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Fatty liver in fasted FABP4/5 null mice is not followed by liver function deterioration
Published in Robert Hofstra, Noriyuki Koibuchi, Suthat Fucharoen, Advances in Biomolecular Medicine, 2017
M.R.A.A. Syamsunarno, M. Ghozali, G.I. Nugraha, R. Panigoro, T. Iso, M. Putri, M. Kurabayashi
In our previous study, we have showed that FABP4/5 was expressed in muscular capillary endothelial type of cells and serve to facilitate fatty acid transport from vascular lumen into the extracellular matrix (Iso et al., 2013). Deletion of FABP4/5 resulted in a marked perturbation of metabolism in response to prolonged fasting, including hyperketotic hypoglycemia, hepatic steatosis, and inability to maintain body temperature under cold exposure (Syamsunarno et al., 2013, Syamsunarno et al., 2014). The purpose of the current study is to investigate whether massive triglyceride accumulation in fasted DKO mice could induce liver function disturbance.
Molecular biology of peritoneal carcinomatosis
Published in Wim P. Ceelen, Edward A. Levine, Intraperitoneal Cancer Therapy, 2015
Riom Kwakman, Nina R. Sluiter, Erienne M.V. de Cuba, Elisabeth (Lisette) A. te Velde
Part of the hallmarks of cancer as described by Hanahan and Weinberg [4] includes the dysregulation and hijacking of the normal metabolism in order to not only sustain proliferation and cell division, but also to function in relatively hypoxic-ischemic conditions. Although much research on metabolism in cancer is available, very little knowledge exists on this process in PC. New research suggests tumor cells produce fatty acid binding protein 4 (FABP4) in the presence of omental or peritoneal adipocytes. Beta-adrenergic stimulation of adipocytes by a FABP4-mediated mechanism induces lipolysis in adipocytes and subsequent beta-oxidation provides free fatty acids. These free fatty acids are transported to the tumor cells, which require them for their high energy metabolism [51]. The exact mechanism of FABP4-mediated tumor–adipocyte fat transfer remains unknown.
FABP4 in Paneth cells regulates antimicrobial protein expression to reprogram gut microbiota
Published in Gut Microbes, 2022
Xiaomin Su, Mengli Jin, Chen Xu, Yunhuan Gao, Yazheng Yang, Houbao Qi, Qianjing Zhang, Xiaorong Yang, Wang Ya, Yuan Zhang, Rongcun Yang
Fatty acid binding protein 4 (FABP4) is a member of the FABP family of intracellular lipid chaperones. 28 It is most abundantly expressed in adipocytes but also detected in macrophages and a subset of endothelial cells such as gut epithelial crypt cells. 29–32 FABP4 exhibits a range of functions in these cell types, including regulation of glucose, lipid metabolism, and inflammation, cell survival and cell proliferation. 33,34 Circulating FABP4 levels are also associated with several aspects of metabolic syndrome and cardiovascular disease. 35 FABP4 is a critical mediator of metabolism and inflammatory processes, both locally and systemically, and therefore is potential therapeutic target for immunometabolic diseases. 36 However, the exact function(s) of FABP4 in gut epithelial crypt cells such as Paneth cells 30 is unclear. Since Paneth cells can highly produce antimicrobials to control gut microbial communities, 37 it is interest to know whether FABP4 in gut Paneth cells could regulate the antimicrobial peptides. Here, we find that FABP4, which can be induced by HFD, downregulates the expression of defensins through degrading PPARγ in Paneth cells.
Jateorhizine alleviates insulin resistance by promoting adipolysis and glucose uptake in adipocytes
Published in Journal of Receptors and Signal Transduction, 2021
Changqin Cheng, Zhiyong Li, Min Zhang, Dezhi Chen
In order to further verify the pro-adipolysis effect of Jat, the expression levels of adipose transcription factors and related proteins were further determined, including PPARγ, C/EBPα, FABP4, perilipin and FAS. Specifically expressed in adipose tissues, PPARγ is an internal regulatory point for adipocyte differentiation, which can affect adipocyte differentiation process by regulating the expression of key enzymes or transporters in lipid metabolism [19]. C/EBPα, which is expressed late in adipocyte differentiation, activates target genes in adipocytes and collaborates with PPARγ to trigger adipocyte differentiation [20]. FABP4 is an important intracellular fatty acid carrier protein that promotes lipid droplet formation by regulating the uptake, transport and oxidation of fatty acids and their derivatives [21]. Perilipin can form a protective cover on the surface of lipid droplets to prevent lipase contact, thus inhibiting fat decomposition [22]. FAS can catalyze the conversion of acetyl-CoA and malonyl-CoA into fatty acids, leading to the deposition of fat in the body [23]. In short, elevated levels of PPARγ, C/EBPα, FABP4, perilipin and FAS represent increased production of fat, while decreases in these indicators accelerates adipolysis. In this present study, we found that the expression levels of PPARγ, C/EBPα, FABP4, perilipin and FAS were significantly increased in MID-induced preadipocytes, which were reversed by Jat in a concentration-dependent manner. These further indicated that Jat could regulate adipolysis in cells by regulating the expression of fat transcription factors and related proteins.
Serum fatty acid binding protein 4 levels are associated with abdominal aortic calcification in peritoneal dialysis patients
Published in Renal Failure, 2021
Sijia Zhou, Xiaoxiao Wang, Junbao Shi, Qingfeng Han, Lian He, Wen Tang, Aihua Zhang
An increase of body fat is common in peritoneal dialysis (PD) patients [2], which is associated with the proinflammatory state and the alteration in lipid profile [3]. Current researches suggest that fat tissue plays an important role in modulating lots of complications among PD patients, mainly through secreting various adipokines [4]. Fatty acid binding protein 4 (FABP4), also known as adipocyte FABP (A-FABP) or adipocyte protein 2 (aP2), is abundantly expressed in adipocytes and activated macrophages [5]. Adipokines may affect intimal arterial calcification in PD patients through regulating atherosclerosis. Studies also showed positive associations between serum FABP4 and other cardiovascular risk factors like obesity, dyslipidemia, and insulin resistance [6–8]. Medial arterial calcification is specific in patients with CKD-MBD, and the transformation of vascular smooth muscle cells into osteoblast-like cells is recognized as a key process in VC. There are many complex cross-talks between adipocytes, vessels, and bone tissues in patients on dialysis. Recent studies found that adipokines may influence the bone metabolism [9,10]. A basic study [11] reported that inhibition of FABP4 could alleviate osteoarthritis induced by high-fat diet in mice. These data corroborate the fact that FABP4 may play an important role in the development of VC among PD patients. However, no research has investigated the relationship between FABP4 and VC.