Yang Siwen, Qu Yunhe, Chen Jiyu, Chen Si, Sun Lin, Zhou Yifa, Fan Yuying
Engineering Research Center of Glycoconjugates Ministry of Education, Jilin Provincial Key Laboratory of Chemistry and Biology of Changbai Mountain Natural Drugs, School of Life Sciences, Northeast Normal University, Changchun, China.
Front Pharmacol. 2021 Jun 28;12:688073. doi: 10.3389/fphar.2021.688073. eCollection 2021.
Insufficient pancreatic β-cell or insulin-producing β-cell are implicated in all types of diabetes mellitus. Our previous studies showed bee pollen polysaccharide RBPP-P improves insulin resistance in type 2 diabetic mice by inhibiting liver fat deposition. However, its potential of regulating β-cell function and integrity is not fully known. Herein, we observed that β-cell proliferation ( = 10), insulin synthesis ( = 5, 0.01684) and insulin incretion ( = 5, 0.02115) were intensely activated in MIN6 cells when treatment with RBPP-P. In alloxan-induced diabetic mice, oral administration of RBPP-P ( = 10) effectively decreased the blood glucose ( 0.0326), drink intake ( < 0.001) and urine ( < 0.001). It directly stimulated phosphorylation of p38 ( 0.00439), ERK ( 0.02951) and AKT ( 0.0072) to maintain the islet function and mass. Thus, our data suggest that RBPP-P is a natural compound to regulate β-cell proliferation and function, indicating it might have therapeutic potential against type 1 diabetes.
所有类型的糖尿病都与胰腺β细胞或产生胰岛素的β细胞不足有关。我们之前的研究表明,蜂花粉多糖RBPP-P通过抑制肝脏脂肪沉积来改善2型糖尿病小鼠的胰岛素抵抗。然而,其调节β细胞功能和完整性的潜力尚未完全明确。在此,我们观察到,用RBPP-P处理时,MIN6细胞中的β细胞增殖(n = 10)、胰岛素合成(n = 5,P = 0.01684)和胰岛素分泌(n = 5,P = 0.02115)被强烈激活。在四氧嘧啶诱导的糖尿病小鼠中,口服RBPP-P(n = 10)有效降低了血糖(P = 0.0326)、饮水量(P < 0.001)和尿量(P < 0.001)。它直接刺激p38(P = 0.00439)、ERK(P = 0.02951)和AKT(P = 0.0072)的磷酸化,以维持胰岛功能和质量。因此,我们的数据表明,RBPP-P是一种调节β细胞增殖和功能的天然化合物,表明它可能对1型糖尿病具有治疗潜力。