mProX™ Human FFAR1 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 Effect of FFAR1 knockdown on mTOR and insulin signaling in INS-1 cells.
Cells underwent transient transfection with 40 nM of either scrambled siRNA or FFAR1 siRNA for a duration of 48 to 72 hours, followed by harvest and subsequent qPCR analysis. Each group was subjected to duplicate cell repetitions, resulting in a transfection efficiency of 75%. This approach led to an approximate 60% reduction in FFAR1 mRNA levels, correlating with a noteworthy decrease in IRS-1 and an elevation in INSR1β mRNA expression. Intriguingly, no discernible impact was observed on other targets within the mTOR and insulin signaling pathways, including PI3k, Raptor, Rictor, and S6K1, with GAPDH employed as the reference gene for standardization.
Ref: Marafie, Sulaiman K., et al. "Palmitic acid-induced lipotoxicity promotes a novel interplay between Akt-mTOR, IRS-1, and FFAR1 signaling in pancreatic β-cells." Biological Research 52.1 (2019): 1-12.
Pubmed: 31426858
DOI: 10.1186/s40659-019-0253-4
Research Highlights
Guan S, et al. "A novel PPARbeta/FFA1 dual agonist Y8 promotes diabetic wound healing.." European journal of pharmacology, 2023.
The study of diabetic ulcer treatment has shown that Y8, a dual agonist of PPARbeta and FFA1, has the potential to be an effective treatment. This new compound molecule has been found to accelerate wound healing in diabetic mice, with increased tissue regeneration and extracellular matrix deposition. Further research has also shown that Y8 promotes keratinocyte proliferation and migration by activating PPARbeta and triggering FFA1. Y8 has also been found to decrease ROS levels in fibroblasts, further contributing to its effectiveness in promoting healing. These findings suggest that Y8 may have a superior therapeutic effect compared to single-target agonists.
Pubmed:
37562666
DOI:
10.1016/j.ejphar.2023.175934
Oteng AB, Liu L. "GPCR-mediated effects of fatty acids and bile acids on glucose homeostasis.." Frontiers in endocrinology, 2023.
The key biomolecules, fatty acids and glucose, have common roles as both energy substrates and signaling molecules. Fatty acids can be produced endogenously from glucose intermediates through de-novo lipogenesis. Similarly, bile acids are synthesized in the liver from cholesterol and also contribute to systemic glucose homeostasis. Insulin and glucagon, two pancreatic hormones, play a significant role in controlling plasma glucose levels during postprandial and fasted states. Several experimental studies have shown that fatty acids and bile acids act as endocrine modulators and regulate the release of key hormones involved in glucose metabolism. These molecules, including short chain fatty acids (SCFAs), unsaturated and saturated fatty acids, and bile acids, act as ligands for specific G-protein coupled receptors (GPCRs). Activation of these GPCRs influences the release of hormones such as incretins, insulin, glucagon, and somatostatin, ultimately maintaining euglycemia and preventing metabolic diseases like type-2 diabetes.
Pubmed:
37484954
DOI:
10.3389/fendo.2023.1206063
