Anderson Emma L, Howe Laura D, Fraser Abigail, Callaway Mark P, Sattar Naveed, Day Chris, Tilling Kate, Lawlor Debbie A
MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, UK; School of Social and Community Medicine, University of Bristol, Bristol, UK.
MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, UK; School of Social and Community Medicine, University of Bristol, Bristol, UK.
J Hepatol. 2014 Sep;61(3):626-32. doi: 10.1016/j.jhep.2014.04.018. Epub 2014 Apr 24.
BACKGROUND & AIMS: Adiposity is a key risk factor for NAFLD. Few studies have examined prospective associations of infant and childhood adiposity with subsequent NAFLD risk. We examined associations of weight-for-height trajectories from birth to age 10 with liver outcomes in adolescence, and assessed the extent to which associations are mediated through fat mass at the time of outcome assessment.
Individual trajectories of weight and height were estimated for participants in the Avon Longitudinal Study of Parents and Children using random-effects linear-spline models. Associations of birthweight (adjusted for birth length) and weight change (adjusted for length/height change) from 0-3 months, 3 months-1 y, 1-3 y, 3-7 y, and 7-10 y with ultrasound scan (USS) determined liver fat and stiffness, and serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyl transferase (GGT) at mean age 17.8 y were assessed with linear and logistic regressions. Mediation by concurrent fat mass was assessed with adjustment for fat mass at mean age 17.8 y.
Birth weight was positively associated with liver stiffness and negatively with ALT and AST. Weight change from birth to 1 y was not associated with outcomes. Weight change from 1-3 y, 3-7 y, and 7-10 y was consistently positively associated with USS and blood-based liver outcomes. Adjusting for fat mass at mean age 17.8 y attenuated associations toward the null, suggesting associations are largely mediated by concurrent body fatness.
Greater rates of weight-for-height change between 1 y and 10 y are consistently associated with adverse liver outcomes in adolescence. These associations are largely mediated through concurrent fatness.
肥胖是NAFLD的关键危险因素。很少有研究探讨婴儿期和儿童期肥胖与后续NAFLD风险之间的前瞻性关联。我们研究了从出生到10岁的身高体重轨迹与青少年肝脏结局的关联，并评估了这些关联在结局评估时通过脂肪量介导的程度。
使用随机效应线性样条模型估计雅芳亲子纵向研究参与者的体重和身高个体轨迹。采用线性回归和逻辑回归评估出生体重（根据出生身长进行调整）以及0至3个月、3个月至1岁、1至3岁、3至7岁和7至10岁的体重变化（根据身长/身高变化进行调整）与超声扫描（USS）测定的肝脏脂肪和硬度，以及平均年龄17.8岁时血清丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）和γ-谷氨酰转移酶（GGT）之间的关联。通过对平均年龄17.8岁时的脂肪量进行调整来评估同期脂肪量的介导作用。
出生体重与肝脏硬度呈正相关，与ALT和AST呈负相关。从出生到1岁的体重变化与结局无关。1至3岁、3至7岁和7至10岁的体重变化与USS及基于血液的肝脏结局始终呈正相关。对平均年龄17.8岁时的脂肪量进行调整后，关联减弱至无效，表明这些关联在很大程度上由同期体脂介导。
1岁至10岁之间较高的身高体重变化率与青少年不良肝脏结局始终相关。这些关联在很大程度上通过同期肥胖介导。
