Zoledronic acid prevents the hepatic changes associated with high fat diet in rats; the potential role of mevalonic acid pathway in nonalcoholic steatohepatitis

2019 ◽  
Vol 858 ◽  
pp. 172469 ◽  
Author(s):  
Reham Hussein Mohamed ◽  
Maha Tarek ◽  
Ghada Galal Hamam ◽  
Samar F. Ezzat
Keyword(s):  
Zoledronic Acid ◽  
Nonalcoholic Steatohepatitis ◽  
High Fat Diet ◽  
Potential Role ◽  
Mevalonic Acid ◽  
High Fat ◽  
Mevalonic Acid Pathway ◽  
Acid Pathway

scholarly journals Deficiency of the Purinergic Receptor 2X7 Attenuates Nonalcoholic Steatohepatitis Induced by High-Fat Diet: Possible Role of the NLRP3 Inflammasome

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Claudia Blasetti Fantauzzi ◽  
Stefano Menini ◽  
Carla Iacobini ◽  
Chiara Rossi ◽  
Eleonora Santini ◽  
...  
Keyword(s):  
Nonalcoholic Steatohepatitis ◽  
Nlrp3 Inflammasome ◽  
High Fat Diet ◽  
Molecular Mechanisms ◽  
Purinergic Receptor ◽  
High Fat ◽  
Liver Sinusoidal Endothelial Cells ◽  
Nonalcoholic Fatty Liver ◽  
Markers Of Inflammation

Molecular mechanisms driving transition from simple steatosis to nonalcoholic steatohepatitis (NASH), a critical step in the progression of nonalcoholic fatty liver disease (NAFLD) to cirrhosis, are poorly defined. This study aimed at investigating the role of the purinergic receptor 2X7 (PR2X7), through the NLRP3 inflammasome, in the development of NASH. To this end, mice knockout for the Pr2x7 gene (Pr2x7−/−) and coeval wild-type (WT) mice were fed a high-fat diet (HFD) or normal-fat diet for 16 weeks. NAFLD grade and stage were lower in Pr2x7−/− than WT mice, and only 1/7 Pr2x7−/− animals showed evidence of NASH, as compared with 4/7 WT mice. Molecular markers of inflammation, oxidative stress, and fibrosis were markedly increased in WT-HFD mice, whereas no or significantly reduced increments were detected in Pr2x7−/− animals, which showed also decreased modulation of genes of lipid metabolism. Deletion of Pr2x7 gene was associated with blunted or abolished activation of NLRP3 inflammasome and expression of its components, which were induced in liver sinusoidal endothelial cells challenged with appropriate stimuli. These data show that Pr2x7 gene deletion protects mice from HFD-induced NASH, possibly through blunted activation of NLRP3 inflammasome, suggesting that PR2X7 and NLRP3 may represent novel therapeutic targets.

scholarly journals Potential Role of Central Microglia Activation in High Fat Diet‐Induced Obesity

2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
Aneesh Singal ◽  
Caitlin R. Coker ◽  
Sarah S. Bingaman ◽  
Amy C. Arnold ◽  
Yuval Silberman
Keyword(s):  
High Fat Diet ◽  
Potential Role ◽  
Microglia Activation ◽  
High Fat ◽  
Diet Induced Obesity

scholarly journals Glucagon-like peptide-2 and mouse intestinal adaptation to a high-fat diet

2013 ◽  
Vol 217 (1) ◽  
pp. 11-20 ◽  
Author(s):  
Sara Baldassano ◽  
Antonella Amato ◽  
Francesco Cappello ◽  
Francesca Rappa ◽  
Flavia Mulè
Keyword(s):  
High Fat Diet ◽  
Caspase 3 ◽  
Potential Role ◽  
Intestinal Adaptation ◽  
Cell Number ◽  
Standard Diet ◽  
High Fat ◽  
Villus Height ◽  
Glucagon Like Peptide

Endogenous glucagon-like peptide-2 (GLP2) is a key mediator of refeeding-induced and resection-induced intestinal adaptive growth. This study investigated the potential role of GLP2 in mediating the mucosal responses to a chronic high-fat diet (HFD). In this view, the murine small intestine adaptive response to a HFD was analyzed and a possible involvement of endogenous GLP2 was verified using GLP2 (3–33) as GLP2 receptor (GLP2R) antagonist. In comparison with animals fed a standard diet, mice fed a HFD for 14 weeks exhibited an increase in crypt–villus mean height (duodenum, 27.5±3.0%; jejunum, 36.5±2.9%;P<0.01), in the cell number per villus (duodenum, 28.4±2.2%; jejunum, 32.0±2.9%;P<0.01), and in Ki67-positive cell number per crypt. No change in the percent of caspase-3-positive cell in the villus–crypt was observed. The chronic exposure to a HFD also caused a significant increase in GLP2 plasma levels and in GLP2R intestinal expression. Daily administration of GLP2 (3–33) (30–60 ng) for 4 weeks did not modify the crypt–villus height in control mice. In HFD-fed mice, chronic treatment with GLP2 (3–33) reduced the increase in crypt–villus height and in the cell number per villus through reduction of cell proliferation and increase in apoptosis. This study provides the first experimental evidence for a role of endogenous GLP2 in the intestinal adaptation to HFD in obese mice and for a dysregulation of the GLP2/GLP2R system after a prolonged HFD.

