Disciplina de Medicina Interna, Laboratório de Metabolismo Hidrossalino, Universidade Estadual de Campinas, 13083-592 Campinas, SP, Brasil ; Departamento de Clínica Médica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, 13083-592 Campinas, SP, Brasil.
Nutr Metab (Lond). 2014 Jun 2;11:25. doi: 10.1186/1743-7075-11-25. eCollection 2014.
Obesity is associated with development of the cardiorenal metabolic syndrome, which is a constellation of risk factors, such as insulin resistance, inflammatory response, dyslipidemia, and high blood pressure that predispose affected individuals to well-characterized medical conditions such as diabetes, cardiovascular and kidney chronic disease. The study was designed to establish relationship between metabolic and inflammatory disorder, renal sodium retention and enhanced blood pressure in a group of obese subjects compared with age-matched, lean volunteers.
The study was performed after 14 h overnight fast after and before OGTT in 13 lean (BMI 22.92 ± 2.03 kg/m(2)) and, 27 obese (BMI 36.15 ± 3.84 kg/m(2)) volunteers. Assessment of HOMA-IR and QUICKI index were calculated and circulating concentrations of TNF-α, IL-6 and C-reactive protein, measured by immunoassay.
THE STUDY SHOWS THAT A HYPERINSULINEMIC (HI: 10.85 ± 4.09 μg/ml) subgroup of well-characterized metabolic syndrome bearers-obese subjects show higher glycemic and elevated blood pressure levels when compared to lean and normoinsulinemic (NI: 5.51 ± 1.18 μg/ml, P < 0.027) subjects. Here, the combination of hyperinsulinemia, higher HOMA-IR (HI: 2.19 ± 0.70 (n = 12) vs. LS: 0.83 ± 0.23 (n = 12) and NI: 0.98 ± 0.22 (n = 15), P < 0.0001) associated with lower QUICKI in HI obese when compared with LS and NI volunteers (P < 0.0001), suggests the occurrence of insulin resistance and a defect in insulin-stimulated peripheral action. Otherwise, the adiponectin measured in basal period was significantly enhanced in NI subjects when compared to HI groups (P < 0.04). The report also showed a similar insulin-mediated reduction of post-proximal urinary sodium excretion in lean (LS: 9.41 ± 0.68% vs. 6.38 ± 0.92%, P = 0.086), and normoinsulinemic (NI: 8.41 ± 0.72% vs. 5.66 ± 0.53%, P = 0.0025) and hyperinsulinemic obese subjects (HI: 8.82 ± 0.98% vs. 6.32 ± 0.67%, P = 0.0264), after oral glucose load, despite elevated insulinemic levels in hyperinsulinemic obeses.
In conclusion, this study highlights the importance of adiponectin levels and dysfunctional inflammatory modulation associated with hyperinsulinemia and peripheral insulin resistance, high blood pressure, and renal dysfunction in a particular subgroup of obeses.
肥胖与心脏代谢综合征的发生有关，后者是一组风险因素，如胰岛素抵抗、炎症反应、血脂异常和高血压，使受影响的个体容易出现糖尿病、心血管和肾脏慢性疾病等明确的医学病症。本研究旨在比较肥胖组与年龄匹配的瘦对照组之间，代谢和炎症紊乱、肾钠潴留和血压升高之间的关系。
在 13 名瘦（BMI 22.92 ± 2.03 kg/m²）和 27 名肥胖（BMI 36.15 ± 3.84 kg/m²）志愿者中，在 OGTT 前后进行了 14 小时的夜间禁食。计算 HOMA-IR 和 QUICKI 指数，并通过免疫测定法测量循环 TNF-α、IL-6 和 C 反应蛋白浓度。
研究表明，一组具有典型代谢综合征特征的高胰岛素血症（HI：10.85 ± 4.09 µg/ml）肥胖者，与瘦和正常胰岛素血症（NI：5.51 ± 1.18 µg/ml，P < 0.027）的肥胖者相比，血糖水平更高，血压水平升高。在此，高胰岛素血症、更高的 HOMA-IR（HI：2.19 ± 0.70（n = 12）与 LS：0.83 ± 0.23（n = 12）和 NI：0.98 ± 0.22（n = 15），P < 0.0001）与 HI 肥胖者中较低的 QUICKI 相关（P < 0.0001），提示发生了胰岛素抵抗和胰岛素刺激外周作用的缺陷。此外，与 HI 组相比，NI 组在基础期测量的脂联素显著升高（P < 0.04）。报告还显示，在瘦（LS：9.41 ± 0.68% 与 6.38 ± 0.92%，P = 0.086）和正常胰岛素血症（NI：8.41 ± 0.72% 与 5.66 ± 0.53%，P = 0.0025）和高胰岛素血症肥胖者中，胰岛素介导的近端尿钠排泄减少相似（HI：8.82 ± 0.98% 与 6.32 ± 0.67%，P = 0.0264），尽管 HI 肥胖者的胰岛素水平升高。
总之，本研究强调了脂联素水平和与高胰岛素血症和外周胰岛素抵抗、高血压和肾功能障碍相关的炎症调节功能障碍在肥胖特定亚组中的重要性。
