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Type 2 diabetes mellitus (T2D) is one of the leading causes of morbidity and mortality in the United States, with approximately 25% of healthcare expenditures directed toward its management and associated metabolic complications. In response to the urgent need for novel therapeutic strategies, recent research has focused on bioactive compounds derived from dietary sources. In light of that, we identified the plant lignan matairesinol (MA) and its gut-derived metabolite, enterolactone (ENL), as agents capable of enhancing glucose uptake in 3T3-L1 differentiated adipocytes. These results suggest that enterolactone may represent a promising dietary supplement for improving glycemic control in patients with T2D. Comparative mechanistic studies indicate that ENL promotes glucose uptake through pathways that intersect with the canonical insulin signaling cascade, particularly Glut4 translocation. Further studies are warranted to elucidate the precise molecular mechanisms underlying these effects and to evaluate their therapeutic potential in vivo.

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Apr 22nd, 1:00 PM Apr 22nd, 3:00 PM

Mechanistic Insights of Enterolactone within 3T3-L1 Adipocyte Cells

Basic

Type 2 diabetes mellitus (T2D) is one of the leading causes of morbidity and mortality in the United States, with approximately 25% of healthcare expenditures directed toward its management and associated metabolic complications. In response to the urgent need for novel therapeutic strategies, recent research has focused on bioactive compounds derived from dietary sources. In light of that, we identified the plant lignan matairesinol (MA) and its gut-derived metabolite, enterolactone (ENL), as agents capable of enhancing glucose uptake in 3T3-L1 differentiated adipocytes. These results suggest that enterolactone may represent a promising dietary supplement for improving glycemic control in patients with T2D. Comparative mechanistic studies indicate that ENL promotes glucose uptake through pathways that intersect with the canonical insulin signaling cascade, particularly Glut4 translocation. Further studies are warranted to elucidate the precise molecular mechanisms underlying these effects and to evaluate their therapeutic potential in vivo.

 

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