miR-182-5p Attenuates High-Fat -Diet-Induced Nonalcoholic Steatohepatitis in Mice

2018 ◽  
Vol 17 (5) ◽  
pp. 0-10
Author(s):  
Qionghe Liang ◽  
Huan Chen ◽  
Xiaoqun Xu ◽  
Weiwei Jiang
Keyword(s):  
Nonalcoholic Steatohepatitis ◽  
High Fat Diet ◽  
Hepg2 Cells ◽  
Treated Group ◽  
High Fat ◽  
Protein Levels ◽  
Tlr4 Mrna ◽  
Increased Risk

Introduction and Aim: Patients with NASH have increased risk for sepsis or cardiovascular disease after Liver transplantation. An important role of Toll-like receptor (TLR) 4 in the pathogenesis of nonalcoholic steatohepatitis (NASH) was demonstrated. Here, we study the role of miR-182-5p in TLR4 expression and high-fat-diet (HFD)-induced NASH in vitro and in vivo. Methods: Following transfection with a miR-182-5p mimic, the effect of miR-182-5p on TLR4 in RAW264.7 and HepG2 cells was investigated. Following administration of the miR-182-5p mimic into the livers of HFD-induced NASH mice, we determined the in vivo expression of TLR4, TNFα, and IL-6 and assessed the histologic features of the livers. Results: Following lipopolysaccharide (LPS) treatment of RAW264.7 cells, real-time RT-PCR and western blot results indicated decreases levels of TLR4 mRNA and protein in the miR-182-5p group as compared with levels observed in controls, with similar trends were observed in TNFα and IL-6 protein levels. Following oleic acid (OA) treatment of HepG2 cells, TLR4, TNFα, and IL-6 levels were significantly decreased in the miR-182-5p group as compared with levels observed in controls. Following miR-182-5p administration, TLR4 mRNA and protein levels decreased along with those of TNFα and IL-6 proteins, and the liver weight/body weight ratio of treated mice was less than that observed in controls. Furthermore, hematoxylin and eosin staining showed that the miR-182-5p-treated group exhibited low adipose-cell cross-sectional areas, and Oil Red O staining showed decreases in the size of lipid droplets in the miR-182-5p-treated group. Conclusions: miR-182-5p ameliorated HFD-induced NASH by suppressing TLR4.

[696] ROLE OF MELATONIN IN TREATMENT OF NONALCOHOLIC STEATOHEPATITIS IN RATS INDUCED BY HIGH FAT DIET

2007 ◽  
Vol 46 ◽  
pp. S263 ◽  
Author(s):  
N. Kuzu ◽  
I.H. Bahcecioglu ◽  
K. Metin ◽  
I.H. Ozercan ◽  
M. Tuzcu ◽  
...  
Keyword(s):  
Nonalcoholic Steatohepatitis ◽  
High Fat Diet ◽  
High Fat

scholarly journals Short-Term High-Fat Diet Promotes Increased Lysine Crotonylation in Cerebral Cortex

2021 ◽  
Author(s):  
Junling Wang ◽  
Jiajia Zhang ◽  
Xiaolu Wang ◽  
Chaojin Xu
Keyword(s):  
High Fat Diet ◽  
Potential Role ◽  
Cell Cycle Gene ◽  
Brain Disorders ◽  
Post Translational Modification ◽  
High Fat ◽  
Human Central Nervous System ◽  
Short Term ◽  
Damage Response

Abstract Protein lysine crotonylation is a newly discovered protein post-translational modification (PTM), which has been associated with cellular metabolism, cell cycle, gene transcription, DNA damage response. However, its potential roles related to human central nervous system diseases remain largely unknown. In the present study, we observed a significant elevated lysine crotonylation in a screening of nine lysine acylations in cortex tissues of HFD-fed mice after short-term overfeeding. On the base of previous reports and molecular weight of proteins, we also speculate that actin, ERK2 or GAPDH and CDK1 might be modified by lysine crotonylation (KCr). Taken together, our findings highlight a potential role of protein lysine crotonylation in HFD-induced brain disorders and as possible therapeutic candidates in the future.

Sign in / Sign up

Export Citation Format

Share Document