scholarly journals Vascepa Protects Against High Fat Diet Induced Glucose Intolerance, Insulin Resistance and Impaired Pancreatic Beta Cell Function in Mice

iScience ◽  
2021 ◽  
pp. 102909
Author(s):  
Dana Al Rijjal ◽  
Ying Liu ◽  
Mi Lai ◽  
Youchen Song ◽  
Zahra Danaei ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Beta Cell ◽  
Glucose Intolerance ◽  
High Fat Diet ◽  
Beta Cell Function ◽  
Cell Function ◽  
Pancreatic Beta Cell ◽  
High Fat ◽  
Pancreatic Beta Cell Function

[I10W]tigerinin-1R enhances both insulin sensitivity and pancreatic beta cell function and decreases adiposity and plasma triglycerides in high-fat mice

2015 ◽  
Vol 53 (2) ◽  
pp. 303-315 ◽  
Author(s):  
Dinesh K. Srinivasan ◽  
Opeolu O. Ojo ◽  
Bosede O. Owolabi ◽  
J. Michael Conlon ◽  
Peter R. Flatt ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Pancreatic Beta Cell ◽  
High Fat ◽  
Plasma Triglycerides ◽  
Pancreatic Beta Cell Function

scholarly journals Insulin and C-peptide levels, pancreatic beta cell function, and insulin resistance across glucose tolerance status in Thais

2007 ◽  
Vol 21 (2) ◽  
pp. 85-90 ◽  
Author(s):  
La-or Chailurkit ◽  
Wallaya Jongjaroenprasert ◽  
Suwannee Chanprasertyothin ◽  
Boonsong Ongphiphadhanakul
Keyword(s):  
Insulin Resistance ◽  
Glucose Tolerance ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Pancreatic Beta Cell ◽  
C Peptide ◽  
Glucose Tolerance Status ◽  
Pancreatic Beta Cell Function

Long-term effect of bezafibrate on pancreatic beta-cell function and insulin resistance in patients with diabetes

2007 ◽  
Vol 194 (1) ◽  
pp. 265-271 ◽  
Author(s):  
Helena Tenenbaum ◽  
Solomon Behar ◽  
Valentina Boyko ◽  
Yehuda Adler ◽  
Enrique Z. Fisman ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Pancreatic Beta Cell ◽  
Term Effect ◽  
Long Term Effect ◽  
Patients With Diabetes ◽  
Pancreatic Beta Cell Function

scholarly journals ZBED6 counteracts high-fat diet-induced glucose intolerance by maintaining beta cell area and reducing excess mitochondrial activation

Diabetologia ◽  
2021 ◽  
Author(s):  
Xuan Wang ◽  
Shady Younis ◽  
Jing Cen ◽  
Yun Wang ◽  
Camilla Krizhanovskii ◽  
...  
Keyword(s):  
Beta Cell ◽  
Glucose Intolerance ◽  
Knockout Mice ◽  
High Fat Diet ◽  
Beta Cell Function ◽  
Cell Function ◽  
Cell Area ◽  
High Fat ◽  
Beta Cell Area

Abstract Aims/hypothesis ZBED6 (zinc finger, BED-type containing 6) is known to regulate muscle mass by suppression of Igf2 gene transcription. In insulin-producing cell lines, ZBED6 maintains proliferative capacity at the expense of differentiation and beta cell function. The aim was to study the impact of Zbed6 knockout on beta cell function and glucose tolerance in C57BL/6 mice. Methods Beta cell area and proliferation were determined in Zbed6 knockout mice using immunohistochemical analysis. Muscle and fat distribution were assessed using micro-computed tomography. Islet gene expression was assessed by RNA sequencing. Effects of a high-fat diet were analysed by glucose tolerance and insulin tolerance tests. ZBED6 was overexpressed in EndoC-βH1 cells and human islet cells using an adenoviral vector. Beta cell cell-cycle analysis, insulin release and mitochondrial function were studied in vitro using propidium iodide staining and flow cytometry, ELISA, the Seahorse technique, and the fluorescent probes JC-1 and MitoSox. Results Islets from Zbed6 knockout mice showed lowered expression of the cell cycle gene Pttg1, decreased beta cell proliferation and decreased beta cell area, which occurred independently from ZBED6 effects on Igf2 gene expression. Zbed6 knockout mice, but not wild-type mice, developed glucose intolerance when given a high-fat diet. The high-fat diet Zbed6 knockout islets displayed upregulated expression of oxidative phosphorylation genes and genes associated with beta cell differentiation. In vitro, ZBED6 overexpression resulted in increased EndoC-βH1 cell proliferation and a reduced glucose-stimulated insulin release in human islets. ZBED6 also reduced mitochondrial JC-1 J-aggregate formation, mitochondrial oxygen consumption rates (OCR) and mitochondrial reactive oxygen species (ROS) production, both at basal and palmitate + high glucose-stimulated conditions. ZBED6-induced inhibition of OCR was not rescued by IGF2 addition. ZBED6 reduced levels of the mitochondrial regulator PPAR-γ related coactivator 1 protein (PRC) and bound its promoter/enhancer region. Knockdown of PRC resulted in a lowered OCR. Conclusions/interpretation It is concluded that ZBED6 is required for normal beta cell replication and also limits excessive beta cell mitochondrial activation in response to an increased functional demand. ZBED6 may act, at least in part, by restricting PRC-mediated mitochondrial activation/ROS production, which may lead to protection against beta cell dysfunction and glucose intolerance in vivo. Graphical abstract

scholarly journals Role of sensory neurons on pancreatic beta cell function and on development of insulin resistance

2009 ◽  
Vol 9 (S2) ◽  
Author(s):  
Barna Peitl ◽  
Róbert Döbrönte ◽  
László Drimba ◽  
Réka Sári ◽  
József Németh ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Beta Cell ◽  
Sensory Neurons ◽  
Beta Cell Function ◽  
Cell Function ◽  
Pancreatic Beta Cell ◽  
Pancreatic Beta Cell Function
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