Cocoa-rich diet attenuates beta cell mass loss and function in young Zucker diabetic fatty rats by preventing oxidative stress and beta cell apoptosis

2015 ◽  
Vol 59 (4) ◽  
pp. 820-824 ◽  
Author(s):  
Elisa Fernández-Millán ◽  
Isabel Cordero-Herrera ◽  
Sonia Ramos ◽  
Fernando Escrivá ◽  
Carmen Alvarez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Beta Cell ◽  
Mass Loss ◽  
Cell Apoptosis ◽  
Cell Mass ◽  
Beta Cell Mass ◽  
Beta Cell Apoptosis ◽  
Zucker Diabetic Fatty Rats ◽  
And Function

scholarly journals Mechanisms of Beta-Cell Apoptosis in Type 2 Diabetes-Prone Situations and Potential Protection by GLP-1-Based Therapies

2021 ◽  
Vol 22 (10) ◽  
pp. 5303
Author(s):  
Safia Costes ◽  
Gyslaine Bertrand ◽  
Magalie A. Ravier
Keyword(s):  
Type 2 Diabetes ◽  
Beta Cell ◽  
Beta Cells ◽  
Cell Apoptosis ◽  
Molecular Mechanisms ◽  
Cell Mass ◽  
Beta Cell Mass ◽  
Beta Cell Apoptosis ◽  
Chronic Hyperglycemia

Type 2 diabetes (T2D) is characterized by chronic hyperglycemia secondary to the decline of functional beta-cells and is usually accompanied by a reduced sensitivity to insulin. Whereas altered beta-cell function plays a key role in T2D onset, a decreased beta-cell mass was also reported to contribute to the pathophysiology of this metabolic disease. The decreased beta-cell mass in T2D is, at least in part, attributed to beta-cell apoptosis that is triggered by diabetogenic situations such as amyloid deposits, lipotoxicity and glucotoxicity. In this review, we discussed the molecular mechanisms involved in pancreatic beta-cell apoptosis under such diabetes-prone situations. Finally, we considered the molecular signaling pathways recruited by glucagon-like peptide-1-based therapies to potentially protect beta-cells from death under diabetogenic situations.

scholarly journals The postnatal growth of the beta-cell mass in pigs

2003 ◽  
Vol 179 (2) ◽  
pp. 245-252 ◽  
Author(s):  
T Bock ◽  
A Kyhnel ◽  
B Pakkenberg ◽  
K Buschard
Keyword(s):  
Beta Cell ◽  
Linear Relationship ◽  
Body Mass ◽  
Cell Apoptosis ◽  
Cell Mass ◽  
Beta Cell Mass ◽  
Postnatal Growth ◽  
The Body ◽  
Constant Level ◽  
Beta Cell Apoptosis

Studies of the postnatal growth of the beta-cell mass in rats have revealed some unexpected and apparently paradoxical results, the most prominent being a beta-cell mass plateau in the early phase of life. We have studied the postnatal growth of the beta-cell mass in the domestic pig to investigate its development in a larger mammal. The pancreases from a total of 86 male pigs from 5 to 100 days of age were studied. The beta-cell mass increased linearly from day 5 to day 40, reached a plateau from day 40 to day 60, and then increased further into adulthood. The relative beta-cell mass (beta-cell mass per body mass) was increased in the early postnatal period but reached a constant level from day 60, after which there was a linear relationship between the beta-cell mass and the body mass. There were high rates of both beta-cell apoptosis and mitosis at 50 and 60 days of age, while the Volume-weighted mean islet Volume increased from birth and reached a plateau at approximately 60 days of age. A beta-cell mass plateau early in life accompanied by a wave of beta-cell apoptosis coinciding with the relative beta-cell mass decreasing to reach a constant level, and a linear relationship between the beta-cell mass and the body mass in later life is exactly what has previously been reported in rats. The coincidence of these events in both rats and pigs, although occurring at different ages in the two species, suggests a causal relationship as previously suggested in a proposed explanatory model for postnatal beta-cell growth.

scholarly journals Reduced beta-cell mass and expression of oxidative stress-related DNA damage in the islet of Japanese Type II diabetic patients

Diabetologia ◽  
2002 ◽  
Vol 45 (1) ◽  
pp. 85-96 ◽  
Author(s):  
H. Sakuraba ◽  
H. Mizukami ◽  
N. Yagihashi ◽  
R. Wada ◽  
C. Hanyu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Beta Cell ◽  
Cell Mass ◽  
Beta Cell Mass ◽  
Diabetic Patients ◽  
Type Ii

scholarly journals Oxidative stress is induced by islet amyloid formation and time-dependently mediates amyloid-induced beta cell apoptosis

Diabetologia ◽  
2009 ◽  
Vol 52 (4) ◽  
pp. 626-635 ◽  
Author(s):  
S. Zraika ◽  
R. L. Hull ◽  
J. Udayasankar ◽  
K. Aston-Mourney ◽  
S. L. Subramanian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Beta Cell ◽  
Cell Apoptosis ◽  
Beta Cell Apoptosis ◽  
Amyloid Formation ◽  
Islet Amyloid

scholarly journals Effect of Hypertriglyceridemia on Beta Cell Mass and Function in ApoC3 Transgenic Mice

