Department of Food and Nutrition, Hanyang University, Seoul, South Korea.
Department of Nutrition, University of California, Davis, Davis, CA, USA.
Adv Nutr. 2022 Oct 2;13(5):1989-2001. doi: 10.1093/advances/nmac064.
The brain and peripheral nervous system provide oversight to muscle physiology and metabolism. Muscle is the largest organ in the body and critical for glucose sensitivity, prevention of diabetes, and control of obesity. The central nervous system produces endocannabinoids (eCBs) that play a role in brain neurobiology, such as inflammation and pain. Interestingly, studies in humans and rodents show that a moderate duration of exercise increases eCBs in the brain and blood and influences cannabinoid receptors. Cannabinoid actions in the nervous system have advanced our understanding of pain, well-being, and disease. Nutrition is an important aspect of brain and eCB physiology because eCBs are biosynthesized from PUFAs. The primary eCB metabolites are derived from arachidonic acid, a 20:4n-6 (ω-6) PUFA, and the n-3 (ω-3) PUFAs, EPA and DHA. The eCBs bind to cannabinoid receptors CB1 and CB2 to exert a wide range of activities, such as stimulating appetite, influencing energy metabolism, supporting the immune system, and facilitating neuroplasticity. A diet containing different essential n-6 and n-3 PUFAs will dominate the formation of specific eCBs, and subsequently their actions as ligands for CB1 and CB2. The eCBs also function as substrates for cyclooxygenase enzymes, including potential substrates for the oxylipins (OxLs), which can be proinflammatory. Together, the eCBs and OxLs act as modulators of neuroinflammation. Thus, dietary PUFAs have implications for exercise responses via synthesis of eCBs and their effects on neuroinflammation. Neurotrophins also participate in interactions between diet and the eCBs, specifically brain-derived neurotrophic factor (BDNF). BDNF supports neuroplasticity in cooperation with the endocannabinoid system (ECS). This review will describe the role of PUFAs in eCB biosynthesis, discuss the ECS and OxLs in neuroinflammation, highlight the evidence for exercise effects on eCBs, and describe eCB and BDNF actions on neuroplasticity.
大脑和外周神经系统为肌肉生理学和代谢提供监督。肌肉是人体最大的器官,对于葡萄糖敏感性、预防糖尿病和控制肥胖至关重要。中枢神经系统产生内源性大麻素 (eCBs),它们在大脑神经生物学中发挥作用,如炎症和疼痛。有趣的是,人类和啮齿动物的研究表明,适度的运动时间会增加大脑和血液中的 eCB,并影响大麻素受体。大麻素在神经系统中的作用促进了我们对疼痛、幸福感和疾病的理解。营养是大脑和 eCB 生理学的一个重要方面,因为 eCB 是由多不饱和脂肪酸 (PUFAs) 生物合成的。主要的 eCB 代谢物来自花生四烯酸,一种 20:4n-6(ω-6)PUFA,以及 n-3(ω-3)PUFAs,EPA 和 DHA。eCB 与大麻素受体 CB1 和 CB2 结合,发挥广泛的作用,如刺激食欲、影响能量代谢、支持免疫系统和促进神经可塑性。含有不同必需 n-6 和 n-3 PUFAs 的饮食将主导特定 eCB 的形成,随后它们作为 CB1 和 CB2 的配体发挥作用。eCB 还作为环氧化酶 (COX) 酶的底物发挥作用,包括可能作为氧化脂素 (OxLs) 的底物,OxLs 可能具有促炎作用。eCB 和 OxLs 共同作为神经炎症的调节剂。因此,饮食中的 PUFAs 通过合成 eCB 及其对神经炎症的影响,对运动反应有影响。神经营养因子也参与了饮食和 eCB 之间的相互作用,特别是脑源性神经营养因子 (BDNF)。BDNF 与内源性大麻素系统 (ECS) 合作支持神经可塑性。这篇综述将描述 PUFAs 在 eCB 生物合成中的作用,讨论 ECS 和 OxLs 在神经炎症中的作用,强调运动对 eCB 的影响,并描述 eCB 和 BDNF 对神经可塑性的作用。