Patients with type 2 diabetes mellitus (T2DM) have impaired arterial baroreflex function, which may be linked to the co-existence of obesity. However, the role of obesity and its related metabolic impairments on baroreflex dysfunction in T2DM is unknown. This study aimed to investigate the role of visceral fat and adiponectin, the most abundant cytokine produced by adipocytes, on baroreflex dysfunction in T2DM rats. Experiments were performed in adult male UCD-T2DM rats assigned to the following experimental groups (n = 6 in each): prediabetic (Pre), diabetes-onset (T0), 4 weeks after onset (T4), and 12 weeks after onset (T12). Age-matched healthy Sprague-Dawley rats were used as controls. Rats were anesthetized and blood pressure was directly measured on a beat-to-beat basis to assess spontaneous baroreflex sensitivity (BRS) using the sequence technique. Dual-energy X-ray absorptiometry (DEXA) was used to assess body composition. Data are presented as mean ± SD. BRS was significantly lower in T2DM rats compared with controls at T0 (T2D: 3.7 ± 3.2 ms/mmHg vs Healthy: 16.1 ± 8.4 ms/mmHg; P = 0.01), but not at T12 (T2D: 13.4 ± 8.1 ms/mmHg vs Healthy: 9.2 ± 6.0 ms/mmHg; P = 0.16). T2DM rats had higher visceral fat mass, adiponectin, and insulin concentrations compared with control rats (all P < 0.01). Changes in adiponectin and insulin concentrations over the measured time-points mirrored one another and were opposite those of the BRS in T2DM rats. These findings demonstrate that obesity-related metabolic impairments may contribute to an attenuated spontaneous BRS in T2DM, suggesting a link between metabolic and autonomic dysfunction.

2 型糖尿病 （T2DM） 患者的动脉压力反射功能受损，这可能与肥胖的共存有关。然而，肥胖及其相关代谢障碍对 T2DM 压力反射功能障碍的作用尚不清楚。本研究旨在探讨脂肪细胞产生的最丰富的细胞因子内脏脂肪和脂联素对 T2DM 大鼠压力反射功能障碍的影响。在被分配到以下实验组 （每个实验组 n = 6） 的成年雄性 UCD-T2DM 大鼠中进行实验：糖尿病前期 （Pre）、糖尿病发作 （T0）、发病后 4 周 （T4） 和发病后 12 周 （T12）。使用年龄匹配的健康 Sprague-Dawley 大鼠作为对照。对大鼠进行麻醉，并在逐次的基础上直接测量血压，以使用序列技术评估自发压力反射敏感性 （BRS）。双能 X 射线吸收测定法 （DEXA） 用于评估身体成分。数据以平均 ± SD 表示。与 T0 对照组相比，T2DM 大鼠的 BRS 显着降低（T2D：3.7 ± 3.2 ms/mmHg vs 健康：16.1 ± 8.4 ms/mmHg;P = 0.01），但在 T12 时没有（T2D：13.4 ± 8.1 ms/mmHg vs 健康：9.2 ± 6.0 ms/mmHg;P = 0.16）。与对照大鼠相比，T2DM 大鼠内脏脂肪量、脂联素和胰岛素浓度较高 （P均 < 0.01）。脂联素和胰岛素浓度在测量时间点上的变化相互镜像，与 T2DM 大鼠的 BRS 相反。这些发现表明，与肥胖相关的代谢障碍可能导致 T2DM 中自发性 BRS 减弱，这表明代谢和自主神经功能障碍之间存在联系。