scholarly journals HRD1, an Important Player in Pancreatic β-Cell Failure and Therapeutic Target for Type 2 Diabetic Mice

Diabetes ◽  
2020 ◽  
Vol 69 (5) ◽  
pp. 940-953 ◽  
Author(s):  
Tijun Wu ◽  
Shuang Zhang ◽  
Jialiang Xu ◽  
Yaqin Zhang ◽  
Tong Sun ◽  
...  
Keyword(s):  
Therapeutic Target ◽  
Pancreatic Β Cell ◽  
Diabetic Mice ◽  
Β Cell ◽  
Important Player ◽  
Type 2 Diabetic

scholarly journals Pterocarpan-Enriched Soy Leaf Extract Ameliorates Insulin Sensitivity and Pancreatic β-Cell Proliferation in Type 2 Diabetic Mice

Molecules ◽  
2014 ◽  
Vol 19 (11) ◽  
pp. 18493-18510 ◽  
Author(s):  
Un-Hee Kim ◽  
Jeong-Hyun Yoon ◽  
Hua Li ◽  
Ji-Hyun Kang ◽  
Hyeon-Seon Ji ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Insulin Sensitivity ◽  
Leaf Extract ◽  
Pancreatic Β Cell ◽  
Diabetic Mice ◽  
Β Cell ◽  
Type 2 Diabetic

scholarly journals BBT improves glucose homeostasis by ameliorating β-cell dysfunction in type 2 diabetic mice

2015 ◽  
Vol 224 (3) ◽  
pp. 327-341 ◽  
Author(s):  
Xin-gang Yao ◽  
Xin Xu ◽  
Gai-hong Wang ◽  
Min Lei ◽  
Ling-ling Quan ◽  
...  
Keyword(s):  
Cell Death ◽  
Protective Action ◽  
Fasting Blood Glucose ◽  
Oral Glucose ◽  
Diabetic Mice ◽  
Β Cells ◽  
Β Cell ◽  
Cell Functions ◽  
Type 2 Diabetic

Impaired glucose-stimulated insulin secretion (GSIS) and increasing β-cell death are two typical dysfunctions of pancreatic β-cells in individuals that are destined to develop type 2 diabetes, and improvement of β-cell function through GSIS enhancement and/or inhibition of β-cell death is a promising strategy for anti-diabetic therapy. In this study, we discovered that the small molecule, N-(2-benzoylphenyl)-5-bromo-2-thiophenecarboxamide (BBT), was effective in both potentiating GSIS and protecting β-cells from cytokine- or streptozotocin (STZ)-induced cell death. Results of further studies revealed that cAMP/PKA and long-lasting (L-type) voltage-dependent Ca2+ channel/CaMK2 pathways were involved in the action of BBT against GSIS, and that the cAMP/PKA pathway was essential for the protective action of BBT on β-cells. An assay using the model of type 2 diabetic mice induced by high-fat diet combined with STZ (STZ/HFD) demonstrated that BBT administration efficiently restored β-cell functions as indicated by the increased plasma insulin level and decrease in the β-cell loss induced by STZ/HFD. Moreover, the results indicated that BBT treatment decreased fasting blood glucose and HbA1c and improved oral glucose tolerance further highlighting the potential of BBT in anti-hyperglycemia research.

scholarly journals Effect of Hydrolyzed Bird’s Nest on β-Cell Function and Insulin Signaling in Type 2 Diabetic Mice

2021 ◽  
Vol 12 ◽  
Author(s):  
Ker Woon Choy ◽  
Zuhaida Md Zain ◽  
Dharmani Devi Murugan ◽  
Nelli Giribabu ◽  
Nor Hisam Zamakshshari ◽  
...  
Keyword(s):  
Insulin Signaling ◽  
Cell Function ◽  
Serum Insulin ◽  
Fasting Blood Glucose ◽  
Diabetic Mice ◽  
Β Cell ◽  
Β Cell Function ◽  
Type 2 Diabetic ◽  
Pro Inflammatory Cytokines

Type 2 diabetes mellitus is characterized by both resistance to the action of insulin and defects in insulin secretion. Bird’s nest, which is derived from the saliva of swiftlets are well known to possess multiple health benefits dating back to Imperial China. However, it’s effect on diabetes mellitus and influence on the actions of insulin action remains to be investigated. In the present study, the effect of standardized aqueous extract of hydrolyzed edible bird nest (HBN) on metabolic characteristics and insulin signaling pathway in pancreas, liver and skeletal muscle of db/db, a type 2 diabetic mice model was investigated. Male db/db diabetic and its euglycemic control, C57BL/6J mice were administered HBN (75 and 150 mg/kg) or glibenclamide (1 mg/kg) orally for 28 days. Metabolic parameters were evaluated by measuring fasting blood glucose, serum insulin and oral glucose tolerance test (OGTT). Insulin signaling and activation of inflammatory pathways in liver, adipose, pancreas and muscle tissue were evaluated by Western blotting and immunohistochemistry. Pro-inflammatory cytokines were measured in the serum at the end of the treatment. The results showed that db/db mice treated with HBN significantly reversed the elevated fasting blood glucose, serum insulin, serum pro-inflammatory cytokines levels and the impaired OGTT without affecting the body weight of the mice in all groups. Furthermore, HBN treatment significantly ameliorated pathological changes and increased the protein expression of insulin, and glucose transporters in the pancreatic islets (GLUT-2), liver and skeletal muscle (GLUT-4). Likewise, the Western blots analysis denotes improved insulin signaling and antioxidant enzyme, decreased reactive oxygen species producing enzymes and inflammatory molecules in the liver and adipose tissues of HBN treated diabetic mice. These results suggest that HBN improves β-cell function and insulin signaling by attenuation of oxidative stress mediated chronic inflammation in the type 2 diabetic mice.

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