Protective effects of an herbal formulation of Radix Astragali , Radix Codonopsis and Cortex Lycii on streptozotocin-induced apoptosis in pancreatic β -cells: an implication for its treatment of diabetes mellitus

2007 ◽  
Vol 22 (2) ◽  
pp. 190-196 ◽  
Author(s):  
Judy Yuet-Wa Chan ◽  
Ping-Chung Leung ◽  
Chun-Tao Che ◽  
Kwok-Pui Fung
Keyword(s):  
Diabetes Mellitus ◽  
Protective Effects ◽  
Radix Astragali ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Astragali Radix ◽  
Herbal Formulation ◽  
Treatment Of Diabetes ◽  
Induced Apoptosis ◽  
Cortex Lycii

Natural Products Modulating Autophagy Pathway Against the Pathogenesis of Diabetes Mellitus

2018 ◽  
Vol 20 (1) ◽  
pp. 96-110 ◽  
Author(s):  
Linghuan Li ◽  
Jiameng Qi ◽  
Hanbing Li
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Natural Products ◽  
Potential Drug ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Drug Candidates ◽  
Peripheral Insulin Resistance ◽  
Treatment Of Diabetes ◽  
Autophagy Pathway

Autophagy is a conserved, regulated cellular process for the degradation of abnormal proteins and disrupted organelles. Literature has described that dysregulation of autophagy is closely related to the pathogenesis of diabetes mellitus in processes such as impaired pancreatic β cells function, peripheral insulin resistance and diabetic complications. Emerging evidence indicates that natural products may possess anti-diabetic activity via regulation of autophagy. In this review, we summarize natural products targeting the pathogenesis of diabetes mellitus through the regulation of autophagy and underline possible mechanisms, providing potential drug candidates or therapies for the treatment of diabetes mellitus.

Electrospun Nanofibers for Diabetes: Tissue Engineering and Cell-Based Therapies

2019 ◽  
Vol 14 (2) ◽  
pp. 152-168 ◽  
Author(s):  
Elham Hoveizi ◽  
Shima Tavakol ◽  
Sadegh Shirian ◽  
Khadije Sanamiri
Keyword(s):  
Diabetes Mellitus ◽  
Tissue Engineering ◽  
Therapeutic Approach ◽  
Electrospun Nanofibers ◽  
Review Article ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Nanofibrous Scaffolds ◽  
Treatment Of Diabetes

Diabetes mellitus is an autoimmune disease which causes loss of insulin secretion producing hyperglycemia by promoting progressive destruction of pancreatic β cells. An ideal therapeutic approach to manage diabetes mellitus is pancreatic β cells replacement. The aim of this review article was to evaluate the role of nanofibrous scaffolds and stem cells in the treatment of diabetes mellitus. Various studies have pointed out that application of electrospun biomaterials has considerably attracted researchers in the field of tissue engineering. The principles of cell therapy for diabetes have been reviewed in the first part of this article, while the usability of tissue engineering as a new therapeutic approach is discussed in the second part.

scholarly journals Synergistic Effects of Milk-Derived Exosomes and Galactose on α-Synuclein Pathology in Parkinson’s Disease and Type 2 Diabetes Mellitus

2021 ◽  
Vol 22 (3) ◽  
pp. 1059
Author(s):  
Bodo C. Melnik
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Dopaminergic Neurons ◽  
Vagal Nerve ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
The Brain

Epidemiological studies associate milk consumption with an increased risk of Parkinson’s disease (PD) and type 2 diabetes mellitus (T2D). PD is an α-synucleinopathy associated with mitochondrial dysfunction, oxidative stress, deficient lysosomal clearance of α-synuclein (α-syn) and aggregation of misfolded α-syn. In T2D, α-syn promotes co-aggregation with islet amyloid polypeptide in pancreatic β-cells. Prion-like vagal nerve-mediated propagation of exosomal α-syn from the gut to the brain and pancreatic islets apparently link both pathologies. Exosomes are critical transmitters of α-syn from cell to cell especially under conditions of compromised autophagy. This review provides translational evidence that milk exosomes (MEX) disturb α-syn homeostasis. MEX are taken up by intestinal epithelial cells and accumulate in the brain after oral administration to mice. The potential uptake of MEX miRNA-148a and miRNA-21 by enteroendocrine cells in the gut, dopaminergic neurons in substantia nigra and pancreatic β-cells may enhance miRNA-148a/DNMT1-dependent overexpression of α-syn and impair miRNA-148a/PPARGC1A- and miRNA-21/LAMP2A-dependent autophagy driving both diseases. MiRNA-148a- and galactose-induced mitochondrial oxidative stress activate c-Abl-mediated aggregation of α-syn which is exported by exosome release. Via the vagal nerve and/or systemic exosomes, toxic α-syn may spread to dopaminergic neurons and pancreatic β-cells linking the pathogenesis of PD and T2D.

