Category
Basic
Description
This research investigates bioactive polyphenol group theaflavins found in black tea and how they affect Akt signaling in skeletal muscle. The black tea polyphenols are a collection of innate compounds in Camillia sinensis, among them being the theaflavin group which is comprised of four compounds: theaflavin (TF1), theaflavin 3-gallate (TF2A), theaflavin 3’-gallate (TF2B), and theaflavin 3,3’ digallate (TF3) (He, 2017). The theaflavins group has been described as bioactive in a variety of different cellular pathways such as apoptosis, cellular division, gene expression and nutrient regulation (Li et al., 2021)(He, 2017)(Lin et al., 2007).
Previous work by Nagano et al., demonstrated that black tea polyphenols induce phosphorylation and activation of targets associated with insulin signaling, ultimately leading to glucose transporter 4 (GLUT4) translocation to the plasma membrane (Nagano et al., 2015). Specifically, Akt, a serine/threonine kinase, is phosphorylated at threonine 308 (Thr308) in response to the black tea polyphenols (Nagano et al., 2015)(Beg et al., 2017) . Additionally, 100nM treatment of TF1 was found to induce Glut 4 translocation comparable to 1µg/mL of the black tea polyphenols in L6 muscle cells (Nagano et al., 2015). This association with glucose metabolism, makes black tea an area of interest as a potential therapy for glucose maintenance especially among insulin resistant populations.
The signaling properties of isolated theaflavin polyphenols have been assessed in various cell types for the induction of Akt phosphorylation. Isolated TF3 induces the phosphorylation of Akt at serine 473 (Ser473) in H9C2 cardiomyocytes with reperfusion injury (Wang et al., 2025). In a study using C2C12 mouse muscle cells, TF1 has been found to induce glucose uptake (Qu et al., 2021).
It is currently unknown how these compounds stimulate these pathways whether it enters the cell via a carrier protein or interacts with elements on the plasma membrane. It is also unknown which polyphenol in black tea causes the signaling events observed in L6 cells observed by Nagano et al. TF3 stimulates Akt phosphorylation in cardiomyocytes within a disease model, but it is unknown if this is the black tea polyphenol that elicits the phosphorylation of Akt Thr308 in L6 cells.
This study examines whether certain bioactive theaflavins at varying concentrations can prompt the phosphorylation of Akt S473 in L6 rat muscle cells. These questions will be tested in differentiated L6 cells that are treated with insulin, black tea extract, TF1, and TF3. Following these treatments, western blot protein assays will examine the phosphorylation status of Akt at S473. Additionally, this study examines the possibility of TF1 entry by testing cell lysates for the presence of TF1 after treatment. The results will lead to further study of the effect of black tea polyphenols on additional activation sites along the insulin pathway and the nature of how black tea induces the activation of these targets.
Pilot Study: Black Tea Extract and Theaflavin Polyphenols Effects on L6 Myotubes
Basic
This research investigates bioactive polyphenol group theaflavins found in black tea and how they affect Akt signaling in skeletal muscle. The black tea polyphenols are a collection of innate compounds in Camillia sinensis, among them being the theaflavin group which is comprised of four compounds: theaflavin (TF1), theaflavin 3-gallate (TF2A), theaflavin 3’-gallate (TF2B), and theaflavin 3,3’ digallate (TF3) (He, 2017). The theaflavins group has been described as bioactive in a variety of different cellular pathways such as apoptosis, cellular division, gene expression and nutrient regulation (Li et al., 2021)(He, 2017)(Lin et al., 2007).
Previous work by Nagano et al., demonstrated that black tea polyphenols induce phosphorylation and activation of targets associated with insulin signaling, ultimately leading to glucose transporter 4 (GLUT4) translocation to the plasma membrane (Nagano et al., 2015). Specifically, Akt, a serine/threonine kinase, is phosphorylated at threonine 308 (Thr308) in response to the black tea polyphenols (Nagano et al., 2015)(Beg et al., 2017) . Additionally, 100nM treatment of TF1 was found to induce Glut 4 translocation comparable to 1µg/mL of the black tea polyphenols in L6 muscle cells (Nagano et al., 2015). This association with glucose metabolism, makes black tea an area of interest as a potential therapy for glucose maintenance especially among insulin resistant populations.
The signaling properties of isolated theaflavin polyphenols have been assessed in various cell types for the induction of Akt phosphorylation. Isolated TF3 induces the phosphorylation of Akt at serine 473 (Ser473) in H9C2 cardiomyocytes with reperfusion injury (Wang et al., 2025). In a study using C2C12 mouse muscle cells, TF1 has been found to induce glucose uptake (Qu et al., 2021).
It is currently unknown how these compounds stimulate these pathways whether it enters the cell via a carrier protein or interacts with elements on the plasma membrane. It is also unknown which polyphenol in black tea causes the signaling events observed in L6 cells observed by Nagano et al. TF3 stimulates Akt phosphorylation in cardiomyocytes within a disease model, but it is unknown if this is the black tea polyphenol that elicits the phosphorylation of Akt Thr308 in L6 cells.
This study examines whether certain bioactive theaflavins at varying concentrations can prompt the phosphorylation of Akt S473 in L6 rat muscle cells. These questions will be tested in differentiated L6 cells that are treated with insulin, black tea extract, TF1, and TF3. Following these treatments, western blot protein assays will examine the phosphorylation status of Akt at S473. Additionally, this study examines the possibility of TF1 entry by testing cell lysates for the presence of TF1 after treatment. The results will lead to further study of the effect of black tea polyphenols on additional activation sites along the insulin pathway and the nature of how black tea induces the activation of these targets.