2016 ◽  
Vol 291 (28) ◽  
pp. 14695-14705 ◽  
Author(s):  
Yun-Zi Liu ◽  
Xiaoyun Cheng ◽  
Ting Zhang ◽  
Sojin Lee ◽  
Jun Yamauchi ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Beta Cell ◽  
Cell Mass ◽  
Beta Cell Mass ◽  
And Function

scholarly journals Mechanisms involved in the beta-cell mass increase induced by chronic sucrose feeding to normal rats

2002 ◽  
Vol 174 (2) ◽  
pp. 225-231 ◽  
Author(s):  
H Del Zotto ◽  
CL Gomez Dumm ◽  
S Drago ◽  
A Fortino ◽  
GC Luna ◽  
...  
Keyword(s):  
Body Weight ◽  
Beta Cell ◽  
Beta Cells ◽  
Cell Mass ◽  
Beta Cell Mass ◽  
Serum Glucose ◽  
Beta Cell Apoptosis ◽  
Cell Replication ◽  
Replication Rate ◽  
Endocrine Tissue

The aim of the present study was to clarify the mechanisms by which a sucrose-rich diet (SRD) produces an increase in the pancreatic beta-cell mass in the rat. Normal Wistar rats were fed for 30 weeks either an SRD (SRD rats; 63% wt/wt), or the same diet but with starch instead of sucrose in the same proportion (CD rats). We studied body weight, serum glucose and triacylglycerol levels, endocrine tissue and beta-cell mass, beta-cell replication rate (proliferating cell nuclear antigen; PCNA), islet neogenesis (cytokeratin immunostaining) and beta-cell apoptosis (propidium iodide). Body weight (g) recorded in the SRD rats was significantly (P<0.05) larger than that of the CD group (556.0+/-8.3 vs 470.0+/-13.1). Both serum glucose and triacylglycerol levels (mmol/l) were also significantly higher (P<0.05) in SRD than in CD rats (serum glucose, 8.11+/-0.14 vs 6.62+/-0.17; triacylglycerol, 1.57+/-0.18 vs 0.47+/-0.04). The number of pancreatic islets per unit area increased significantly (P<0.05) in SRD rats (3.29+/-0.1 vs 2.01+/-0.2). A significant increment (2.6 times) in the mass of endocrine tissue was detected in SRD animals, mainly due to an increase in the beta-cell mass (P=0.0025). The islet cell replication rate, measured as the percentage of PCNA-labelled beta cells increased 6.8 times in SRD rats (P<0.03). The number of apoptotic cells in the endocrine pancreas decreased significantly (three times) in the SRD animals (P=0.03). The cytokeratin-positive area did not show significant differences between CD and SRD rats. The increase of beta-cell mass induced by SRD was accomplished by an enhanced replication of beta cells together with a decrease in the rate of beta-cell apoptosis, without any evident participation of islet neogenesis. This pancreatic reaction was unable to maintain serum glucose levels of these rats at the level measured in CD animals.

scholarly journals Insulin mutations impair beta-cell development in a patient-derived iPSC model of neonatal diabetes

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Diego Balboa ◽  
Jonna Saarimäki-Vire ◽  
Daniel Borshagovski ◽  
Mantas Survila ◽  
Päivi Lindholm ◽  
...  
Keyword(s):  
Beta Cell ◽  
Er Stress ◽  
Cell Mass ◽  
Gene Mutations ◽  
Beta Cell Mass ◽  
Neonatal Diabetes ◽  
Beta Cell Apoptosis ◽  
Beta Cell Proliferation ◽  
Sequencing Analysis ◽  
Mtorc1 Signaling

Insulin gene mutations are a leading cause of neonatal diabetes. They can lead to proinsulin misfolding and its retention in endoplasmic reticulum (ER). This results in increased ER-stress suggested to trigger beta-cell apoptosis. In humans, the mechanisms underlying beta-cell failure remain unclear. Here we show that misfolded proinsulin impairs developing beta-cell proliferation without increasing apoptosis. We generated induced pluripotent stem cells (iPSCs) from people carrying insulin (INS) mutations, engineered isogenic CRISPR-Cas9 mutation-corrected lines and differentiated them to beta-like cells. Single-cell RNA-sequencing analysis showed increased ER-stress and reduced proliferation in INS-mutant beta-like cells compared with corrected controls. Upon transplantation into mice, INS-mutant grafts presented reduced insulin secretion and aggravated ER-stress. Cell size, mTORC1 signaling, and respiratory chain subunits expression were all reduced in INS-mutant beta-like cells, yet apoptosis was not increased at any stage. Our results demonstrate that neonatal diabetes-associated INS-mutations lead to defective beta-cell mass expansion, contributing to diabetes development.

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