scholarly journals Teucrium polium: Potential Drug Source for Type 2 Diabetes Mellitus

Biology ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 128
Author(s):  
Yaser Albadr ◽  
Andrew Crowe ◽  
Rima Caccetta
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Insulin Secretion ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Glucose Levels ◽  
Teucrium Polium

The prevalence of type 2 diabetes mellitus is rising globally and this disease is proposed to be the next pandemic after COVID-19. Although the cause of type 2 diabetes mellitus is unknown, it is believed to involve a complex array of genetic defects that affect metabolic pathways which eventually lead to hyperglycaemia. This hyperglycaemia arises from an inability of the insulin-sensitive cells to sufficiently respond to the secreted insulin, which eventually results in the inadequate secretion of insulin from pancreatic β-cells. Several treatments, utilising a variety of mechanisms, are available for type 2 diabetes mellitus. However, more medications are needed to assist with the optimal management of the different stages of the disease in patients of varying ages with the diverse combinations of other medications co-administered. Throughout modern history, some lead constituents from ancient medicinal plants have been investigated extensively and helped in developing synthetic antidiabetic drugs, such as metformin. Teucrium polium L. (Tp) is a herb that has a folk reputation for its antidiabetic potential. Previous studies indicate that Tp extracts significantly decrease blood glucose levels r and induce insulin secretion from pancreatic β-cells in vitro. Nonetheless, the constituent/s responsible for this action have not yet been elucidated. The effects appear to be, at least in part, attributable to the presence of selected flavonoids (apigenin, quercetin, and rutin). This review aims to examine the reported glucose-lowering effect of the herb, with a keen focus on insulin secretion, specifically related to type 2 diabetes mellitus. An analysis of the contribution of the key constituent flavonoids of Tp extracts will also be discussed.

scholarly journals G protein-coupled receptor 119 agonist DS-8500a effects on pancreatic β-cells in Japanese type 2 diabetes mellitus patients

2018 ◽  
Vol 10 (1) ◽  
pp. 84-93 ◽  
Author(s):  
Hirotaka Watada ◽  
Masanari Shiramoto ◽  
Shin Irie ◽  
Yasuo Terauchi ◽  
Yuichiro Yamada ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
G Protein ◽  
G Protein Coupled Receptor ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
G Protein Coupled

Delphinidin-induced autophagy protects pancreatic β cells against apoptosis resulting from high-glucose stress via AMPK signaling pathway

2019 ◽  
Vol 51 (12) ◽  
pp. 1242-1249 ◽  
Author(s):  
Dengni Lai ◽  
Mingyong Huang ◽  
Lingyan Zhao ◽  
Yan Tian ◽  
Yong Li ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
High Glucose ◽  
Cell Mass ◽  
Protective Role ◽  
Common Disease ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Ampk Signaling ◽  
Compound C ◽  
Induced Apoptosis

Abstract Hyperglycemia, a diagnostic characteristic of diabetes mellitus, is detrimental to pancreatic β cells. Delphinidin, a member of the anthocyanin family, inhibits glucose absorption, increases glucagon-like peptide-1 (GLP-1) secretion, and improves insulin secretion in diabetes. However, whether delphinidin plays a protective role in pancreatic β-cell mass and function is not clear. In this study, delphinidin was found to decrease the high-glucose-induced apoptosis of RIN-m5F pancreatic β cells. In addition, delphinidin induced autophagy in RIN-m5F cells under the normal and high-glucose conditions, while 3-methyladenine (3-MA) inhibition of autophagy significantly diminished the protective role of delphinidin against high-glucose-induced apoptosis of pancreatic β cells. Delphinidin also decreased the level of cleaved caspase 3 and increased the phosphorylation level of AMP-activated protein kinase α (AMPKα) Thr172. Compound C, an AMPK inhibitor, was found to decrease the ratio of LC3-II/LC3-I, and the apoptotic rate of high-glucose-injured cells was increased after treatment with delphinidin, indicating that delphinidin attenuated the negative effects of high-glucose stress to cells. In conclusion, our data demonstrate that delphinidin protects pancreatic β cells against high-glucose-induced injury by autophagy regulation via the AMPK signaling pathway. These findings might shed light on the underlying mechanisms of diabetes and help improve the prevention and therapy of this common disease.

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