Mulberry branch bark powder significantly improves hyperglycemia and regulates insulin secretion in type II diabetic mice

Abstract

This experiment, based on the previous study on R. mori, introduces whole mulberry branch powder into the diet to treat diabetic mice. Mulberry branch bark powder (MBBP) was administered orally to streptozotocin (STZ)-induced type II diabetic (T2D) mice to investigate hypoglycemic effects. After a 4-week period of diet consumption containing 5%, 10% and 20% MBBP, the fasting blood glucose, body weight and the related western blotting were measured, pathologic and immunohistochemical were observed. The 20% MBBP group showed a significant reduction in hyperglycemia and hyperinsulinemia; fasting blood glucose and insulin decreased from 25.0 to 14.8 mmol/L and 26.5 to 16.0 mU/L, respectively. Pathologic and immunohistochemical observation showed that MBBP administration lead to the repair of pancreas cells and restoration of insulin secretion. Dietary MBBP was associated with the decrease in the contents of 3, 4-methylenedioxeamphetamine, 8-OHdG, aspartate aminotransferase, and alanine aminotransferase, and the increase in antioxidative ability and glucose tolerance. Western blotting (WB) analysis suggested that MBBP decreased the TNF-α levels, thus relieving inflammation and improving liver function. It also led to the downregulation of apoptosis factor expression. WB also confirmed that MBBP enhanced the gene expression of the key enzymes: insulin receptor, insulin receptor substrate, p-AKT, GSK3β, glycogen synthase, G6Pase and phosphoenolpyruvate carboxykinase, which are related to glucose metabolism in the liver, and increase the expression of the genes PDX-1, GLUT2, MafA, and glucokinase, related to insulin secretion. Thus, oral administration of MBBP regulated insulin secretion and effectively maintained normal levels of glucose metabolism in mice, which may be done by improving the antioxidant capacity and activating insulin signaling with T2D..

Retracted: Bilobalide alleviates tumor necrosis factor‐alpha‐induced pancreatic beta‐cell MIN6 apoptosis and dysfunction through upregulation of miR‐153

“…Moreover, TNF‐α is investigated to involve in insulin secretion. The increase of TNF‐α promoted apoptosis and suppressed insulin secretion in pancreatic cells of T2DM (Yin, Liu, & Zhang, ). In our research, we had consistent results in T1DM.…”

MicroRNA-17-92 Regulates Beta-Cell Restoration After Streptozotocin Treatment

“…Diabetes mellitus shows features of hyperglycemia because of absolutely or relatively insufficient serum insulin secretion. Pancreatic beta-cells have fundamental functions to modulate insulin synthesis and secretion, which is regulated by various transcriptional activators such as Pdx-1 (pancreas/duodenum homeobox factor-1) (54), MafA (55,56), and Glut2 (57)(58)(59) and transcriptional repressors including Sox6 (60) and Crem (61). Pdx-1 plays pivotal roles in the early differentiation, maturation and regeneration of pancreatic islet cells (57).…”

“…Pancreatic beta-cells have fundamental functions to modulate insulin synthesis and secretion, which is regulated by various transcriptional activators such as Pdx-1 (pancreas/duodenum homeobox factor-1) (54), MafA (55,56), and Glut2 (57)(58)(59) and transcriptional repressors including Sox6 (60) and Crem (61). Pdx-1 plays pivotal roles in the early differentiation, maturation and regeneration of pancreatic islet cells (57). MafA is highly expressed in pancreatic beta-cells, which activates the transcription of the insulin gene by targeting RIPE3b1, a cisregulatory element (62)(63)(64).…”

“…The expression of MafA gene is down-regulated, thus inhibiting the transcription of insulin in diabetes mellitus (55,56). MafA can regulate the expression of insulin gene as well as other related factors including Pdx-1 and Glut2 (57). Glut2 is a glucose transporter in pancreatic betacells, which can transport glucose and regulate ion channels on cell membrane, thus promoting insulin secretion (57).…”

“…MafA can regulate the expression of insulin gene as well as other related factors including Pdx-1 and Glut2 (57). Glut2 is a glucose transporter in pancreatic betacells, which can transport glucose and regulate ion channels on cell membrane, thus promoting insulin secretion (57). Sox6, a member of the high mobility group box superfamily, acts as a co-repressor with Pdx-1 and plays critical roles in pancreatic beta-cell replication and insulin gene transcription (65).…”