scholarly journals Role of Bioactive Food Components in Diabetes Prevention: Effects on Beta-Cell Function and Preservation

2014 ◽  
Vol 7 ◽  
pp. NMI.S13589 ◽  
Author(s):  
Yoon Sin Oh ◽  
Hee-Sook Jun
Keyword(s):  
Beta Cell ◽  
Bioactive Compounds ◽  
Fruits And Vegetables ◽  
Cell Function ◽  
Published Data ◽  
Diabetic Patients ◽  
Beta Cell Apoptosis ◽  
Beta Cell Proliferation ◽  
Clinical Effects ◽  
Beneficial Effects

Bioactive compounds found in fruits and vegetables can have anti-oxidant, anti-inflammatory, and anti-carcinogenic effects and can be protective against various diseases and metabolic disorders. These beneficial effects make them good candidates for the development of new functional foods with potential protective and preventive properties for type 1 and type 2 diabetes. This review summarizes the most relevant results concerning the effects of various bioactive compounds such as flavonoids, vitamins, and carotenoids on several aspects of beta-cell functionality. Studies using animal models with induced diabetes and diabetic patients support the hypothesis that bioactive compounds could ameliorate diabetic phenotypes. Published data suggest that there might be direct effects of bioactive compounds on enhancing insulin secretion and preventing beta-cell apoptosis, and some compounds might modulate beta-cell proliferation. Further research is needed to establish any clinical effects of these compounds.

scholarly journals Melatonin and diabetes: from pathophysiology to the treatment perspectives

2013 ◽  
Vol 16 (2) ◽  
pp. 11-16 ◽  
Author(s):  
Vladimir Iosifovich Konenkov ◽  
Vadim Valerievich Klimontov ◽  
Svetlana Viktorovna Michurina ◽  
M A Prudnikova ◽  
I Ju Ishenko
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Cell Function ◽  
Association Studies ◽  
Diabetes Mellitus Type 1 ◽  
Experimental Models ◽  
Diabetic Patients ◽  
Beta Cell Proliferation ◽  
Genome Wide Association Studies ◽  
Genome Wide

Pineal hormone melatonin synchronizes insulin secretion and glucose homeostasis with solar periods. Misalliance between melatonin-mediated circadian rhythms and insulin secretion characterizes diabetes mellitus type 1 (T1DM) and type 2 (T2DM). Insulin deficiency in T1DM is accompanied by increased melatonin production. Conversely, T2DM is characterized by diminished melatonin secretion. In genome-wide association studies the variants of melatonin receptor MT2 gene (rs1387153 and rs10830963) were associated with fasting glucose, beta-cell function and T2DM. In experimental models of diabetes melatonin enhanced beta-cell proliferation and neogenesis, improved insulin resistance and alleviated oxidative stress in retina and kidneys. However, further investigation is required to assess the therapeutic value of melatonin in diabetic patients.

scholarly journals Serum CA19-9 Level Associated with Metabolic Control and Pancreatic Beta Cell Function in Diabetic Patients

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Haoyong Yu ◽  
Ruixia Li ◽  
Lei Zhang ◽  
Haibing Chen ◽  
Yuqian Bao ◽  
...  
Keyword(s):  
Glycemic Control ◽  
Beta Cell ◽  
Total Cholesterol ◽  
Beta Cell Function ◽  
Cell Function ◽  
Total Cholesterol Level ◽  
Pancreatic Beta Cell ◽  
Elevated Serum ◽  
Diabetic Patients ◽  
Pancreatic Beta Cell Function

CA19-9 is a tumor-associated antigen. It is also a marker of pancreatic tissue damage that might be caused by diabetes. Long-term poor glycemic control may lead to pancreatic beta cell dysfunction which is reflected by elevated serum CA19-9 level. Intracellular cholesterol accumulation leads to islet dysfunction and impaired insulin secretion which provide a new lipotoxic model. This study firstly found total cholesterol was one of the independent contributors to CA19-9. Elevated serum CA19-9 level in diabetic patients may indicate further investigations of glycemic control, pancreatic beta cell function, and total cholesterol level.

scholarly journals Bergenin protects pancreatic beta cells against cytokine-induced apoptosis in INS-1E cells

