scholarly journals Jinlida granule inhibits palmitic acid induced-intracellular lipid accumulation and enhances autophagy in NIT-1 pancreatic β cells through AMPK activation

2015 ◽  
Vol 161 ◽  
pp. 99-107 ◽  
Author(s):  
Dingkun Wang ◽  
Min Tian ◽  
Yuan Qi ◽  
Guang Chen ◽  
Lijun Xu ◽  
...  
Keyword(s):  
Palmitic Acid ◽  
Lipid Accumulation ◽  
Ampk Activation ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Intracellular Lipid ◽  
Intracellular Lipid Accumulation

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.

Zinc alpha2 glycoprotein alleviates palmitic acid-induced intracellular lipid accumulation in hepatocytes

2017 ◽  
Vol 439 ◽  
pp. 155-164 ◽  
Author(s):  
Xinhua Xiao ◽  
Han Li ◽  
Xiaoyan Qi ◽  
Yadi Wang ◽  
Canxin Xu ◽  
...  
Keyword(s):  
Palmitic Acid ◽  
Lipid Accumulation ◽  
Intracellular Lipid ◽  
Intracellular Lipid Accumulation

scholarly journals Diosgenin ameliorates palmitic acid-induced lipid accumulation via AMPK/ACC/CPT-1A and SREBP-1c/FAS signaling pathways in LO2 cells

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Ke Fang ◽  
Fan Wu ◽  
Guang Chen ◽  
Hui Dong ◽  
Jingbin Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Liver Disease ◽  
Fatty Liver ◽  
Palmitic Acid ◽  
Mitochondrial Function ◽  
Lipid Accumulation ◽  
Lipid Synthesis ◽  
Underlying Mechanism ◽  
Intracellular Lipid

Abstract Background Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease and is characterized by excessive hepatic lipid accumulation. Many studies have suggested that lipid overload is the key initial factor that contributes to hepatic steatosis. Our previous study indicated that diosgenin (DSG) has a beneficial effect on energy metabolism, but the underlying mechanism remains unclear. Methods Human normal hepatocytes (LO2 cells) were incubated with palmitic acid to establish the cell model of nonalcoholic fatty liver. The effects of DSG on lipid metabolism, glucose uptake and mitochondrial function were evaluated. Furthermore, the mechanism of DSG on oxidative stress, lipid consumption and lipid synthesis in LO2 cells was investigated. Results The results indicated that palmitic acid induced obvious lipid accumulation in LO2 cells and that DSG treatment significantly reduced the intracellular lipid content. DSG treatment upregulated expression of lipolysis proteins, including phospho-AMP activated protein kinase (p-AMPK), phospho-acetyl-coA carboxylase (p-ACC) and carnitine acyl transferase 1A (CPT-1A), and inhibited expression of lipid synthesis-related proteins, including sterol regulatory element-binding protein 1c (SREBP-1c) and fatty acid synthase (FAS). Additionally, DSG-treated cells displayed a marked improvement in mitochondrial function, with less production of reactive oxygen species and a higher mitochondrial membrane potential compared with the model group. Conclusion This study suggests that DSG can reduce intracellular lipid accumulation in LO2 cells and that the underlying mechanism may be related to the improving oxidative stress, increasing fatty acid β-oxidation and decreasing lipid synthesis. The above changes might be mediated by the activation of the AMPK/ACC/CPT-1A pathway and inhibition of the SREBP-1c/FAS pathway.

scholarly journals Association of intracellular lipid accumulation in subcutaneous adipocyte precursors and plasma adipokines in bariatric surgery candidates

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Ioana Hristov ◽  
Veronica Mocanu ◽  
Florin Zugun-Eloae ◽  
Luminita Labusca ◽  
Iustina Cretu-Silivestru ◽  
...  
Keyword(s):  
Bariatric Surgery ◽  
Lipid Accumulation ◽  
Intracellular Lipid ◽  
Intracellular Lipid Accumulation

Dysregulation of low-density lipoprotein receptor contributes to podocyte injuries in diabetic nephropathy

2015 ◽  
Vol 308 (12) ◽  
pp. E1140-E1148 ◽  
Author(s):  
Yang Zhang ◽  
Kun Ling Ma ◽  
Jing Liu ◽  
Yu Wu ◽  
Ze Bo Hu ◽  
...  
Keyword(s):  
High Glucose ◽  
Lipid Accumulation ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Lipoprotein Receptor ◽  
Intracellular Lipid ◽  
Phenotypic Alteration ◽  
Density Lipoprotein Receptor ◽  
Intracellular Lipid Accumulation

Dyslipidemia plays crucial roles in the progression of diabetic nephropathy (DN). This study investigated the effects of high glucose on lipid accumulation in podocytes and explored its underlying mechanisms. Male db/m and db/db mice were fed a normal chow diet for 8 wk. Immortalised mouse podocytes were treated with or without high glucose for 24 h. The changes to the morphology and ultramicrostructures of the kidneys in mice were examined using pathological staining and electron microscopy. Intracellular lipid accumulation was evaluated by Oil Red O staining and a free cholesterol quantitative assay. The expressions of the molecules involved in low-density lipoprotein receptor (LDLr) pathway and podocyte injury were examined using immunofluorescent staining, real-time PCR, and Western blot. There were increased levels of plasma lipid, serum creatinine, and proteinuria in db/db mice compared with db/m mice. Moreover, there was significant mesangial matrix expansion, basement membrane thickening, podocyte foot process effacement, and phenotypic alteration in the db/db group. Additionally, lipid accumulation in the kidneys of db/db mice was increased due to increased protein expressions of LDLr, sterol regulatory element-binding protein (SREBP) cleavage-activating protein, and SREBP-2. These effects were further confirmed by in vitro studies. Interestingly, the treatment with LDLr siRNA inhibited lipid accumulation in podocytes and decreased the protein expression of molecules associated with phenotypic alteration in podocytes. High glucose disrupted LDLr feedback regulation in podocytes, which may cause intracellular lipid accumulation and alteration of podocyte phenotype, thereby accelerating DN progression.

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