scholarly journals The role of gut microbiota and amino metabolism in the effects of improvement of islet β-cell function after modified jejunoileal bypass

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Cai Tan ◽  
Zhihua Zheng ◽  
Xiaogang Wan ◽  
Jiaqing Cao ◽  
Ran Wei ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Cell Function ◽  
Body Weight Gain ◽  
Fasting Blood Glucose ◽  
Jejunoileal Bypass ◽  
Β Cell ◽  
Β Cell Function ◽  
Branched Chain

AbstractThe change in gut microbiota is an important mechanism of the amelioration of type 2 diabetes mellitus (T2DM) after bariatric surgery. Here, we observe that the modified jejunoileal bypass effectively decreases body weight gain, fasting blood glucose, and lipids level in serum; additionally, islet β-cell function, glucose tolerance, and insulin resistance were markedly ameliorated. The hypoglycemic effect and the improvement in islet β-cell function depend on the changes in gut microbiota structure. modified jejunoileal bypass increases the abundance of gut Escherichia coli and Ruminococcus gnavus and the levels of serum glycine, histidine, and glutamine in T2DM rats; and decreases the abundance of Prevotella copri and the levels of serum branched chain amino acids, which are significantly related to the improvement of islet β-cell function in T2DM rats. Our results suggest that amino acid metabolism may contribute to the islet β-cell function in T2DM rats after modified jejunoileal bypass and that improving gut microbiota composition is a potential therapeutic strategy for T2DM.

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.

scholarly journals The Role of the Gut Microbiota in the Pathogenesis of Diabetes

2022 ◽  
Vol 23 (1) ◽  
pp. 480
Author(s):  
Weronika Bielka ◽  
Agnieszka Przezak ◽  
Andrzej Pawlik
Keyword(s):  
Gut Microbiota ◽  
Cell Function ◽  
Bacterial Composition ◽  
New Developments ◽  
Β Cell Function ◽  
Therapeutic Problem

Diabetes mellitus is a significant clinical and therapeutic problem because it can lead to serious long-term complications. Its pathogenesis is not fully understood, but there are indications that dysbiosis can play a role in the development of diabetes, or that it appears during the course of the disease. Changes in microbiota composition are observed in both type 1 diabetes (T1D) and type 2 diabetes (T2D) patients. These modifications are associated with pro-inflammation, increased intestinal permeability, endotoxemia, impaired β-cell function and development of insulin resistance. This review summarizes the role of the gut microbiota in healthy individuals and the changes in bacterial composition that can be associated with T1D or T2D. It also presents new developments in diabetes therapy based on influencing the gut microbiota as a promising method to alter the course of diabetes. Moreover, it highlights the lacking data and suggests future directions needed to prove the causal relationship between dysbiosis and diabetes, both T1D and T2D.

scholarly journals The Role of Markers of Low-Grade Inflammation for the Early Time Course of Glycemic Control, Glucose Disappearance Rate, and β-Cell Function in Recently Diagnosed Type 1 and Type 2 Diabetes

Diabetes Care ◽  
2015 ◽  
Vol 38 (9) ◽  
pp. 1758-1767 ◽  
Author(s):  
Katharina S. Weber ◽  
Bettina Nowotny ◽  
Klaus Strassburger ◽  
Giovanni Pacini ◽  
Karsten Müssig ◽  
...  
Keyword(s):  
Time Course ◽  
Cell Function ◽  
Early Time ◽  
Low Grade ◽  
Β Cell ◽  
Β Cell Function ◽  
Low Grade Inflammation

scholarly journals The pathogenetic role of β-cell mitochondria in type 2 diabetes

2018 ◽  
Vol 236 (3) ◽  
pp. R145-R159 ◽  
Author(s):  
Malin Fex ◽  
Lisa M Nicholas ◽  
Neelanjan Vishnu ◽  
Anya Medina ◽  
Vladimir V Sharoyko ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Mitochondrial Dysfunction ◽  
Translational Regulation ◽  
Cell Function ◽  
Rare Condition ◽  
Β Cells ◽  
Β Cell ◽  
Β Cell Function

Mitochondrial metabolism is a major determinant of insulin secretion from pancreatic β-cells. Type 2 diabetes evolves when β-cells fail to release appropriate amounts of insulin in response to glucose. This results in hyperglycemia and metabolic dysregulation. Evidence has recently been mounting that mitochondrial dysfunction plays an important role in these processes. Monogenic dysfunction of mitochondria is a rare condition but causes a type 2 diabetes-like syndrome owing to β-cell failure. Here, we describe novel advances in research on mitochondrial dysfunction in the β-cell in type 2 diabetes, with a focus on human studies. Relevant studies in animal and cell models of the disease are described. Transcriptional and translational regulation in mitochondria are particularly emphasized. The role of metabolic enzymes and pathways and their impact on β-cell function in type 2 diabetes pathophysiology are discussed. The role of genetic variation in mitochondrial function leading to type 2 diabetes is highlighted. We argue that alterations in mitochondria may be a culprit in the pathogenetic processes culminating in type 2 diabetes.

scholarly journals Branched Chain Amino Acids Associate Negatively with Postprandial Insulin Secretion in Recent-Onset Diabetes

2021 ◽  
Author(s):  
Yanislava Karusheva ◽  
Klaus Strassburger ◽  
Daniel F Markgraf ◽  
Oana-Patricia Zaharia ◽  
Kálmán Bódis ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Cell Function ◽  
Branched Chain Amino Acids ◽  
Β Cell ◽  
C Peptide ◽  
Β Cell Function ◽  
Branched Chain

Abstract Context In addition to unfavourable effects on insulin sensitivity, elevated plasma branched-chain amino acids (BCAA) stimulate insulin secretion, which in the long-term could impair pancreatic β-cell function. Objective To investigate cross-sectional and prospective associations between circulating BCAA and postprandial β-cell function in recently diagnosed type 1 and type 2 diabetes. Methods The study included individuals with well-controlled type 1 and type 2 diabetes (known diabetes duration <12 months) and glucose tolerant humans (control) of similar age, sex and BMI (n=10/group) underwent mixed meal tolerance tests. Plasma BCAA levels were quantified by gas chromatography-mass spectrometry, postprandial β-cell function was assessed from serum C-peptide levels and insulin sensitivity from PREDIM index (PREDIcted M-value). Results In type 1 diabetes, postprandial total BCAA, valine and leucine levels were 25%, 18% and 19% higher versus control, and total as well as individual postprandial BCAA related inversely to C-peptide levels. In type 2 diabetes, postprandial isoleucine was 16% higher versus the respective controls, while neither total nor individual BCAA correlated with C-peptide levels. Whole body insulin sensitivity was lower in both diabetes groups than in corresponding controls. In conclusion, insulin deficiency associates with sustained high BCAA concentrations which could contribute to exhausting the insulin secretory reserve in early type 1 diabetes.

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