Fatty acid oxidation

脂肪酸氧化
  • 文章类型: Journal Article
    肿瘤相关巨噬细胞(TAM)是浸润肿瘤微环境(TME)的重要免疫细胞。最近的研究表明,TAM在表型方面表现出多样性,函数,时间,和空间分布,这允许TAM亚型的进一步分类。脂肪酸氧化(FAO)的代谢效率在TAM亚型之间有所不同。粮农组织与活性氧(ROS)的产生密切相关,在氧化应激等过程中发挥作用。目前的证据表明,粮农组织和ROS可以影响TAMs的招募,极化,和吞噬能力单独或组合,从而影响肿瘤进展。但与这些关系相关的具体机制仍需进一步调查。我们将从ROS和TAMs三个方面综述TAMs与肿瘤发生发展关系的研究现状,粮农组织和TAM,以及粮农组织的相互联系,ROS,和TAM。
    Tumor-associated macrophages (TAMs) are significant immunocytes infiltrating the tumor microenvironment(TME). Recent research has shown that TAMs exhibit diversity in terms of their phenotype, function, time, and spatial distribution, which allows for further classification of TAM subtypes. The metabolic efficiency of fatty acid oxidation (FAO) varies among TAM subtypes. FAO is closely linked to the production of reactive oxygen species (ROS), which play a role in processes such as oxidative stress. Current evidence demonstrates that FAO and ROS can influence TAMs\' recruitment, polarization, and phagocytosis ability either individually or in combination, thereby impacting tumor progression. But the specific mechanisms associated with these relationships still require further investigation. We will review the current status of research on the relationship between TAMs and tumor development from three aspects: ROS and TAMs, FAO and TAMs, and the interconnectedness of FAO, ROS, and TAMs.
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  • 文章类型: Journal Article
    在系统性红斑狼疮(SLE)的免疫发病机制中,特异性免疫细胞失调,包括T细胞。T细胞中的代谢重编程引起不同的影响。代谢程序是免疫反应中的关键检查点,并且涉及自身免疫性疾病的病因。例如,静息淋巴细胞通过氧化磷酸化(OXPHOS)和脂肪酸氧化(FAO)产生能量,而活化的淋巴细胞迅速转移到糖酵解途径。具体来说,线粒体功能障碍,氧化应激,异常代谢(包括葡萄糖,脂质,和氨基酸代谢),和mTOR信号是SLE中T淋巴细胞代谢功能障碍的标志。本文总结了代谢缺陷如何促进SLE中的T细胞反应,和一些与疾病有关的表观遗传学改变。最后,它显示了代谢缺陷如何可以被治疗性地改变。
    In the immunopathogenesis of systemic lupus erythematosus (SLE), there is a dysregulation of specific immune cells, including T cells. The metabolic reprogramming in T cells causes different effects. Metabolic programs are critical checkpoints in immune responses and are involved in the etiology of autoimmune disease. For instance, resting lymphocytes generate energy through oxidative phosphorylation (OXPHOS) and fatty acid oxidation (FAO), whereas activated lymphocytes rapidly shift to the glycolytic pathway. Specifically, mitochondrial dysfunction, oxidative stress, abnormal metabolism (including glucose, lipid, and amino acid metabolism), and mTOR signaling are hallmarks of T lymphocyte metabolic dysfunction in SLE. Herein it is summarized how metabolic defects contribute to T cell responses in SLE, and some epigenetic alterations involved in the disease. Finally, it is shown how metabolic defects could be modified therapeutically.
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  • 文章类型: Journal Article
    Nonalcoholic fatty liver disease (NAFLD) is closely linked to the metabolic syndrome and is highly prevalent in bariatric patients. The criterion standard to diagnose NAFLD is a liver biopsy specifically to detect inflammatory changes characteristic of nonalcoholic steatohepatitis. Technologic advancements will improve the accuracy of current noninvasive modalities. Modification of risk factors via food management is important to prevent the progression of NAFLD to nonalcoholic steatohepatitis and cirrhosis. Several clinical trials are underway for pharmacologic treatment of NAFLD; currently the mainstay of treatment is insulin sensitizers and vitamin E. There is strong evidence bariatric surgery improves biochemical and histologic features of NAFLD and therefore, bariatric surgery should be considered as a treatment of NAFLD in patients with obesity. Gastric bypass exhibits antilipogenic, antiinflammatory, antioxidant, and antidiabetic properties in the livers of laboratory animals; thereby, providing a unique window to study regulation of body adiposity and insulin resistance.
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  • 文章类型: Journal Article
    In mammals, excess energy is stored primarily as triglycerides, which are mobilized when energy demands arise and cannot be covered by feed intake. This review mainly focuses on the role of long chain fatty acids in disturbed energy metabolism of the bovine species. Long chain fatty acids regulate energy metabolism as ligands of peroxisome proliferator-activated receptors. Carnitine acts as a carrier of fatty acyl groups as long-chain acyl-CoA derivatives do not penetrate the mitochondrial inner membrane. There are two different types of disorders in lipid metabolism which can occur in cattle, namely the hypoglycaemic-hypoinsulinaemic and the hyperglycaemic-hyperinsulinaemic type with the latter not always associated with ketosis. There is general agreement that fatty acid β-oxidation capability is limited in the liver of (ketotic) cows. In accord, supplemental L-carnitine decreased liver lipid accumulation in periparturient Holstein cows. Of note, around parturition concurrent oxidation of fatty acids in skeletal muscle is highly activated. Also peroxisomal β-oxidation in liver of dairy cows may be part of the hepatic adaptations to a negative energy balance (NEB) to break down fatty acids. An elevated blood concentration of nonesterified fatty acids is one of the indicators of NEB in cattle among others like increased β-hydroxy butyrate concentration, and decreased concentrations of glucose, insulin, and insulin-like growth factor-I. Assuming that liver carnitine concentrations might limit hepatic fatty acid oxidation capacity in dairy cows, further study of the role of acyl-CoA dehydrogenases and/or riboflavin in bovine ketosis is warranted.
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