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，肥胖及其相关代谢损伤对 T2DM 压力感受反射功能障碍的作用尚不清楚。本研究旨在探讨内脏脂肪和脂联素（脂肪细胞产生的最丰富的细胞因子）对 T2DM 大鼠压力感受反射功能障碍的作用。实验在成年雄性 UCD-T2DM 大鼠中进行，分配到以下实验组（每组 n = 6）：糖尿病前期（Pre）、糖尿病发病（T0）、发病后 4 周（T4）和发病后 12 周（T4）。 T12）。使用年龄匹配的健康 Sprague-Dawley 大鼠作为对照。将大鼠麻醉并直接逐次测量血压，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。数据以平均值±标准差表示。与 T0 时的对照组相比，T2DM 大鼠的 BRS 显着降低（T2D：3.7 ± 3.2 ms/mmHg 对比健康：16.1 ± 8.4 ms/mmHg；P = 0.01），但在 T12 时则不然（T2D：13.4 ± 8.1 ms/mmHg 对比健康：9.2 ± 6.0 ms/mmHg；P = 0.16）。与对照大鼠相比，T2DM 大鼠的内脏脂肪量、脂联素和胰岛素浓度较高（均 P < 0.01）。在测量的时间点上脂联素和胰岛素浓度的变化彼此镜像，并且与 T2DM 大鼠的 BRS 的变化相反。这些发现表明，肥胖相关的代谢损伤可能导致 T2DM 中自发 BRS 减弱，这表明代谢与自主神经功能障碍之间存在联系。