scholarly journals The effect of fermented tempeh aerobic anaerobic (FETAA) on pancreatic duodenal homeobox 1 (Pdx1) gene expression and HOMA-beta index in diabetic mice

2021 ◽  
pp. 11
Author(s):  
Hendi Wicaksono ◽  
Prasetyastuti Prasetyastuti ◽  
Pramudji Hastuti ◽  
Ahmad Hamim Sadewa
Keyword(s):  
Oxidative Stress ◽  
Blood Glucose ◽  
Mrna Expression ◽  
Cell Function ◽  
Model Assessment ◽  
Diabetic Mice ◽  
Β Cell ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Β Cell Function

Background: Diabetes is a result of oxidative stress which causes the impaired function of pancreatic beta-cells. Fermented tempeh aerobic anaerobic (FETAA) containing gamma-aminobutyric acid and isoflavones can reduce oxidative stress in diabetes. Objective: The aim of this study is to evaluate FETAA in improving pancreatic β-cell function in diabetic mice. Methods: Twenty streptozotocin-induced diabetic mice, divided into four groups (n = 5 each group): DM, DM + FETAA 10 mg/100 g BW, DM + FETAA 20 mg/100 g BW, DM + FETAA 40 mg/100 g BW as well as normal group (n = 5). DM mice were treated with FETAA for 21 days. Fasting glucose was determined using the GOD-PAP method, while insulin level was determined by ELISA. The homeostasis model assessment of β-cell function (HOMA-β) was calculated using the HOMA2 calculator, and the Pdx1 mRNA level was determined by Real Time-PCR. Results: The DM mice group treated with FETAA had lower glucose levels than the DM mice group. FETAA dosage of 40 mg/100 g BW was able to reduce the highest blood glucose levels (p<0.05). DM mice group treated with FETAA had higher levels of insulin and HOMA-β than the DM mice group (p <0.05). Treatment of FETAA 10 mg/100 g BW produced the highest insulin content of 57.44 ± 8.132 pmol/L, while treatment of FETAA 40 mg/100 g BW had a HOMA-β value of 72.86 ± 21.85%. Pdx1 mRNA expression in group FETAA-treated DM mice was higher than the DM mice group, although it was not statistically significant (p> 0.05). Conclusion: FETAA could improve HOMA-β, blood glucose levels, but did not affect Pdx1 mRNA expression.

scholarly journals Effect of Probiotics on the Glucose Levels of Pregnant Women: A Meta-Analysis of Randomized Controlled Trials

Medicina ◽  
2018 ◽  
Vol 54 (5) ◽  
pp. 77 ◽  
Author(s):  
Tzu-Rong Peng ◽  
Ta-Wei Wu ◽  
You-Chen Chao
Keyword(s):  
Blood Glucose ◽  
Randomized Controlled Trials ◽  
Pregnant Women ◽  
Cell Function ◽  
Fasting Blood Glucose ◽  
Controlled Trials ◽  
Model Assessment ◽  
Glucose Levels ◽  
Randomized Controlled ◽  
Blood Glucose Levels

Background: Gestational diabetes mellitus (GDM) is a condition, in which women develop high blood sugar levels during pregnancy without having diabetes. Evidence on the effects of probiotics on the blood glucose levels of women with GDM is inconsistent. Objective: The present study aimed to investigate the effects of probiotics on the blood glucose levels of pregnant women. Methods: Online databases, such as PubMed, Cochrane, and Excerpta Medica Database (EMBASE) were searched for randomized controlled trials (RCTs) published before July 2018. Trials had to meet the inclusion criteria of our study. Methodological quality and risk bias were independently assessed by two reviewers. Data were pooled using a random effects model and were expressed as the mean difference (MD) and 95% confidence interval (CI). Heterogeneity was evaluated and quantified as I2. Results: In total, 12 RCTs were included in this study. Studies have shown that the use of probiotics significantly reduced the fasting blood glucose (FBG) level (MD: −0.10 mmol/L; 95% CI: −0.19, −0.02), insulin concentration (MD: −2.24 μIU/mL; 95% CI: −3.69, −0.79), Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) score (MD: −0.47; 95% CI: −0.74, −0.21), and Homeostasis model of assessment-estimated β cell function (HOMA-B) score (MD: −20.23; 95% CI: −31.98, −8.49) of pregnant women. In a subgroup analysis, whether the blood glucose-lowering effect of probiotics influenced the diagnosis of pregnant women with GDM was assessed. The results showed that probiotics had significantly reduced the fasting blood glucose (FBG) level (MD: −0.10 mmol/L; 95% CI: −0.17, −0.04) and HOMA-IR score (MD: −0.37; 95% CI: −0.72, −0.02) of pregnant women who were not diagnosed with GDM. Conclusion: Probiotics reduce the blood glucose level of pregnant women, especially without GDM diagnosis. However, further research using RCTs must be conducted to validate the results of the present study.

