Cyanidin Stimulates Insulin Secretion and Pancreatic β-Cell Gene Expression through Activation of l-type Voltage-Dependent Ca2+ Channels

Cyanidin is a natural anthocyanidin present in fruits and vegetables with anti-diabetic properties including stimulation of insulin secretion. However, its mechanism of action remains unknown. In this study, we elucidated the mechanisms of cyanidin for stimulatory insulin secretion from pancreatic β-cells. Rat pancreatic β-cells INS-1 were used to investigate the effects of cyanidin on insulin secretion, intracellular Ca2+ signaling, and gene expression. We detected the presence of cyanidin in the intracellular space of β-cells. Cyanidin stimulated insulin secretion and increased intracellular Ca2+ signals in a concentration-dependent manner. The Ca2+ signals were abolished by nimodipine, an l-type voltage-dependent Ca2+ channel (VDCC) blocker or under extracellular Ca2+ free conditions. Stimulation of cells with cyanidin activated currents typical for VDCCs and up-regulated the expression of glucose transporter 2 (GLUT2), Kir6.2, and Cav1.2 genes. Our findings indicate that cyanidin diffuses across the plasma membrane, leading to activation of l-type VDCCs. The increase in intracellular Ca2+ stimulated insulin secretion and the expression of genes involved in this process. These findings suggest that cyanidin could be used as a promising agent to stimulate insulin secretion

Capability of polygonum cuspidatum extract in inhibiting AGEs and preventing diabetes

Diabetes is a metabolic disorder disease associated with advanced glycation end products (AGEs) and protein glycation. The effect of polygonum cuspidatum extract (PE) on AGEs and Nε‐(Carboxymethyl)‐L‐lysine formation, protein glycation, and diabetes was investigated. Six primary phenolics in a range of 12.36 mg/g for ellagic acid to 0.01 mg/g for piceid were determined in PE. In an intermediate‐moisture‐foods model, inhibition rate of PE was as high as 54.2% for AGEs and 78.9% for CML under aw 0.75. The protein glycation was also inhibited by PE. In a diabetic rat model, the levels of blood glucose, serum malondialdehyde, cholesterol, triglycerides, and low‐density lipoproteins were effectively reduced by PE treatment. The antioxidation capacity (T‐AOC) and superoxide dismutase (SOD) activity were also mediated by PE. Additionally, the activates of liver function‐related enzymes including alkaline phosphatase (ALP), glutamate pyruvate transaminase (GPT), and glutamate oxaloacetate transaminase (GOT) in diabetic rat were improved by PE