Kurajoh Masafumi, Koyama Hidenori, Kadoya Manabu, Naka Mariko, Miyoshi Akio, Kanzaki Akinori, Kakutani-Hatayama Miki, Okazaki Hirokazu, Shoji Takuhito, Moriwaki Yuji, Yamamoto Tetsuya, Emoto Masanori, Inaba Masaaki, Namba Mitsuyoshi
Division of Diabetes, Endocrinology and Metabolism, Department of Internal Medicine, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo, 663-8501, Japan.
Department of Endocrinology, Metabolism and Molecular Medicine, Osaka City University Graduate School of Medicine, Osaka, Japan.
Cardiovasc Diabetol. 2015 Sep 4;14:117. doi: 10.1186/s12933-015-0280-6.
It has been shown that visceral fat accumulation is associated with autonomic dysfunction, though the precise mechanism remains unclear. A recent basic study found that leptin can directly modulate autonomic function through the dorsomedial hypothalamus in relation to obesity. Here, we investigated the mutual relationships among plasma leptin, visceral fat accumulation, and cardiac autonomic dysfunction in patients with type 2 diabetes.
This cross-sectional study included 100 diabetic patients, and 100 age- and gender-matched non-diabetic patients with cardiovascular risk factors. Plasma leptin and soluble leptin receptor levels, visceral fat area (VFA), and heart rate variability (HRV) were determined in addition to classical cardiovascular risk factors.
In the type 2 diabetic patients, VFA was significantly (p < 0.05) and inversely associated with HRV parameters (SDNN: r = -0.243; SDANN5: r = -0.238), while the plasma level of leptin, but not soluble leptin receptor, was also significantly (p < 0.05) and inversely associated with HRV parameters (SDNN: r = -0.243; SDANN5: r = -0.231). Multiple regression analysis showed that plasma leptin was significantly associated with SDNN and SDANN5 independent of other factors, including age, gender, presence of hypertension and dyslipidemia, duration of diabetes, HbA1c, and eGFR. Furthermore, the relationship of leptin with SDNN and SDANN5 (β = -0.279 and -0.254, respectively) remained significant (p < 0.05) after adjustment for VFA. In patients without diabetes, no significant associations were observed between leptin and any of the HRV parameters.
Hyperleptinemia may be involved in cardiac autonomic dysfunction in patients with type 2 diabetes and visceral obesity.
已有研究表明内脏脂肪堆积与自主神经功能障碍有关,但其确切机制仍不清楚。最近一项基础研究发现,瘦素可通过下丘脑背内侧核直接调节与肥胖相关的自主神经功能。在此,我们研究了2型糖尿病患者血浆瘦素、内脏脂肪堆积和心脏自主神经功能障碍之间的相互关系。
这项横断面研究纳入了100例糖尿病患者以及100例年龄和性别匹配、有心血管危险因素的非糖尿病患者。除了经典的心血管危险因素外,还测定了血浆瘦素和可溶性瘦素受体水平、内脏脂肪面积(VFA)以及心率变异性(HRV)。
在2型糖尿病患者中,VFA与HRV参数(SDNN:r = -0.243;SDANN5:r = -0.238)显著负相关(p < 0.05),而血浆瘦素水平而非可溶性瘦素受体水平也与HRV参数显著负相关(p < 0.05)(SDNN:r = -0.243;SDANN5:r = -0.231)。多元回归分析显示,血浆瘦素与SDNN和SDANN5显著相关,独立于其他因素,包括年龄、性别、高血压和血脂异常的存在、糖尿病病程、糖化血红蛋白(HbA1c)和估算肾小球滤过率(eGFR)。此外,在调整VFA后,瘦素与SDNN和SDANN5的关系(β分别为-0.279和-0.254)仍然显著(p < 0.05)。在无糖尿病患者中,未观察到瘦素与任何HRV参数之间存在显著关联。
高瘦素血症可能参与2型糖尿病和内脏肥胖患者的心脏自主神经功能障碍。