scholarly journals Palmitic acid-induced lipotoxicity promotes a novel interplay between Akt-mTOR, IRS-1, and FFAR1 signaling in pancreatic β-cells

2019 ◽  
Vol 52 (1) ◽  
Author(s):  
Sulaiman K. Marafie ◽  
Eman M. Al-Shawaf ◽  
Jehad Abubaker ◽  
Hossein Arefanian
Keyword(s):  
Palmitic Acid ◽  
Β Cells ◽  
Pancreatic Β Cells

scholarly journals DGAT1 inhibitors protect pancreatic β-cells from palmitic acid-induced apoptosis

2020 ◽  
Author(s):  
Jun-shang Huang ◽  
Bin-bin Guo ◽  
Gai-hong Wang ◽  
Li-min Zeng ◽  
You-hong Hu ◽  
...  
Keyword(s):  
Palmitic Acid ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Induced Apoptosis

scholarly journals Mitigation of Glucolipotoxicity-Induced Apoptosis, Mitochondrial Dysfunction, and Metabolic Stress by N-Acetyl Cysteine in Pancreatic β-Cells

Biomolecules ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 239 ◽  
Author(s):  
Arwa Alnahdi ◽  
Annie John ◽  
Haider Raza
Keyword(s):  
Energy Metabolism ◽  
Palmitic Acid ◽  
Mitochondrial Dysfunction ◽  
High Glucose ◽  
High Energy ◽  
Metabolic Adaptation ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Mitochondrial Energy Metabolism ◽  
Acetyl Cysteine

Glucolipotoxicity caused by hyperglycemia and hyperlipidemia are the common features of diabetes-induced complications. Metabolic adaptation, particularly in energy metabolism; mitochondrial dysfunction; and increased inflammatory and oxidative stress responses are considered to be the main characteristics of diabetes and metabolic syndrome. However, due to various fluctuating endogenous and exogenous stimuli, the precise role of these factors under in vivo conditions is not clearly understood. In the present study, we used pancreatic β-cells, Rin-5F, to elucidate the molecular and metabolic changes in glucolipotoxicity. Cells treated with high glucose (25 mM) and high palmitic acid (up to 0.3 mM) for 24 h exhibited increased caspase/poly-ADP ribose polymerase (PARP)-dependent apoptosis followed by DNA fragmentation, alterations in mitochondrial membrane permeability, and bioenergetics, accompanied by alterations in glycolytic and mitochondrial energy metabolism. Our results also demonstrated alterations in the expression of mammalian target of rapamycin (mTOR)/5′ adenosine monophosphate-activated protein kinase (AMPK)-dependent apoptotic and autophagy markers. Furthermore, pre-treatment of cells with 10 mM N-acetyl cysteine attenuated the deleterious effects of high glucose and high palmitic acid with improved cellular functions and survival. These results suggest that the presence of high energy metabolites enhance mitochondrial dysfunction and apoptosis by suppressing autophagy and adapting energy metabolism, mediated, at least in part, via enhanced oxidative DNA damage and mTOR/AMPK-dependent cell signaling.

scholarly journals JunD Regulates Pancreatic β-Cells Function by Altering Lipid Accumulation

2021 ◽  
Vol 12 ◽  
Author(s):  
Kexin Wang ◽  
Yixin Cui ◽  
Peng Lin ◽  
Zhina Yao ◽  
Yu Sun
Keyword(s):  
Gene Expression ◽  
Insulin Secretion ◽  
Lipid Metabolism ◽  
Palmitic Acid ◽  
Lipid Accumulation ◽  
Activator Protein 1 ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Intracellular Lipid Accumulation ◽  
Glucose Stimulated Insulin Secretion

The impairment of pancreatic β-cells function is partly caused by lipotoxicity, which aggravates the development of type 2 diabetes mellitus. Activator Protein 1 member JunD modulates apoptosis and oxidative stress. Recently, it has been found that JunD regulates lipid metabolism in hepatocytes and cardiomyocytes. Here, we studied the role of JunD in pancreatic β-cells. The lipotoxic effects of palmitic acid on INS-1 cells were measured, and JunD small-interfering RNA was used to assess the effect of JunD in regulating lipid metabolism and insulin secretion. The results showed that palmitic acid stimulation induced the overexpression of JunD, impaired glucose-stimulated insulin secretion, and increased intracellular lipid accumulation of β-cells. Moreover, the gene expression involved in lipid metabolism (Scd1, Fabp4, Fas, Cd36, Lpl, and Plin5) was upregulated, while gene expression involved in the pancreatic β-cells function (such as Pdx1, Nkx6.1, Glut2, and Irs-2) was decreased. Gene silencing of JunD reversed the lipotoxic effects induced by PA on β-cells. These results suggested that JunD regulated the function of pancreatic β-cells by altering lipid accumulation.

Cinnamtannin D-1 Protects Pancreatic β-Cells from Palmitic Acid-Induced Apoptosis by Attenuating Oxidative Stress

2014 ◽  
Vol 62 (22) ◽  
pp. 5038-5045 ◽  
Author(s):  
Ting Wang ◽  
Peng Sun ◽  
Liang Chen ◽  
Qi Huang ◽  
Kaixian Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Palmitic Acid ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Induced Apoptosis

MICROCHEMICAL ASSAYS OF GLUCOSE AND GLUCOSE-6-PHOSPHATE IN MAMMALIAN PANCREATIC β-CELLS

1968 ◽  
Vol 59 (3) ◽  
pp. 479-486 ◽  
Author(s):  
Lars-Ake Idahl ◽  
Bo Hellman
Keyword(s):  
Glucose Level ◽  
Exocrine Pancreas ◽  
The Other ◽  
Wide Concentration Range ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Enzymatic Cycling ◽  
Glucose Diffusion ◽  
Significant Barrier ◽  
The Brain

ABSTRACT The combination of enzymatic cycling and fluorometry was used for measuring glucose and glucose-6-phosphate in pancreatic β-cells from obese-hyperglycaemic mice. The glucose level of the β-cells corresponded to that of serum over a wide concentration range. In the exocrine pancreas, on the other hand, a significant barrier to glucose diffusion across the cell membranes was demonstrated. During 5 min of ischaemia, the glucose level remained practically unchanged in the β-cells while it increased in the liver and decreased in the brain. The observation that the pancreatic β-cells are characterized by a relatively low ratio of glucose-6-phosphate to glucose may be attributed to the presence of a specific glucose-6-phosphatase.

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