Ebenibo Sotonte, Edeoga Chimaroke, Owei Ibiye, Dagogo-Jack Sam
Division of Endocrinology, Diabetes and Metabolism, University of Tennessee Health Science Center, Memphis, TN, United States.
Front Endocrinol (Lausanne). 2018 Jan 26;9:12. doi: 10.3389/fendo.2018.00012. eCollection 2018.
Fasting plasma leptin levels reflect fat mass, but dynamic leptin responses to secretagogues, and the influence of race/ethnicity, have not been well studied. Here, we compared basal and stimulated leptin levels in relation to cardiometabolic risk and weight trajectories in black and white subjects.
We studied 254 (127 black and 127 white) normoglycemic adults enrolled in the Pathobiology of Prediabetes in a Biracial Cohort (POP-ABC) study. At baseline and annually, POP-ABC participants underwent physical examination, oral glucose tolerance test, and measurements of body fat (dual energy X-ray absorptiometry), fasting plasma leptin, insulin, cortisol, lipids, and leptin secretory response to single-dose (2 mg) dexamethasone (dex). The interactions among basal and stimulated leptin and changes in adiposity/cardiometabolic measures during the ensuing year were then analyzed.
The mean (±SD) fasting leptin level (50.6 ± 47.7 vs. 39.5 ± 37.6 ng/mL, = 0.004) and body mass index (BMI) (31.9 ± 7.14 vs. 29.0 ± 7.66 kg/m, = 0.0043) were higher in black women vs. white women, but similar in black men vs. white men (leptin: 12.4 ± 2.07 vs. 11.1 ± 1.40 ng/mL; BMI: 29.4 ± 7.68 vs. 28.1 ± 4.23 kg/m). The peak leptin response to dex (~200% baseline) did not differ significantly by gender or race. Total body fat correlated positively with fasting leptin ( = 0.81, < 0.0001) and inversely stimulated leptin levels ( = -0.26, < 0.0001). Fasting leptin was unrelated to 1-year change in weight or fat mass, whereas stimulated leptin levels were significantly associated with 1-year trajectories in weight ( = 0.0016) and total fat mass ( = 0.0035). Stimulated leptin levels also had significant interactions with insulin sensitivity (homeostasis model of insulin resistance, = 0.01), triglycerides ( = 0.0078), fasting glucose ( = 0.027), systolic blood pressure ( = 0.037), and high-sensitivity C-reactive protein ( = 0.027).
We found no significant ethnic disparities in basal or dynamic leptin secretion in relation to adiposity. Fasting leptin levels were not associated with 1-year weight change, while stimulated levels showed weak though significant association with 1-year weight change.
空腹血浆瘦素水平反映脂肪量,但瘦素对促分泌素的动态反应以及种族/民族的影响尚未得到充分研究。在此,我们比较了黑人和白人受试者基础和刺激后的瘦素水平与心脏代谢风险及体重轨迹的关系。
我们研究了254名(127名黑人与127名白人)血糖正常的成年人,他们参与了双种族队列中糖尿病前期病理生物学(POP-ABC)研究。在基线时及每年,POP-ABC参与者接受体格检查、口服葡萄糖耐量试验,并测量体脂(双能X线吸收法)、空腹血浆瘦素、胰岛素、皮质醇、血脂,以及单剂量(2毫克)地塞米松(地米)刺激后的瘦素分泌反应。然后分析基础和刺激后瘦素与随后一年中肥胖/心脏代谢指标变化之间的相互作用。
黑人女性的平均(±标准差)空腹瘦素水平(50.6±47.7对39.5±37.6纳克/毫升,P = 0.004)和体重指数(BMI)(31.9±7.14对29.0±7.66千克/米²,P = 0.0043)高于白人女性,但黑人男性与白人男性相似(瘦素:12.4±2.07对11.1±1.40纳克/毫升;BMI:29.4±7.68对28.1±4.23千克/米²)。地米刺激后瘦素的峰值反应(约为基线的200%)在性别或种族上无显著差异。全身脂肪与空腹瘦素呈正相关(r = 0.81,P < 0.0001),与刺激后瘦素水平呈负相关(r = -0.26,P < 0.0001)。空腹瘦素与1年体重或脂肪量变化无关,而刺激后瘦素水平与1年体重轨迹(P = 0.0016)和总脂肪量轨迹(P = 0.0035)显著相关。刺激后瘦素水平还与胰岛素敏感性(胰岛素抵抗稳态模型,P = 0.01)、甘油三酯(P = 0.0078)、空腹血糖(P = 0.027)、收缩压(P = 0.037)和高敏C反应蛋白(P = 0.027)有显著相互作用。
我们发现基础或动态瘦素分泌与肥胖相关方面不存在显著的种族差异。空腹瘦素水平与1年体重变化无关,而刺激后瘦素水平与1年体重变化呈弱但显著的关联。