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FFAR4 Membrane Protein Introduction

Introduction of FFAR4

FFAR4, also known as G-protein coupled receptor 120 (GPR120), G-protein coupled receptor 129 (GPR129), G-protein coupled receptor GT01, GT01, G-protein coupled receptor PGR4, PGR4, or Omega-3 fatty acid receptor 1 (O3FAR1), is a 43 kDa protein belongs to the rhodopsin family of G protein-coupled receptors. In humans, it is encoded by the GPR120 gene of the chromosome 10q23.33. FFAR4 is ubiquitously expressed in various tissues and organs, including lungs, colon, small intestine, thymus, brain, liver, taste buds, heart, skeletal muscle, and adipose tissue. Additionally, its expression in heart, skeletal muscle, and adipose tissue is elevated by a high-fat diet (HFD).

Basic Information of FFAR4
Protein Name Free fatty acid receptor 4
Gene Name FFAR4
Aliases GT01, PGR4, BMIQ10, GPR120, GPR129, O3FAR1
Organism Homo sapiens (Human)
UniProt ID Q5NUL3
Transmembrane Times 7
Length (aa) 377
Sequence MSPECARAAGDAPLRSLEQANRTRFPFFSDVKGDHRLVLAAVETTVLVLIFAVSLLGNVC
ALVLVARRRRRGATACLVLNLFCADLLFISAIPLVLAVRWTEAWLLGPVACHLLFYVMTL
SGSVTILTLAAVSLERMVCIVHLQRGVRGPGRRARAVLLALIWGYSAVAALPLCVFFRVV
PQRLPGADQEISICTLIWPTIPGEISWDVSFVTLNFLVPGLVIVISYSKILQTSEHLLDA
RAVVTHSEITKASRKRLTVSLAYSESHQIRVSQQDFRLFRTLFLLMVSFFIMWSPIIITI
LLILIQNFKQDLVIWPSLFFWVVAFTFANSALNPILYNMTLCRNEWKKIFCCFWFPEKGA
ILTDTSVKRNDLSIISG

Function of FFAR4 Membrane Protein

FFAR4, a seven transmembrane receptor, functions as a receptor for ω3 fatty acid (ω3-FA), regulating the secretion of gastrointestinal peptide hormone, adipogenesis, and adipogenic differentiation, as well as the anti-inflammatory process. ω3-FA, including, α-linolenic acid (α-LA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA), are endogenous ligands for FFAR4. Consistent with the multiple effects of ω3-FA, FFAR4 has participated in many different processes, such as insulin sensitization, anti-inflammation, release of gut peptides, and alteration of food preference. A wide variety of incidents that can be positively influenced by FFAR4 makes it potentially significant in the prevention and treatment of metabolic diseases. In view that the dysfunction of FFAR4 is closely associated with metabolic disorders, it may be considered as a novel potential target for the therapeutic treatment of obesity, insulin resistance, type 2 diabetes and the like.

(a) Snake-like topographical representation of human GPR120 receptor depicted by the residue-based diagram generator program. (b) FFAR4 functions as a ω3-FA receptor/sensor to mediate broad anti-inflammatory and insulin sensitization effects. Fig.1 (a) Snake-like topographical representation of human GPR120 receptor depicted by the residue-based diagram generator program. (b) FFAR4 functions as a ω3-FA receptor/sensor to mediate broad anti-inflammatory and insulin sensitization effects. (Li, 2015)

Application of FFAR4 Membrane Protein in Literature

  1. Muredda L., et al. IL-1β and TNFα inhibit GPR120 (FFAR4) and stimulate GPR84 (EX33) and GPR41 (FFAR3) fatty acid receptor expression in human adipocytes: implications for the anti-inflammatory action of n-3 fatty acids. Arch Physiol Biochem. 2018, 124(2): 97-108. PubMed ID: 28835131

    The result showed that TNFα and IL-1β induced a significant decrease of GPR120 expression. GPR120 and GP84 gene levels in human adipocytes are highly sensitive to pro-inflammatory mediators. And the inflammation-induced inhibition of GPR120 might compromise the anti-inflammation of GPR120 agonists.

  2. Nakamoto K., et al. DHA supplementation prevent the progression of NASH via GPR120 signaling. Eur J Pharmacol. 2018, 820: 31-38. PubMed ID: 29221950

    This article found that DHA supplementation may be prevented the development of nonalcoholic steatohepatitis (NASH) by the GPR120/FFAR4 signaling. Moreover, a reduction of GPR120/FFAR4 signaling is likely to be promoting an inflammatory response during NASH progressions.

  3. Li J., et al. FFAR4 is involved in regulation of neurotensin release from neuroendocrine cells and male C57BL/6 mice. Endocrinology. 2018, 159(8): 2939-2952. PubMed ID: 29796668

    From this paper, the final results demonstrated that FFAR4 plays more crucial role in contrast with FFAR1 in the mediation of fat-regulated NT (13-amino acid peptide) release, as well as an inhibitory crosstalk between MEK/ERK1/2 and AMPK in the control of NT release downstream of FFAR1/FFAR4.

  4. Serna-Marquez N., et al. Linoleic acid induces migration and invasion through FFAR4- and PI3K-/Akt-dependent pathway in MDA-MB-231 breast cancer cells. Med Oncol. 2017, 34(6): 111. PubMed ID: 28456993

    Here, scientists indicated that linoleic acid (LA) can induce Akt2 activation, invasion, as well as a rising in NFκB-DNA binding activity, miR34a upregulation and miR9 downregulation in MDA-MB-231 breast cancer cells. Their findings firstly revealed that LA induces migration and invasion via an EGFR-/PI3K-/Akt-dependent pathway in MDA-MB-231 cells.

  5. Shewale S. V., et al. In vivo activation of leukocyte GPR120/FFAR4 by PUFAs has minimal impact on atherosclerosis in LDL receptor knockout miceJ Lipid Res. 2017, 58(1): 236-246. PubMed ID: 27811230

    This paper concluded that GPR120/FFAR4 expression in leukocytes has minimal influences on dietary PUFA-induced plasma lipid/lipoprotein decrease and atheroprotection. Furthermore, there is no distinction between n-3 and n-6 PUFAs in activating anti-inflammatory effects on leukocyte GPR120 levels in vivo.

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