Miranda Merce, Ceperuelo-Mallafré Victòria, Lecube Albert, Hernandez Cristina, Chacon Matilde R, Fort Jose M, Gallart Lluís, Baena-Fustegueras Juan A, Simó Rafael, Vendrell Joan
Unitat de Recerca, Hospital Universitari de Tarragona Joan XXIII, IISPV, 43007 Tarragona, Spain.
Metabolism. 2009 Dec;58(12):1762-8. doi: 10.1016/j.metabol.2009.06.004. Epub 2009 Jul 16.
The trafficking of glycerol from adipose and hepatic tissue is mainly mediated by 2 aquaporin channel proteins: AQP7 and AQP9, respectively. In rodents, both aquaporins were found to act in a coordinated manner. The aim was to study the relationship between adipose AQP7 and hepatic AQP9 messenger RNA expression and the presence of glucose abnormalities simultaneously in morbid obesity. Adipose tissue (subcutaneous [SAT] and visceral [VAT]) and liver biopsies from the same patient were obtained during bariatric surgery in 30 (21 male and 9 female) morbidly obese subjects. Real-time quantification of AQP7 in SAT and VAT and hepatic AQP9 gene expression were performed. A 75-g oral glucose tolerance test was performed in all subjects. The homeostasis model assessment of insulin resistance and lipidic profile were also determined. Visceral adipose tissue AQP7 expression levels were significantly higher than SAT AQP7 (P = .009). Subcutaneous adipose tissue AQP7 positively correlated with both VAT AQP7 and hepatic AQP9 messenger RNA expression (r = 0.44, P = .013 and r = 0.45, P = .012, respectively). The correlation between SAT AQP7 and liver AQP9 was stronger in intolerant and type 2 diabetes mellitus subjects (r = 0.602, P = .011). We have found no differences in compartmental AQP7 adipose tissue distribution or AQP9 hepatic gene expression according to glucose tolerance classification. The present study provides, for the first time, evidence of coordinated regulation between adipose aquaglyceroporins, with a greater expression found in visceral fat, and between subcutaneous adipose AQP7 and hepatic AQP9 gene expression within the context of human morbid obesity.
水通道蛋白7(AQP7)和水通道蛋白9(AQP9)。在啮齿动物中,发现这两种水通道蛋白以协同方式发挥作用。本研究旨在探讨病态肥胖患者脂肪组织AQP7和肝脏AQP9信使核糖核酸表达之间的关系以及同时存在的血糖异常情况。在30例(21例男性和9例女性)病态肥胖受试者接受减重手术期间,获取了同一患者的脂肪组织(皮下脂肪组织[SAT]和内脏脂肪组织[VAT])以及肝脏活检样本。对SAT和VAT中的AQP7以及肝脏AQP9基因表达进行了实时定量分析。所有受试者均进行了75克口服葡萄糖耐量试验。还测定了胰岛素抵抗的稳态模型评估指标和血脂谱。内脏脂肪组织AQP7表达水平显著高于SAT AQP7(P = 0.009)。皮下脂肪组织AQP7与VAT AQP7和肝脏AQP9信使核糖核酸表达均呈正相关(分别为r = 0.44,P = 0.013和r = 0.45,P = 0.012)。在糖耐量异常和2型糖尿病受试者中,SAT AQP7与肝脏AQP9之间的相关性更强(r = 0.602,P = 0.011)。根据葡萄糖耐量分类,我们未发现不同部位脂肪组织中AQP7分布或肝脏AQP9基因表达存在差异。本研究首次提供了在人类病态肥胖背景下,脂肪组织水甘油通道蛋白之间协同调节的证据,其中在内脏脂肪中表达更高,以及皮下脂肪AQP7与肝脏AQP9基因表达之间协同调节的证据。