Fasting is part of many weight management and health-boosting regimens. Fasting causes substantial metabolic adaptations in the liver that include the stimulation of fatty acid oxidation and ketogenesis. The induction of fatty acid oxidation and ketogenesis during fasting is mainly driven by interrelated changes in plasma levels of various hormones and an increase in plasma nonesterified fatty acid (NEFA) levels and is mediated transcriptionally by the peroxisome proliferator-activated receptor (PPAR)α, supported by CREB3L3 (cyclic AMP-responsive element-binding protein 3 like 3). Compared with men, women exhibit higher ketone levels during fasting, likely due to higher NEFA availability, suggesting that the metabolic response to fasting shows sexual dimorphism. Here, we synthesize the current molecular knowledge on the impact of fasting on hepatic fatty acid oxidation and ketogenesis.

禁食是许多体重管理和促进健康方案的一部分。禁食会引起肝脏的大量代谢适应，包括刺激脂肪酸氧化和生酮。禁食期间脂肪酸氧化和生酮的诱导主要是由各种激素血浆水平的相互关联变化和血浆非酯化脂肪酸（NEFA）水平的增加驱动的，并由过氧化物酶体增殖物激活受体（PPAR）α转录介导，由 CREB3L3（环 AMP 响应元件结合蛋白 3 类似 3）支持。与男性相比，女性在禁食期间表现出更高的酮水平，这可能是由于 NEFA 可用性更高，这表明禁食的代谢反应表现出性别二态性。在这里，我们综合了当前关于禁食对肝脏脂肪酸氧化和生酮影响的分子知识。