scholarly journals Aerobic Exercise Improves Sepsis via Impairing LPS-induced Lactate and HMGB1 Release in Mice

2021 ◽  
Author(s):  
xishuai Wang ◽  
zhiqing Wang ◽  
donghui Tang
Keyword(s):  
Oxidative Stress ◽  
Blood Glucose ◽  
Aerobic Exercise ◽  
Mrna Expression ◽  
Aerobic Glycolysis ◽  
Aortic Injury ◽  
Organ Injury ◽  
Stress Injury ◽  
Glucose Levels ◽  
Blood Glucose Levels

Abstract Purpose: In the present study, we attempted to investigate whether aerobic exercise (AE) could prevent sepsis and its complications and explored the related mechanisms. Methods: Forty ICR mice were divided into four groups: Control (Con), Lipopolysaccharide (LPS), Exercise (Ex), and Exercise + LPS (Ex + LPS) groups. Ex and Ex + LPS mice were performed with low-intensity AE for 4 weeks. LPS and Ex + LPS mice received 5 mg/kg LPS intraperitoneally for induction of sepsis. Histopathological micrographs showed the organ injury. This study examined the effects of AE on LPS-induced changes in systemic inflammation, pulmonary inflammation, lung permeability, oxidative stress-related indicators in the lung, blood glucose levels, plasma lactate levels, and plasma high-mobility group box 1 (HMGB1) levels, and bronchoalveolar lavage fluid (BALF) cell count. Sixty mice were used to perform survival rate analysis. Results: AE improved survival rates, MODS, and aortic injury in mice with sepsis. AE decreased LPS-induced oxidative stress injury in lung tissue. AE reduced the infiltration of neutrophils in the lung, liver, kidney, and heart tissues. AE suppressed CXCL-1, CXCL-8, IL-6, and TNF-α mRNA expression but activated IL-1RN, IL-10, Sirt-1, and Nrf-2 mRNA expression in the lung. AE decreased the serum levels of lactate and HMGB1 but increased blood glucose levels during sepsis. Conclusions: AE improves sepsis-associated lung, liver, kidney, heart, and aortic injury and death. AE modulates the inflammatory-anti-inflammatory and oxidative-antioxidative balance in the lung. AE, which can regulate the Warburg effect and impair LPS-induced lactate and HMGB1 release, is a novel therapeutic strategy for sepsis targeting aerobic glycolysis.

scholarly journals The Role of Oxidative Stress in Pancreatic β Cell Dysfunction in Diabetes

2021 ◽  
Vol 22 (4) ◽  
pp. 1509
Author(s):  
Natsuki Eguchi ◽  
Nosratola D. Vaziri ◽  
Donald C. Dafoe ◽  
Hirohito Ichii
Keyword(s):  
Oxidative Stress ◽  
Cell Function ◽  
Pancreatic Β Cell ◽  
Antioxidative Capacity ◽  
Β Cells ◽  
Β Cell ◽  
Glucose Levels ◽  
Cell Dysfunction ◽  
Elevated Glucose ◽  
Β Cell Function

Diabetes is a chronic metabolic disorder characterized by inappropriately elevated glucose levels as a result of impaired pancreatic β cell function and insulin resistance. Extensive studies have been conducted to elucidate the mechanism involved in the development of β cell failure and death under diabetic conditions such as hyperglycemia, hyperlipidemia, and inflammation. Of the plethora of proposed mechanisms, endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and oxidative stress have been shown to play a central role in promoting β cell dysfunction. It has become more evident in recent years that these 3 factors are closely interrelated and importantly aggravate each other. Oxidative stress in particular is of great interest to β cell health and survival as it has been shown that β cells exhibit lower antioxidative capacity. Therefore, this review will focus on discussing factors that contribute to the development of oxidative stress in pancreatic β cells and explore the downstream effects of oxidative stress on β cell function and health. Furthermore, antioxidative capacity of β cells to counteract these effects will be discussed along with new approaches focused on preserving β cells under oxidative conditions.

