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 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 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 MIF in Type 1 and Type 2 Diabetes Mellitus

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Yuriko I. Sánchez-Zamora ◽  
Miriam Rodriguez-Sosa
Keyword(s):  
Diabetes Mellitus ◽  
Macrophage Migration Inhibitory Factor ◽  
Inflammatory Responses ◽  
Current Knowledge ◽  
Low Grade ◽  
Clinical Environment ◽  
Low Grade Inflammation

Autoimmunity and chronic low-grade inflammation are hallmarks of diabetes mellitus type one (T1DM) and type two (T2DM), respectively. Both processes are orchestrated by inflammatory cytokines, including the macrophage migration inhibitory factor (MIF). To date, MIF has been implicated in both types of diabetes; therefore, understanding the role of MIF could affect our understanding of the autoimmune or inflammatory responses that influence diabetic pathology. This review highlights our current knowledge about the involvement of MIF in both types of diabetes in the clinical environment and in experimental disease models.

scholarly journals The Anna Karenina model of β cell maturation in development and their dedifferentiation in type 1 and type 2 diabetes

2021 ◽  
Author(s):  
Sutichot D. Nimkulrat ◽  
Zijian Ni ◽  
Jared Brown ◽  
Christina Kendziorski ◽  
Barak Blum
Keyword(s):  
Type 2 Diabetes ◽  
Cell Function ◽  
Lineage Tracing ◽  
Β Cells ◽  
Β Cell ◽  
Cell Dedifferentiation ◽  
Anna Karenina ◽  
Β Cell Function

AbstractLoss of mature β cell function and identity, or β cell dedifferentiation, is seen in all types of diabetes mellitus. Two competing models explain β cell dedifferentiation in diabetes. In the first model, β cells dedifferentiate in the reverse order of their developmental ontogeny. This model predicts that dedifferentiated β cells resemble β cell progenitors. In the second model, β cell dedifferentiation depends on the type of diabetogenic stress. This model, which we call the “Anna Karenina” model, predicts that in each type of diabetes, β cells dedifferentiate in their own way, depending on how their mature identity is disrupted by any particular diabetogenic stress. We directly tested the two models using a β cell-specific lineage-tracing system coupled with RNA-sequencing in mice. We constructed a multidimensional map of β cell transcriptional trajectories during the normal course of β cell postnatal development and during their dedifferentiation in models of both type 1 diabetes (NOD) and type 2 diabetes (BTBR-Lepob/ob). Using this unbiased approach, we show here that despite some similarities between immature and dedifferentiated β cells, β cells dedifferentiation in the two mouse models is not a reversal of developmental ontogeny and is different between different types of diabetes.

scholarly journals The Anna Karenina Model of β Cell Maturation in Development and their Dedifferentiation in Type 1 and Type 2 Diabetes

2021 ◽  
Author(s):  
Sutichot D. Nimkulrat ◽  
Matthew N. Bernstein ◽  
Zijian Ni ◽  
Jared Brown ◽  
Christina Kendziorski ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Cell Function ◽  
Lineage Tracing ◽  
Β Cells ◽  
Β Cell ◽  
Cell Dedifferentiation ◽  
Anna Karenina ◽  
Β Cell Function

Loss of mature β cell function and identity, or β cell dedifferentiation, is seen in both type 1 and type 2 diabetes. Two competing models explain β cell dedifferentiation in diabetes. In the first model, β cells dedifferentiate in the reverse order of their developmental ontogeny. This model predicts that dedifferentiated β cells resemble β cell progenitors. In the second model, β cell dedifferentiation depends on the type of diabetogenic stress. This model, which we call the “Anna Karenina” model, predicts that in each type of diabetes, β cells dedifferentiate in their own way, depending on how their mature identity is disrupted by any particular diabetogenic stress. We directly tested the two models using a β cell-specific lineage-tracing system coupled with RNA-sequencing in mice. We constructed a multidimensional map of β cell transcriptional trajectories during the normal course of β cell postnatal development and during their dedifferentiation in models of both type 1 diabetes (NOD) and type 2 diabetes (BTBR-<i>Lep<sup>ob/ob</sup></i>). Using this unbiased approach, we show here that despite some similarities between immature and dedifferentiated β cells, <a>β cells dedifferentiation in the two mouse models is not a reversal of developmental ontogeny and is different between </a>different types of diabetes.

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