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Adipokines, Inflammation, and Metabolic Diseases · Journal article
Molecular Medicine Reports · September 3, 2026
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This is a first mechanistic study demonstrating that licoisoflavone A (LIC-A), a natural compound from licorice, upregulates METTL3 expression in cultured adipocytes and improves metabolic parameters in a diet-induced obesity mouse model. The work is novel in linking LIC-A to METTL3-dependent regulation but remains preclinical; no human efficacy or safety data are provided, and animal sample sizes and study conduct details are not disclosed.
In vitro cell culture and in vivo diet-induced obesity mouse model with molecular docking screen. Diet-induced obesity mice; 3T3-L1 mouse adipogenic cell line. Intervention: Licoisoflavone A (LIC-A) treatment. Compared with: Untreated or vehicle control in cells and mice; TNF-α and lipopolysaccharide as inflammatory stimuli.
LIC-A identified as upstream positive regulator of METTL3 expression via molecular docking and cell culture TNF-α and lipopolysaccharide-induced inhibition of adipogenesis in 3T3-L1 cells was recovered by LIC-A treatment, dependent on METTL3 In vivo LIC-A administration recovered body weight, lipid metabolism, insulin resistance, and gluconeogenesis in diet-induced obesity mice with reduced adipose deposition
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This work identifies a potential natural compound target and mechanism for obesity-related metabolic dysfunction but is preclinical. No human trials, safety data, or clinical dosing are provided; further development and validation in animal models with explicit sample sizes and then human studies would be needed before clinical use.
First-in-vivo mechanistic study of a natural compound in diet-induced obesity using surrogate endpoints (body weight, lipid metabolism, insulin resistance) without clinical outcomes or human data.
As stated by the source record.
This work identifies a potential natural compound target and mechanism for obesity-related metabolic dysfunction but is preclinical. No human trials, safety data, or clinical dosing are provided; further development and validation in animal models with explicit sample sizes and then human studies would be needed before clinical use.
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With the development of obese adipose tissue (aT), adipocytes undergo pathological changes from inert energy storage to excessive and active endocrine organs associated with disease hazards.Methyltransferase 3 (MeTTl3) is an rna methyltransferase with key roles in aT development, functional maintenance and metabolic homeostasis.Licoisoflavone A (LIC-A) is a prenylated flavonoid compound derived from licorice, which has anti-inflammatory, antihypertrophic and antiproliferative activities; however, whether it directly modulates MeTTl3 expression and affects aT function in obesity remains unknown. in the present study, molecular docking of compounds from the traditional chinese medicine formula Fangji-Huangqi decoction against MeTTl3, identified 16 top-ranked candidate molecules.Among these candidates, LIC-A was identified as a potential upstream regulator of MeTTl3 and markedly increased MeTTl3 expression.The effects of TnF-α and lipopolysaccharide treatments on the inhibition of adipogenesis were successfully recovered by lic-a treatment of the adipogenic 3T3-l1 cells, via the regulation of adipogenic cytokines, as well as the expression of inflammatory factors.These protective effects were similarly abolished by MeTTl3 knockdown, suggesting that the role of lic-a relies on MeTTl3.Moreover, in vivo data demonstrated that the administration of lic-a could notably recover body weight lipid metabolism, insulin resistance and gluconeogenesis in mice with reduced adipose deposition, as well as abate systemic inflammation.The novelty of the present study lies in three aspects: i) LIC-A was identified as a previously unrecognized upstream positive regulator of MeTTl3 expression; ii) lic-a was demonstrated to alleviate adipokine dysregulation and AT inflammation through a METTL3-dependent mechanism; and iii) the first in vivo experimental evidence that lic-a can improve obesity-related metabolic disorders by promoting MeTTl3-mediated m6a methylation in aT was provided.To the best of our knowledge, this is the first study to link a natural isoflavone compound from licorice to MeTTl3-mediated post-transcriptional regulation in the context of aT dysfunction.
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