scholarly journals Trypanosoma cruziInfection and Host Lipid Metabolism

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Qianqian Miao ◽  
Momar Ndao
Keyword(s):  
Lipid Metabolism ◽  
Metabolic Pathways ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipid Homeostasis ◽  
Low Density ◽  
Host Interactions ◽  
Density Lipoprotein Receptor ◽  
The Status ◽  
Potential Impact

Trypanosoma cruziis the causative agent of Chagas disease. Approximately 8 million people are thought to be affected worldwide. Several players in host lipid metabolism have been implicated inT. cruzi-host interactions in recent research, including macrophages, adipocytes, low density lipoprotein (LDL), low density lipoprotein receptor (LDLR), and high density lipoprotein (HDL). All of these factors are required to maintain host lipid homeostasis and are intricately connected via several metabolic pathways. We reviewed the interaction ofT. cruziwith each of the relevant host components, in order to further understand the roles of host lipid metabolism inT. cruziinfection. This review sheds light on the potential impact ofT. cruziinfection on the status of host lipid homeostasis.

scholarly journals CREBH Systemically Regulates Lipid Metabolism by Modulating and Integrating Cellular Functions

Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 3204
Author(s):  
Yoshimi Nakagawa ◽  
Masaya Araki ◽  
Song-iee Han ◽  
Yuhei Mizunoe ◽  
Hitoshi Shimano
Keyword(s):  
Small Intestine ◽  
Lipid Metabolism ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipid Homeostasis ◽  
Transcriptional Level ◽  
Cellular Functions ◽  
Density Lipoprotein Receptor ◽  
Element Binding Protein ◽  
Severe Atherosclerosis

Cyclic AMP-responsive element-binding protein H (CREBH, encoded by CREB3L3) is a membrane-bound transcriptional factor expressed in the liver and small intestine. The activity of CREBH is regulated not only at the transcriptional level but also at the posttranslational level. CREBH governs triglyceride metabolism in the liver by controlling gene expression, with effects including the oxidation of fatty acids, lipophagy, and the expression of apolipoproteins related to the lipoprotein lipase activation and suppression of lipogenesis. The activation and functions of CREBH are controlled in response to the circadian rhythm. On the other hand, intestinal CREBH downregulates the absorption of lipids from the diet. CREBH deficiency in mice leads to severe hypertriglyceridemia and fatty liver in the fasted state and while feeding a high-fat diet. Therefore, when crossing CREBH knockout (KO) mice with an atherosclerosis model, low-density lipoprotein receptor KO mice, these mice exhibit severe atherosclerosis. This phenotype is seen in both liver- and small intestine-specific CREBH KO mice, suggesting that CREBH controls lipid homeostasis in an enterohepatic interaction. This review highlights that CREBH has a crucial role in systemic lipid homeostasis to integrate cellular functions related to lipid metabolism.

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