Ramírez-Vélez Robinson, González-Ruíz Katherine, González-Jiménez Emilio, Schmidt-RioValle Jacqueline, Correa-Rodríguez María, García-Hermoso Antonio, Palomino-Echeverría Sara, Izquierdo Mikel
Navarrabiomed, Complejo Hospitalario de Navarra (CHN)-Universidad Pública de Navarra (UPNA), IDISNA, 31008, Pamplona, Spain; CIBER of Frailty and Healthy Aging (CIBERFES), Institute of Health Carlos III, Madrid, Spain.
Physical Exercise and Sports Research Group, Vice Chancellor for Research, Manuela Beltrán University (UMB), Bogotá, DC, 110231, Colombia.
Nutr Metab Cardiovasc Dis. 2021 Apr 9;31(4):1308-1316. doi: 10.1016/j.numecd.2020.12.014. Epub 2021 Feb 19.
The relationship between insulin resistance (IR) and hepatic steatosis (fatty liver) is well known; however, the extent to which the satiety hormone leptin acts as a confounder or mediator in this relationship is uncertain. We examined whether the association between IR and hepatic steatosis is mediated by leptin in Colombian adolescents with excess adiposity.
A total of 122 adolescents (mean age: 13.4 years; 68% girls) participated in the study. We assessed body composition, hepatic steatosis (as defined by the controlled attenuation parameter [CAP]), cardiometabolic risk factors (body mass index, waist circumference, body composition), biochemical variables (leptin, insulin, glucose, lipid profile, cardiometabolic Z-score, transaminases, etc.), and physical fitness (cardiorespiratory fitness and grip strength). Partial correlation, regression, and mediation analyses were conducted using the Barron and Kenny framework.
Ninety-two youths (75.4%) had IR. Mediation analysis revealed a positive relationship between Homeostasis Model Assessment-IR (HOMA-IR) and CAP (β = 3.414, 95% confidence interval [CI]: 1.012 to 5.816, p < 0.001), which was attenuated when leptin was included in the model, thus indicating that leptin mediates this relationship (β = 1.074, 95% CI: 0.349 to 2.686, p < 0.001). The percentage of the total effect mediated by leptin was 21%. Regarding sex, the mediation effect of leptin remains significant among boys (β = 0.962, 95% CI: 0.009 to 2.615, p < 0.001), but not in girls (β = 0.991, 95% CI: 1.263 to 5.483, p = 0.477).
The findings are clinically relevant to consider leptin levels as a surrogate marker of insulin sensitivity when assessing youths with excess adiposity and/or suspected Nonalcoholic hepatic steatosis or nonalcoholic fatty liver disease (NAFLD).
胰岛素抵抗（IR）与肝脂肪变性（脂肪肝）之间的关系已为人熟知；然而，饱腹感激素瘦素在这种关系中作为混杂因素或中介因素的程度尚不确定。我们研究了在哥伦比亚肥胖青少年中，IR与肝脂肪变性之间的关联是否由瘦素介导。
共有122名青少年（平均年龄：13.4岁；68%为女孩）参与了该研究。我们评估了身体成分、肝脂肪变性（由受控衰减参数[CAP]定义）、心脏代谢危险因素（体重指数、腰围、身体成分）、生化变量（瘦素、胰岛素、葡萄糖、血脂谱、心脏代谢Z评分、转氨酶等）以及身体素质（心肺适能和握力）。使用巴伦和肯尼框架进行了偏相关、回归和中介分析。
92名青少年（75.4%）存在IR。中介分析显示，稳态模型评估-IR（HOMA-IR）与CAP之间呈正相关（β = 3.414，95%置信区间[CI]：1.012至5.816，p < 0.001），当模型中纳入瘦素时，这种相关性减弱，这表明瘦素介导了这种关系（β = 1.074，95% CI：0.349至2.686，p < 0.001）。瘦素介导的总效应百分比为21%。就性别而言，瘦素的中介效应在男孩中仍然显著（β = 0.962，95% CI：0.009至2.615，p < 0.001），但在女孩中不显著（β = 0.991，95% CI：1.263至5.483，p = 0.477）。
在评估肥胖和/或疑似非酒精性肝脂肪变性或非酒精性脂肪性肝病（NAFLD）的青少年时，将瘦素水平视为胰岛素敏感性的替代标志物，这些发现具有临床相关性。
