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.

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.

ADAMTS13 deficiency promotes microthrombosis in a murine model of diet-induced liver steatosis

2017 ◽  
Vol 117 (01) ◽  
pp. 19-26 ◽  
Author(s):  
Lotte Geys ◽  
Dries Bauters ◽  
Elien Roose ◽  
Claudia Tersteeg ◽  
Karen Vanhoorelbeke ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Potential Role ◽  
Liver Steatosis ◽  
High Fat ◽  
Markers Of Inflammation ◽  
Normal Chow ◽  
Adamts13 Deficiency ◽  
Von Willebrand ◽  
Willebrand Factor

SummaryADAMTS13 cleaves ultralarge multimeric von Willebrand Factor (VWF), thereby preventing formation of platelet-rich microthrombi. ADAMTS13 is mainly produced by hepatic stellate cells, and numerous studies have suggested a functional role of ADAMTS13 in the pathogenesis of liver diseases. The aim of our study was to investigate a potential role of ADAMTS13 in formation of hepatic microthrombi and development of non-alcoholic steatohepatitis (NASH), and furthermore to evaluate whether plasmin can compensate for the absence of ADAMTS13 in removal of thrombi. Therefore, we used a model of high-fat diet-induced steatosis in Adamts13 deficient (Adamts13−/−) and wild-type (WT) control mice. Microthrombi were more abundant in the liver of obese Adamts13−/− as compared to obese WT or to lean Adamts13−/− mice. Obese Adamts13−/− mice displayed lower platelet counts and higher prevalence of ultra-large VWF multimers. Hepatic plasmin-α2-antiplasmin complex levels were comparable for obese WT and Adamts13−/− mice and were lower for lean Adamts13−/− than WT mice, not supporting marked activation of the fibrinolytic system. High fat diet feeding, as compared to normal chow, resulted in enhanced liver triglyceride levels for both genotypes (p < 0.0001) and steatosis (p < 0.0001 for WT mice, p = 0.002 for Adamts13−/− mice) without differences between the genotypes. Expression of markers of inflammation, oxidative stress, steatosis and fibrosis was affected by diet, but not by genotype. Thus, our data confirm that obesity promotes NASH, but do not support a detrimental role of ADAMTS13 in its development. However, Adamts13 deficiency in obese mice promotes hepatic microthrombosis, whereas a compensatory role of plasmin in removal of microthrombi in the absence of ADAMTS13 could not be demonstrated.

scholarly journals The role of glucokinase and insulin receptor substrate-2 in the proliferation of pancreatic beta cells induced by short-term high-fat diet feeding in mice

Metabolism ◽  
2018 ◽  
Vol 85 ◽  
pp. 48-58 ◽  
Author(s):  
Naoyuki Kitao ◽  
Akinobu Nakamura ◽  
Hideaki Miyoshi ◽  
Hiroshi Nomoto ◽  
Kiyohiko Takahashi ◽  
...  
Keyword(s):  
Insulin Receptor ◽  
Beta Cells ◽  
High Fat Diet ◽  
Pancreatic Beta Cells ◽  
Insulin Receptor Substrate ◽  
High Fat ◽  
Short Term
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