期间没有明显升高的许多炎症标志物,在停止治疗后显着下降。这些是C反应蛋白(中位数为1.78至1.23 mg / L,P <.05),可溶性细胞间粘附分子1(范围为210 +/- 10至204 +/- 10 microg / L,P <.02),铜蓝蛋白(256 +/- 17至231 +/- 17 microg / L,P <.02)和红细胞沉降速率(从6.4 +/- 1.3至4.7 +/- 0.9 mm / h,P <.02)。白细胞介素6的浓度不受治疗的影响,但在治疗后明显降低(从2.18 +/- 0.46降至1.65 +/- 0.43 ng / L,P <.05)。总之,尽管用13-顺-视黄酸治疗会导致葡萄糖和脂质代谢紊乱,但矛盾的是血清脂联素浓度会增加。 13-顺式视黄酸对炎症标志物的调节具有深远的影响。

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