China
Africa
Explore chapters and articles related to this topic
Molecular sport nutrition
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Mark Hearris, Nathan Hodson, Javier Gonzalez, James P. Morton
The increased availability of fatty acids that occurs in response to fat adaptation provides the primary signal that serves to activate the complex signalling transduction pathway that controls the synthesis of new fatty acid transport proteins, such as CD36 and CPT-1. This signalling pathway is initiated by the binding of fatty acids to a group of nuclear receptor proteins, known as the peroxisome proliferator-activated receptors (PPARs), which function as transcription factors to control the mRNA expression of fatty acid transporters. Of the family of PPARs, PPARδ is the most abundant PPAR within skeletal muscle. Once activated, these transcription factors bind to specific sequences of DNA that code for the transporter proteins of interest (e.g. CD36 and CPT-1) to create new messenger RNA which can be ultimately used to synthesise new fatty acid transport proteins.
Placental transport and metabolism
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
In addition, placental lipoprotein lipase, which is localized in the MVM, hydrolyzes lipoproteins (43). The free fatty acids (FFA) released diffuse across the plasma membrane. Fatty acid transport proteins, fatty acid translocase, and plasma membrane fatty acid–binding proteins (FABPpm) facilitate unesterified fatty acid uptake into the placental cells (44). An isoform of FABPpm unique to the placenta occurs only in the MVM of the syncytiotrophoblast, suggesting that it may be important in placental FFA uptake (45). While they are thought to encourage transmembrane passage of FFA, the manner in which this is accomplished by FABP is uncertain. Once transported into the syncytial cytoplasm, FFA bind to FABP and are presented to the BM through which they are presumed to be transported to the fetus via either diffusion or facilitation by FABPs (46).
Energy Provision, Fuel Use and Regulation of Skeletal Muscle Metabolism During The Exercise Intensity/Duration Continuum
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
On the fat side, we now understand that FFAs are moved across the muscle membrane and t-tubules via protein-mediated transport systems during exercise (11, 27, 40, 86). These transport proteins include the plasma membrane fatty acid–binding protein (FABPpm), fatty acid transport proteins (FATPs), and fatty acid translocase (FAT/CD36). And unique to fat metabolism, FFAs are bound to protein chaperones in order to be transported in the cytoplasm for storage as IMTG or delivery to the mitochondria (28). At the mitochondrial membranes, all the FFA transported into the cell and released from IMTG must be transported across the mitochondrial membranes with the help of the carnitine palmitoyl transferase I (CPT I) system and FATPs (mainly FAT/CD36) (9, 15, 80, 81). During exercise, FATPs are also moved to the muscle membrane (mainly FABPpm) and mitochondrial (mainly FAT/CD36) membranes to help bring fat into the cell, but this occurs over a slower time course (∼15–30 min) than GLUT4 translocation (12, 13, 40). It is expected that Ca2+ and the factors related to the energy status of the cell (e.g., free ADP, AMP, Pi, and AMPK activation) are involved, as they play an important role in activating the transport and docking of GLUT4 into the muscle membrane. For more detail on the regulation of these processes see (25, 31, 49, 50).
Lipid-associated macrophages in the tumor-adipose microenvironment facilitate breast cancer progression
Published in OncoImmunology, 2022
Zhou Liu, Zhijie Gao, Bei Li, Juanjuan Li, Yangyang Ou, Xin Yu, Zun Zhang, Siqin Liu, Xiaoyu Fu, Hongzhong Jin, Juan Wu, Si Sun, Shengrong Sun, Qi Wu
Adipocytes account for a large portion of the mammary stroma,4 and cancer-associated adipose is able to release abundant free fatty acids (FFAs) to satisfy the increased demand for membrane synthesis and energy metabolism in favor of rapid growth and proliferation.5 More importantly, FFAs are actively involved in the crosstalk among tumor cells and stromal cells, wherein FFA transporters, including fatty acid binding proteins (FABPs) and fatty acid transport protein (FATP), play an important role.6 The tissue origin of FABPs is strictly regulated. For example, FABP3 is highly expressed in the heart and skeletal muscles, FABP4 is enriched in adipose and FABP5 mainly derived from the epithelium.7 FABPs mainly act as intracellular fatty acid transporters to participate in lipid metabolism or directly interact with intracellular proteins.8 Similarly, extracellular FABPs, such as circulating A-FABP, function as new adipokines to enhance obesity-associated breast cancer development.9 The family of fatty acid transport proteins is composed of six members that are localized on cell membranes and intracellular organelle membranes, and they participate in the absorption of long chain FFAs.7,8 FATP1 predominantly originates from tissues with prolific FFAs metabolism, such as heart, adipose and skeletal muscle.10–12 Notably, FATP1 participates in the esterification and oxidation of FAs in parallel.13 It has been reported that tumor cells with elevated FATP1 expression could take up more FFAs from the TME to remain energetic.14,15 Overall, FABPs and FATP1 mediate tumor progression by regulating energy metabolism of tumor cells and tumor neovascularization,14,16–19 while the role of FFA transporters in the ontogeny and functions of immune cells in the TAME remains unclear.