scholarly journals Effects of the long-acting somatostatin analogue Lanreotide Autogel on glucose tolerance and insulin resistance in acromegaly

2006 ◽  
Vol 155 (1) ◽  
pp. 73-78 ◽  
Author(s):  
B Steffin ◽  
B Gutt ◽  
M Bidlingmaier ◽  
C Dieterle ◽  
F Oltmann ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Glucose ◽  
Glucose Tolerance ◽  
Cell Function ◽  
Oral Glucose ◽  
Model Assessment ◽  
Β Cell ◽  
Igf I ◽  
Β Cell Function ◽  
Lanreotide Autogel

Object: Treatment with somatostatin analogues (SA) not only inhibits GH secretion but may also impair insulin secretion. In order to evaluate the influence of SA on glucose metabolism, we investigated insulin resistance (IR) and β-cell function, using the recommended combination of homeostatic model assessment of IR (HOMA-IR) and β-cell function (HOMA-β). Design and methods: This is a prospective, cross-sectional study. We measured fasting insulin, blood glucose and IGF-I. Insulin and blood glucose measurements were taken 120 min after an oral glucose tolerance test with 75 g glucose. We studied 51 patients (27 female/24 male, age 54 years (20–75)). Eighteen patients were on Lanreotide Autogel (LA) treatment, 33 had no medical treatment. GH-levels of more than 2.5 ng/ml was reached by 59% of the patients, 74.5% had normal IGF-I levels. Results: We found no significant influence of disease activity on HOMA-IR and HOMA-β. In the 33 of 51 subjects without any drug treatment, median HOMA-β was 170.4% (36.0–624.0%). In contrast, in the 18 patients on LA treatment, median HOMA-β was found to be significantly lower (84.2% (36.5–346.2%); P = 0.001). Despite this, there was no difference in HOMA-IR in both groups (2.4 (0.7–8.4) vs 2.3 (0.7–6.1); P < 0.001) despite similar insulin values. Conclusion: In conclusion, we found that LA decreases β-cell function significantly without affecting IR. Therefore, we think that insulin secretagogues are probably more effective in the treatment of diabetes mellitus in acromegalic patients on LA therapy than insulin sensitizers.

scholarly journals The Effect of Pumpkin on GLP-1 and HOMA-β in Hypercholesterolemic Rats

2016 ◽  
Vol 23 (1) ◽  
pp. 19-25
Author(s):  
◽  
Dianandha Septiana Rubi ◽  
Ahmad Hamim Sadewa
Keyword(s):  
Oxidative Stress ◽  
Cell Function ◽  
Model Assessment ◽  
High Fat ◽  
Β Cell ◽  
Cholesterol Levels ◽  
Before And After ◽  
Homeostatic Model Assessment ◽  
Β Cell Function ◽  
Glucagon Like Peptide 1

AbstractBackground and aim: High fat and fructose diet may impair β cell function through oxidative stress that is induced by subsequent hypercholesterolemia. The β cell function is usually quantified by homeostatic model assessment beta-cell function (HOMA-β). Oxidative stress may be decreased by β-carotene from pumpkin (Cucurbita maxima). This study aimed to evaluate the effects of pumpkin powder on glucagon-like peptide-1 (GLP-1) level and HOMA-β in rats with high fat and fructose diet.Material and method: A total 25 rats were administered a high fat and fructose diet during 25 days. They were divided into five groups 1) normal, 2) hypercholesterolemic rats 3) hypercholesterolemic rats with 0.16 g pumpkin/200g bodyweight (BW); 4) hypercholesterolemic rats with 0.32 g pumpkin/200 g BW, and 5) hypercholesterolemic rats with 0.64 g of pumpkin/200 g BW. The lipid levels were measured before and after administration of pumpkin for 4 weeks, and at the end of the study, GLP-1 level and HOMA-β were analyzed.Results: Administration of pumpkin to the rats on a high fat and fructose diet reduced total cholesterol, triglyceride, and increased HDL levels. Changes were positively correlated with the amount of pumpkin intake. The decrease of cholesterol levels was positively associated with GLP-1 level, and negatively correlated with HOMA-βConclusions: This study suggested that pumpkin can improve the HOMA-β and decrease GLP-1 levels, possibly by reducing cholesterol levels.