PLoS ONE ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. e0241349
Author(s):  
Sajid Ali Rajput ◽  
Munazza Raza Mirza ◽  
M. Iqbal Choudhary
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Beta Cells ◽  
Proinflammatory Cytokines ◽  
Cell Apoptosis ◽  
Pancreatic Beta Cells ◽  
Cell Function ◽  
Beta Cell Apoptosis ◽  
Atp Levels ◽  
Induced Apoptosis

Beta cell apoptosis induced by proinflammatory cytokines is one of the hallmarks of diabetes. Small molecules which can inhibit the cytokine-induced apoptosis could lead to new drug candidates that can be used in combination with existing therapeutic interventions against diabetes. The current study evaluated several effects of bergenin, an isocoumarin derivative, in beta cells in the presence of cytokines. These included (i) increase in beta cell viability (by measuring cellular ATP levels) (ii) suppression of beta cell apoptosis (by measuring caspase activity), (iii) improvement in beta cell function (by measuring glucose-stimulated insulin secretion), and (iv) improvement of beta cells mitochondrial physiological functions. The experiments were carried out using rat beta INS-1E cell line in the presence or absence of bergenin and a cocktail of proinflammatory cytokines (interleukin-1beta, tumor necrosis factor-alpha, and interferon- gamma) for 48 hr. Bergenin significantly inhibited beta cell apoptosis, as inferred from the reduction in the caspase-3 activity (IC50 = 7.29 ± 2.45 μM), and concurrently increased cellular ATP Levels (EC50 = 1.97 ± 0.47 μM). Bergenin also significantly enhanced insulin secretion (EC50 = 6.73 ± 2.15 μM) in INS-1E cells, presumably because of the decreased nitric oxide production (IC50 = 6.82 ± 2.83 μM). Bergenin restored mitochondrial membrane potential (EC50 = 2.27 ± 0.83 μM), decreased ROS production (IC50 = 14.63 ± 3.18 μM), and improved mitochondrial dehydrogenase activity (EC50 = 1.39 ± 0.62 μM). This study shows for the first time that bergenin protected beta cells from cytokine-induced apoptosis and restored insulin secretory function by virtue of its anti-inflammatory, antioxidant and anti-apoptotic properties. To sum up, the above mentioned data highlight bergenin as a promising anti-apoptotic agent in the context of diabetes.

Beta Cell Function in Insulin-Treated Non-Insulin-Dependent Diabetic Patients

Pancreas ◽  
1986 ◽  
Vol 1 (5) ◽  
pp. 411-414
Author(s):  
Ambady Ramachandran ◽  
Chamukuttan Snehalatha ◽  
Viswanathan Mohan ◽  
Appa Rao ◽  
Moopil Viswanathan
Keyword(s):  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Diabetic Patients ◽  
Insulin Dependent ◽  
Insulin Dependent Diabetic

Effect of beta-blocking drugs on beta-cell function and insulin sensitivity in hypertensive non-diabetic patients

1984 ◽  
Vol 26 (1) ◽  
pp. 13-17 ◽  
Author(s):  
K. T�tterman ◽  
L. Groop ◽  
P. -H. Groop ◽  
R. Kala ◽  
E. -M. Tolppanen ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Diabetic Patients ◽  
Beta Blocking

scholarly journals Role of C-Peptide in the Regulation of Microvascular Blood Flow

2008 ◽  
Vol 2008 ◽  
pp. 1-8 ◽  
Author(s):  
T. Forst ◽  
T. Kunt ◽  
B. Wilhelm ◽  
M. M. Weber ◽  
A. Pfützner
Keyword(s):  
Blood Flow ◽  
Beta Cell ◽  
Cell Function ◽  
Pancreatic Beta Cell ◽  
Microvascular Blood Flow ◽  
Diabetic Patients ◽  
C Peptide ◽  
Glucose Levels ◽  
Peptide Secretion

During the recent years, the role of C-peptide, released from the pancreatic beta cell, in regulating microvascular blood flow, has received increasing attention. In type 1 diabetic patients, intravenous application of C-peptide in physiological concentrations was shown to increase microvascular blood flow, and to improve microvascular endothelial function and the endothelial release of NO. C-peptide was shown to impact microvascular blood flow by several interactive pathways, like stimulatingNa+K+ATPase or the endothelial release of NO. There is increasing evidence, that in patients with declining beta cell function, the lack of C-peptide secretion might play a putative role in the development of microvascular blood flow abnormalities, which go beyond the effects of declining insulin secretion or increased blood glucose levels.

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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