mProX™ Human FFAR4 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 The receptor FFAR4, specializing in the recognition of extended-chain fatty acids, orchestrates oleate-triggered signaling pathways.
Assessing FFAR4 knockdown effects in Huh7 cells: Open bars denote cells with stable FFAR4 shRNA expression, closed bars represent cells transfected with an empty pLKO vector, vertical-striped bars indicate additional FFAR4-GFP transfection, and horizontal-striped bars denote supplementary transfection with a non-functional FFAR4RH mutant. Oleate (OA) was employed. Data is presented as mean±s.e.m. Associated P-values are as follows: 15 min FFAR4 shRNA knockdown, P = 0.014; 15 min FFAR4 shRNA knockdown+FFAR4-GFP, P = 0.093; 180 min FFAR4 shRNA knockdown, P = 0.375; 180 min FFAR4 shRNA knockdown+FFAR4-GFP, P = 0.531; 15 min FFAR4 shRNA knockdown+FFAR4RH, P = 0.078; 180 min FFAR4 shRNA knockdown+FFAR4RH, P = 0.391 (Mann-Whitney U test).
Ref: Rohwedder, Arndt, et al. "Lipid droplet formation in response to oleic acid in Huh-7 cells is mediated by the fatty acid receptor FFAR4." Journal of cell science 127.14 (2014): 3104-3115.
Pubmed: 24876224
DOI: 10.1242/jcs.145854
Research Highlights
Wang Z, et al. "Akkermansia muciniphila supplementation improves glucose tolerance in intestinal ." mSystems, 2023.
The disruption of blood glucose utilization can lead to diabetes mellitus, a complex disease with both genetic and environmental factors. Free fatty acid receptors (FFARs) are believed to link these aspects together. Recently, FFAR4 has been identified as a potential target for diabetes treatment. Therefore, it is essential to understand how FFAR4 affects glucose homeostasis. Previous studies have shown that mice lacking FFAR4 have impaired glucose tolerance when fed a high-fat diet. However, the results for mice under a regular diet have been conflicting. This study aims to investigate the role of FFAR4 in glucose utilization rhythm and its possible mechanism. Results from both total Ffar4 knockout mice and mice with gut-specific Ffar4 deletion indicated a clear diurnal rhythm in glucose tolerance. Moreover, intestinal FFAR4 deficiency was found to cause significant changes in fecal microbiota at different time points. Further analysis revealed that Akkermansia muciniphila, an important bacteria in regulating intestinal hormone secretion, was the main target of FFAR4 at a specific time point. Additionally, supplementation of Akkermansia muciniphila significantly improved glucose tolerance in mice with gut-specific Ffar4 deletion at that time point. These findings suggest that intestinal FFAR4 plays a critical role in the regulation of glucose tolerance, particularly at specific time points. Moreover, alterations in the intestinal environment may contribute to the development of certain diseases.
Pubmed:
37787527
DOI:
10.1128/msystems.00573-23
Wei L, et al. "Double knockout of FFAR4 and FGF21 aggravates metabolic disorders in mice.." International journal of biological macromolecules, 2023.
Multiple investigations have been conducted regarding the involvement of free fatty acid receptor 4 (FFAR4) in metabolic disorders, with conflicting results. To further understand the role of FFAR4 in regulating metabolic status, a team of researchers generated FFAR4/FGF21 double knockout (DKO) mice and examined the effects of FGF21, a fibroblast growth factor, on glucose and lipid metabolism in FFAR4 knockout mice on a high-fat diet. Results showed that levels of FGF21 were significantly elevated in FFAR4-deficient mice and the double deletion of FGF21 and FFAR4 resulted in severe metabolic disruptions. The study also found that FFAR4/FGF21 DKO mice had metabolic irregularities, possibly attributed to decreased energy expenditure. Overall, this study provided insight into the role of endogenous FGF21 as a key regulator in the absence of FFAR4.
Pubmed:
37657572
DOI:
10.1016/j.ijbiomac.2023.126553