scholarly journals Notable Underlying Mechanism for Pancreatic β-Cell Dysfunction and Atherosclerosis: Pleiotropic Roles of Incretin and Insulin Signaling

2020 ◽  
Vol 21 (24) ◽  
pp. 9444
Author(s):  
Hideaki Kaneto ◽  
Atsushi Obata ◽  
Tomohiko Kimura ◽  
Masashi Shimoda ◽  
Junpei Sanada ◽  
...  
Keyword(s):  
Cell Function ◽  
Early Stage ◽  
Receptor Expression ◽  
Protective Effects ◽  
Β Cells ◽  
Β Cell ◽  
Glucose Levels ◽  
Cell Dysfunction ◽  
Blood Glucose Levels ◽  
Β Cell Function

Under healthy conditions, pancreatic β-cells produce and secrete the insulin hormone in response to blood glucose levels. Under diabetic conditions, however, β-cells are compelled to continuously secrete larger amounts of insulin to reduce blood glucose levels, and thereby, the β-cell function is debilitated in the long run. In the diabetic state, expression levels of insulin gene transcription factors and incretin receptors are downregulated, which we think is closely associated with β-cell failure. These data also suggest that it would be better to use incretin-based drugs at an early stage of diabetes when incretin receptor expression is preserved. Indeed, it was shown that incretin-based drugs exerted more protective effects on β-cells at an early stage. Furthermore, it was shown recently that endothelial cell dysfunction was also associated with pancreatic β-cell dysfunction. After ablation of insulin signaling in endothelial cells, the β-cell function and mass were substantially reduced, which was also accompanied by reduced expression of insulin gene transcription factors and incretin receptors in β-cells. On the other hand, it has been drawing much attention that incretin plays a protective role against the development of atherosclerosis. Many basic and clinical data have underscored the importance of incretin in arteries. Furthermore, it was shown recently that incretin receptor expression was downregulated in arteries under diabetic conditions, which likely diminishes the protective effects of incretin against atherosclerosis. Furthermore, a series of large-scale clinical trials (SPAED-A, SPIKE, LEADER, SUSTAIN-6, REWIND, PIONEER trials) have shown that various incretin-related drugs have beneficial effects against atherosclerosis and subsequent cardiovascular events. These data strengthen the hypothesis that incretin plays an important role in the arteries of humans, as well as rodents.

scholarly journals Loss of β-cell identity and diabetic phenotype in mice caused by disruption of CNOT3-dependent mRNA deadenylation

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Dina Mostafa ◽  
Akiko Yanagiya ◽  
Eleni Georgiadou ◽  
Yibo Wu ◽  
Theodoros Stylianides ◽  
...  
Keyword(s):  
Cell Function ◽  
Cell Mass ◽  
Cell Maturation ◽  
Β Cells ◽  
Β Cell ◽  
Cell Identity ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Β Cell Function ◽  
And Function

AbstractPancreatic β-cells are responsible for production and secretion of insulin in response to increasing blood glucose levels. Defects in β-cell function lead to hyperglycemia and diabetes mellitus. Here, we show that CNOT3, a CCR4–NOT deadenylase complex subunit, is dysregulated in islets in diabetic db/db mice, and that it is essential for murine β cell maturation and identity. Mice with β cell-specific Cnot3 deletion (Cnot3βKO) exhibit impaired glucose tolerance, decreased β cell mass, and they gradually develop diabetes. Cnot3βKO islets display decreased expression of key regulators of β cell maturation and function. Moreover, they show an increase of progenitor cell markers, β cell-disallowed genes, and genes relevant to altered β cell function. Cnot3βKO islets exhibit altered deadenylation and increased mRNA stability, partly accounting for the increased expression of those genes. Together, these data reveal that CNOT3-mediated mRNA deadenylation and decay constitute previously unsuspected post-transcriptional mechanisms essential for β cell identity.

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