Flores Monar Gabriela Vanessa, Sanchez Cruz Camila, Calderon Martinez Ernesto
Department of Endocrinology, Albany Medical Center Endocrinology Group, Albany, New York, USA.
Faculty of Medicine, Universidad Nacional Autónoma de México, Coyoacán, Ciudad de México, Mexico.
J Nutr Metab. 2025 Apr 21;2025:5571686. doi: 10.1155/jnme/5571686. eCollection 2025.
Fructose, a common sweetener in modern diets, has profound effects on both metabolism and brain function, primarily due to its distinct metabolic pathways. Unlike glucose, fructose bypasses critical regulatory steps in metabolism, particularly the phosphofructokinase-1 (PFK-1) feedback inhibition, leading to uncontrolled metabolism and increased fat storage. This review delves into the metabolic consequences of fructose consumption, including its limited role in directly stimulating insulin secretion, which affects satiety signaling and contributes to increased food intake. The small intestine initially helps metabolize ingested fructose, shielding the liver and brain from excessive exposure. However, when consumed in excess, particularly in diets high in processed foods, this protective mechanism becomes overwhelmed, contributing to metabolic disorders such as insulin resistance, obesity, and fatty liver disease. The review also explores fructose's impact on the brain, with a focus on the hippocampus, a key region for memory and learning. Chronic high fructose intake has been linked to mitochondrial dysfunction, increased production of reactive oxygen species (ROS), and neuroinflammation, all of which contribute to cognitive decline and impairments in memory and learning. Additionally, fructose-induced alterations in insulin signaling in the brain are associated with increased risk for neurodegenerative diseases. These findings underscore the potential long-term neurological consequences of excessive fructose intake and highlight the need for further human studies to assess the full spectrum of its effects on brain health. Addressing the rising consumption of fructose, particularly in processed foods, is essential for developing targeted strategies to mitigate its adverse metabolic and cognitive outcomes.
果糖是现代饮食中常见的甜味剂，对新陈代谢和大脑功能都有深远影响，主要是由于其独特的代谢途径。与葡萄糖不同，果糖绕过了新陈代谢中的关键调节步骤，特别是磷酸果糖激酶-1（PFK-1）的反馈抑制，导致新陈代谢不受控制并增加脂肪储存。本综述深入探讨了食用果糖的代谢后果，包括其在直接刺激胰岛素分泌方面的有限作用，这会影响饱腹感信号并导致食物摄入量增加。小肠最初有助于代谢摄入的果糖，使肝脏和大脑免受过度暴露。然而，当过量食用时，尤其是在高加工食品的饮食中，这种保护机制会不堪重负，导致胰岛素抵抗、肥胖和脂肪肝疾病等代谢紊乱。该综述还探讨了果糖对大脑的影响，重点是海马体，它是记忆和学习的关键区域。长期高果糖摄入与线粒体功能障碍、活性氧（ROS）产生增加和神经炎症有关，所有这些都会导致认知能力下降以及记忆和学习障碍。此外，果糖引起的大脑胰岛素信号改变与神经退行性疾病风险增加有关。这些发现强调了过量摄入果糖可能产生的长期神经后果，并突出了进一步开展人体研究以评估其对大脑健康全面影响的必要性。解决果糖摄入量不断上升的问题，特别是在加工食品中的摄入量，对于制定有针对性的策略以减轻其不良代谢和认知后果至关重要。
