Anorexia nervosa (AN) is a disease resulting in extreme weight loss. It is caused by multiple factors, including psychosocial, environmental, and genetic factors. A genetic abnormality affecting lipid metabolism has been recently reported in patients with AN. However, it is unknown whether lipid metabolism abnormalities in AN are caused by eating behavior, undernutrition, and/or genetic factors. The meaning of lipid metabolism in AN remains unclear. In particular, differences in the profiles of very long-chain fatty acids (VLCFAs) in patients with various types of AN have not been studied. This study aimed to determine changes to the fatty acid profile over a 3-month period, specifically that of long-chain fatty acids (LCFAs) and VLCFAs in patients with various types of AN. We evaluated 69 female patients with AN, subclassified as AN-restricting type (AN-R) and AN-Binge-Eating/Purging type (AN-BP). On admission and after 3 months of treatment, height, weight, body mass index, plasma and serum parameters, and plasma fatty acid concentrations were measured in all patients. The control group included 25 healthy, age-matched women. Comparisons between the groups were made using one-way ANOVA, while those between the various parameters at admission and after 3 months within each group were made using the Wilcoxon signed rank test. On admission, the AN-R and the AN-BP groups had significantly higher levels of 18-24C and > 14C fatty acids (LCFAs and VLCFAs, respectively) than the control group. After 3 months of treatment, both groups showed high levels of 14-24C fatty acids. The levels of VLCFAs (C22:0 and C24:0) and LCFA (C18:3) after 3 months of treatment remained high in both AN groups relative to the control group. Eating behaviors appear to be associated with levels of LCFAs. Lipid metabolism abnormalities under conditions of starvation in AN might have a genetic basis and appear to be associated with VLCFA (C22:0 and C24:0) and LCFA (C18:3) levels.

中文翻译：

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超长链脂肪酸是神经性厌食症患者营养状况的重要标志：病例对照研究。

神经性厌食症 (AN) 是一种导致极度体重减轻的疾病。它是由多种因素引起的，包括社会心理、环境和遗传因素。最近在 AN 患者中报道了影响脂质代谢的遗传异常。然而，尚不清楚 AN 中的脂质代谢异常是否是由饮食行为、营养不良和/或遗传因素引起的。AN中脂质代谢的意义仍不清楚。特别是，尚未研究各种类型 AN 患者的超长链脂肪酸 (VLCFA) 分布的差异。本研究旨在确定 3 个月内脂肪酸谱的变化，特别是各种类型 AN 患者的长链脂肪酸 (LCFA) 和 VLCFA 的变化。我们评估了 69 名女性 AN 患者，细分为 AN 限制型 (AN-R) 和 AN-Binge-Eating/Purging 型 (AN-BP)。入院时和治疗 3 个月后，测量所有患者的身高、体重、体重指数、血浆和血清参数以及血浆脂肪酸浓度。对照组包括 25 名健康、年龄匹配的女性。使用单因素方差分析进行组间比较，而在每组入院时和3个月后的各种参数之间使用Wilcoxon符号秩检验进行比较。入院时，AN-R 和 AN-BP 组的 18-24C 和 > 14C 脂肪酸（分别为 LCFA 和 VLCFA）水平显着高于对照组。治疗 3 个月后，两组均显示出高水平的 14-24C 脂肪酸。VLCFAs (C22:0 和 C24:0) 和 LCFA (C18: 3) 治疗 3 个月后，两个 AN 组相对于对照组均保持较高水平。饮食行为似乎与 LCFA 水平有关。AN饥饿条件下的脂质代谢异常可能具有遗传基础，并且似乎与VLCFA（C22：0和C24：0）和LCFA（C18：3）水平有关。