ReferenceID 870
Mori Ramulus Inhibits Pancreatic β-Cell Apoptosis and Prevents Insulin Resistance by Restoring Hepatic Mitochondrial Function
Antioxidants (Basel)
Type 2 diabetes mellitus is characterized by insulin resistance and pancreatic beta (beta)-cell dysfunction. Accumulating evidence suggests that mitochondrial dysfunction may cause insulin resistance in peripheral tissue
Relationship Network
Interactive first-hop connections across herbs, ingredients, formulas, targets, diseases, symptoms, syndromes, evidence, and monographs.
Click a node to open it in a new tab
Herb: 1Reference: 1Links: 1
Arranging relationship network...
Record Fields
Scalar fields from the final reference record.
- Reference Id
- 870
- Evidence Id
- 17460
- Core Evidence Id
- 17460
- Source Reference Id
- 1736
- Herb2 Reference Id
- HBREF002533
- Subject Paper Key
- HERB004837_34204891
- Pubmed Id
- 34204891
- Doi
- 10.3390/antiox10060901
- Paper Title
- Mori Ramulus Inhibits Pancreatic β-Cell Apoptosis and Prevents Insulin Resistance by Restoring Hepatic Mitochondrial Function
- Paper Abstract
- Type 2 diabetes mellitus is characterized by insulin resistance and pancreatic beta (beta)-cell dysfunction. Accumulating evidence suggests that mitochondrial dysfunction may cause insulin resistance in peripheral tissues. As commercial hypoglycemic drugs have side effects, it is necessary to develop safe and effective natural compound-based hypoglycemic treatments. This study aimed to investigate the hypoglycemic effects of Mori Ramulus ethanol extract (ME) in a high-fat diet (HFD)-induced diabetes mouse model to decipher the underlying mechanisms focusing on apoptosis and mitochondrial function. ME significantly decreased tunicamycin-induced apoptotic cell death and increased insulin secretion following glucose stimulation in NIT-1 pancreatic beta-cells. Tunicamycin-exposed NIT-1 pancreatic beta-cells showed elevated reactive oxygen species levels and reduced mitochondrial membrane potential, which were reversed by ME treatment. ME inhibited the tunicamycin-induced apoptosis cascade in tunicamycin-exposed NIT-1 pancreatic beta-cells. In HFD diabetic mice, the serum-free fatty acid and insulin levels decreased following a 15-week ME administration. Glucose and insulin tolerance tests showed that ME improved insulin sensitivity. Moreover, ME ameliorated pancreatic beta-cell mass loss in diabetic mice. Finally, ME-treated HFD-fed mice showed improved hepatic mitochondrial function resulting in insulin sensitivity in target tissues. Thus, ME provides protection against pancreatic beta-cell apoptosis and prevents insulin resistance by improving mitochondrial function.
- Journal
- Antioxidants (Basel)
- Publish Year
- 2021
- Experiment Subject
- mouse; nit-1 pancreatic beta-cells; tunicamycin-exposed nit-1 pancreatic beta-cells
- Experiment Type
- Animal Experiment
- Phenotype Related
- Mitochondrial Dysfunction; Type 2 Diabetes Mellitus; Diabetic; Pancreatic Beta (beta)-cell Dysfunction; Diabetes
- Paper Title Cn
- Paper Title En
- Mori Ramulus Inhibits Pancreatic β-Cell Apoptosis and Prevents Insulin Resistance by Restoring Hepatic Mitochondrial Function
- Bilingual Status
- semi_complete