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. 2024 Jun 17;13(12):1908.
doi: 10.3390/foods13121908.

Effect of Black Tea Polysaccharides on Alleviating Type 2 Diabetes Mellitus by Regulating PI3K/Akt/GLUT2 Pathway

Zhenbiao Zhang  1   2 , Xuming Deng  1 , Ruohong Chen  2 , Qiuhua Li  2 , Lingli Sun  2 , Junxi Cao  2 , Zhaoxiang Lai  2 , Xingfei Lai  2 , Zaihua Wang  3 , Shili Sun  2 , Lingzhi Zhang  1
Affiliations

Effect of Black Tea Polysaccharides on Alleviating Type 2 Diabetes Mellitus by Regulating PI3K/Akt/GLUT2 Pathway

Zhenbiao Zhang et al. Foods. .

Abstract

The bioactivity of tea polysaccharides (TPs) has been widely reported, but studies to date have focused on green tea. Some human health investigations have implied that black tea may possess potential antidiabetic effects, but less is known about their potential role and related antidiabetic mechanism. The present study was, therefore, conducted to investigate the chemical properties and antidiabetic activity of TPs from black tea. Monosaccharide composition revealed that Alduronic acid (77.8 mol%) considerably predominated in the fraction. TP conformation analysis indicated that three components in TPs were all typical of high-branching structures. Oral administration of TPs could effectively alleviate fasting blood glucose in type 2 diabetes mellitus (T2D) mice, with the values 23.6 ± 1.42, 19.6 ± 2.25, and 16.4 ± 2.07 mmol/L in the 200, 400, and 800 mg/kg·BW groups, respectively. Among these TPs groups, the 800 mg/kg·BW groups significantly decreased by 37.88% when compared with the T2D+water group (p < 0.05). Further studies demonstrated that TP treatment upregulated the expression of p-Akt/p-PI3K (p < 0.001). Additionally, TP treatment significantly promoted glucose transporter protein 2 (GLUT2) translocation in the liver (p < 0.001). These findings suggest that TPs from black tea protect against T2D by activating PI3K/Akt/GLUT2 signaling and might serve as a novel therapeutic candidate for T2D.

Keywords: PI3K-Akt; black tea; chemical property; hypoglycemic effect; tea polysaccharides.

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Conflict of interest statement

The authors declare that they have no conflicts of interest concerning this article.

Figures

Figure 1
Figure 1
(A) Effect of TPs treatment on body weight of each group of mice. (B) Effect of TPs treatment on water consumption of each group of mice. (C) Effect of TPs treatment on diet consumption of each group of mice. (D) List of results of one-way ANOVA of values in the diet consumption among different groups. Data are expressed as means ± SD (n = 9). * p < 0.05 as compared to the T2D+water group.
Figure 2
Figure 2
(A) Effect of TP treatment on blood glucose levels in each group of mice. (B) Effect of TP treatment on OGTT blood glucose levels in each group of mice. (C) AUC (Area under the curve) of the OGTT. Data are expressed as means ± SD (n = 9). * p < 0.05 as compared to the T2D+water group.
Figure 3
Figure 3
(A) Effect of TP treatment on fasting blood glucose levels in each group of mice. (B) Effect of TP treatment on serum insulin levels in each group of mice. (C) Effect of TP treatment on insulin resistance in each group of mice. (D) Effect of TP treatment on insulin sensitivity in each group of mice. Data are expressed as means ± SD (n = 9). * p < 0.05 and ** p < 0.001 as compared to the T2D+water group.
Figure 4
Figure 4
Antihyperlipidemia effects of TPs in each group of mice on serum lipid levels: (A) triglyceride; (B) total cholesterol; (C) low-density lipoprotein cholesterol; and (D) high-density lipoprotein cholesterol. Data are expressed as means ± SD (n = 9). * p < 0.05 as compared to the T2D+water group.
Figure 5
Figure 5
TP treatment increased the level of phosphorylated Akt in each group of diabetic mice: (A) immunofluorescent staining for p-Akt in liver sections; (B) Western blot analysis of p-Akt and Akt protein levels in mouse liver; and (C) relative expression of p-Akt to Akt levels. Data are expressed as means ± SD (n = 9). The scale bar represents 50 μm. * p < 0.05 and ** p < 0.001 as compared to the T2D+water group.
Figure 6
Figure 6
TP treatment upregulated the expression of p-PI3K, mTOR, and Rictor in each group of diabetic mice: (A) Western blot analysis of p-PI3K, PI3K, mTOR, Rictor, and β-actin protein levels in mouse liver; (B) relative expression of p-PI3K to PI3K levels; and (C,D) relative expression of mTOR and Rictor to β-actin levels, respectively. Data are expressed as means ± SD (n = 9). * p < 0.05 and ** p < 0.001 as compared to the T2D+water group.
Figure 7
Figure 7
TP treatment promoted the expression of p-GSK-3β and Glut2 translocation in each group of diabetic mice: (A) Western blot analysis of p-GSK-3β, GSK-3β, Glut2 (in plasmalemma) and Glut2 (in all) protein levels in mouse liver; (B) Relative expression of p-GSK3β to GSK3β levels; (C) Relative expression of Glut2 (in plasma membrane) to Glut2 (in all). Data were expressed as means ± SD (n = 9). * p < 0.05 and ** p < 0.001 as compared to the T2D+water group.
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