scholarly journals Glutamine Stimulates Biosynthesis and Secretion of Insulin-like Growth Factor 2 (IGF2), an Autocrine Regulator of Beta Cell Mass and Function

2014 ◽  
Vol 289 (46) ◽  
pp. 31972-31982 ◽  
Author(s):  
Honey Modi ◽  
Marion Cornu ◽  
Bernard Thorens
Keyword(s):  
Growth Factor ◽  
Beta Cell ◽  
Cell Mass ◽  
Beta Cell Mass ◽  
Insulin Like Growth Factor ◽  
And Function

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 Verapamil can be used as a Type 2 Diabetes Mellitus Saviour and Stopping the need for Insulin in Uncontrolled Type 2 Diabetes Mellitus

2021 ◽  
pp. 1-8
Author(s):  
Mahmoud Younis ◽  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Beta Cell ◽  
Cell Mass ◽  
Beta Cell Mass ◽  
Interacting Protein ◽  
Significant Difference ◽  
And Function

Introduction: Diabetes mellitus is not just a disease as it is already known, the matter is more complicated, and it is considered as an assembly of metabolic defects with end result of hyperglycemia.verapamil can decrease the expression of thioredoxin-interacting protein (TXNIP), which is recognized as an important factor in pancreatic beta cells.verapamil could enhance beta cell mass and function. Materials and Methods: 160 type 2 diabetes patients in 2 parallel groups. Results: show statistically significant difference in favour of verapamil in increasing c-peptide levels and decreasing hba1c levels. Conclusion: Verapamil could be used as a type 2 diabetes saviour by increasing beta cell mass and function.

scholarly journals Genetic evidence of the programming of beta cell mass and function by glucocorticoids in mice

Diabetologia ◽  
2010 ◽  
Vol 54 (2) ◽  
pp. 350-359 ◽  
Author(s):  
B. Valtat ◽  
C. Dupuis ◽  
D. Zenaty ◽  
A. Singh-Estivalet ◽  
F. Tronche ◽  
...  
Keyword(s):  
Beta Cell ◽  
Cell Mass ◽  
Beta Cell Mass ◽  
Genetic Evidence ◽  
And Function

scholarly journals Role of Ink4a/Arf Locus in Beta Cell Mass Expansion under Physiological and Pathological Conditions

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Elisabet Salas ◽  
Nabil Rabhi ◽  
Philippe Froguel ◽  
Jean-Sébastien Annicotte
Keyword(s):  
Beta Cell ◽  
Cell Mass ◽  
Beta Cell Mass ◽  
Primary Source ◽  
Tumour Suppressor Genes ◽  
General View ◽  
Diabetes Research ◽  
And Function ◽  
Cdkn2a Locus

The ARF/INK4A (Cdkn2a) locus includes the linked tumour suppressor genes p16INK4a and p14ARF (p19ARF in mice) that trigger the antiproliferative activities of both RB and p53. With beta cell self-replication being the primary source for new beta cell generation in adult animals, the network by which beta cell replication could be increased to enhance beta cell mass and function is one of the approaches in diabetes research. In this review, we show a general view of the regulation points at transcriptional and posttranslational levels of Cdkn2a locus. We describe the molecular pathways and functions of Cdkn2a in beta cell cycle regulation. Given that aging reveals increased p16Ink4a levels in the pancreas that inhibit the proliferation of beta cells and decrease their ability to respond to injury, we show the state of the art about the role of this locus in beta cell senescence and diabetes development. Additionally, we focus on two approaches in beta cell regeneration strategies that rely on Cdkn2a locus negative regulation: long noncoding RNAs and betatrophin.

scholarly journals Aberrant methylation underlies insulin gene expression in human insulinoma

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Esra Karakose ◽  
Huan Wang ◽  
William Inabnet ◽  
Rajesh V. Thakker ◽  
Steven Libutti ◽  
...  
Keyword(s):  
Beta Cell ◽  
Cell Mass ◽  
Beta Cell Mass ◽  
Methylation Pattern ◽  
Congenital Hyperinsulinism ◽  
Aberrant Methylation ◽  
Chromosome 11 ◽  
Distal Enhancer ◽  
Human Insulinoma ◽  
And Function

Abstract Human insulinomas are rare, benign, slowly proliferating, insulin-producing beta cell tumors that provide a molecular “recipe” or “roadmap” for pathways that control human beta cell regeneration. An earlier study revealed abnormal methylation in the imprinted p15.5-p15.4 region of chromosome 11, known to be abnormally methylated in another disorder of expanded beta cell mass and function: the focal variant of congenital hyperinsulinism. Here, we compare deep DNA methylome sequencing on 19 human insulinomas, and five sets of normal beta cells. We find a remarkably consistent, abnormal methylation pattern in insulinomas. The findings suggest that abnormal insulin (INS) promoter methylation and altered transcription factor expression create alternative drivers of INS expression, replacing canonical PDX1-driven beta cell specification with a pathological, looping, distal enhancer-based form of transcriptional regulation. Finally, NFaT transcription factors, rather than the canonical PDX1 enhancer complex, are predicted to drive INS transactivation.

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