Faculty of Pharmacy, Department of Toxicology, Gazi University, Hipodrom, Ankara, Turkey.
Faculty of Medicine, Department of General Surgery, Gazi University, Besevler, Ankara, Turkey.
Adv Exp Med Biol. 2024;1460:73-95. doi: 10.1007/978-3-031-63657-8_3.
In this chapter, intestinal lipid transport, which plays a central role in fat homeostasis and the development of obesity in addition to the mechanisms of fatty acids and monoacylglycerol absorption in the intestinal lumen and reassembly of these within the enterocyte was described. A part of the resynthesized triglycerides (triacylglycerols; TAG) is repackaged in the intestine to form the hydrophobic core of chylomicrons (CMs). These are delivered as metabolic fuels, essential fatty acids, and other lipid-soluble nutrients, from enterocytes to the peripheral tissues following detachment from the endoplasmic reticulum membrane. Moreover, the attitudes of multiple receptor functions in dietary lipid uptake, synthesis, and transport are highlighted. Additionally, intestinal fatty acid binding proteins (FABPs), which increase the cytosolic flux of fatty acids via intermembrane transfer in enterocytes, and the functions of checkpoints for receptor-mediated fatty acid signaling are debated. The importance of the balance between storage and secretion of dietary fat by enterocytes in determining the physiological fate of dietary fat, including regulation of blood lipid concentrations and energy balance, is mentioned. Consequently, promising checkpoints regarding how intestinal fat processing affects lipid homeostatic mechanisms and lipid stores in the body and the prevention of obesity-lipotoxicity due to excessive intestinal lipid absorption are evaluated. In this context, dietary TAG digestion, pharmacological inhibition of TAG hydrolysis, the regulation of long-chain fatty acid uptake traffic into adipocytes, intracellular TAG resynthesis, the enlargement of cytoplasmic lipid droplets in enterocytes and constitutional alteration of their proteome, CD36-mediated conversion of diet-derived fatty acid into cellular lipid messengers and their functions are discussed.
在本章中，描述了肠道脂质转运，它除了在肠腔中脂肪酸和单酰甘油吸收以及肠细胞内重新组装的机制外，还在脂肪稳态和肥胖发展中起核心作用。一部分重新合成的三酰基甘油（TAG）在肠道中重新包装，形成乳糜微粒（CM）的疏水区核心。这些 CM 从肠细胞脱离内质网膜后，作为代谢燃料、必需脂肪酸和其他脂溶性营养素被输送到外周组织。此外，强调了多种受体功能在膳食脂质摄取、合成和转运中的作用。此外，肠道脂肪酸结合蛋白（FABP）通过肠细胞的膜间转移增加了脂肪酸的细胞质通量，以及受体介导的脂肪酸信号的检查点功能也存在争议。肠道细胞中储存和分泌膳食脂肪之间的平衡对确定膳食脂肪的生理命运的重要性，包括调节血脂浓度和能量平衡，也被提及。因此，评估了关于肠道脂肪处理如何影响体内脂质稳态机制和脂质储存以及预防由于过度肠道脂肪吸收而导致的肥胖-脂肪毒性的有前途的检查点。在这方面，讨论了膳食 TAG 的消化、TAG 水解的药理学抑制、长链脂肪酸进入脂肪细胞摄取流量的调节、细胞内 TAG 的重新合成、肠细胞细胞质脂滴的增大以及它们的蛋白质组的组成改变、CD36 介导的饮食来源脂肪酸向细胞内脂质信使的转化及其功能。
