Novel therapeutic drugs for hyperlipidemia to regulate lipid metabolism genes, selective PPAR-alpha modulator (SPPARMα)

2019 ◽  
Vol 131 (2) ◽  
pp. 103-105
Author(s):  
Kiyoshi Teshigawara
Keyword(s):  
Lipid Metabolism ◽  
Ppar Alpha ◽  
Therapeutic Drugs ◽  
Lipid Metabolism Genes ◽  
Regulate Lipid Metabolism ◽  
Novel Therapeutic

scholarly journals ANGPLT3: A novel modulator of lipid metabolism

2017 ◽  
Vol 2017 (1) ◽  
Author(s):  
Mohamed Hassan
Keyword(s):  
Lipid Metabolism ◽  
Endothelial Lipase ◽  
Loss Of Function ◽  
New Class ◽  
Irreversible Inhibition ◽  
Cholesterol Levels ◽  
Important Regulator ◽  
Activity Loss ◽  
Regulate Lipid Metabolism ◽  
Novel Therapeutic

Angiopoietin-like proteins (ANGPTLs) have emerged as an important regulator of lipid and glucose metabolism as well as insulin sensitivity. ANGPTL3 plays a key role in regulating circulating triglycerides (TG) and cholesterol levels through reversible inhibition of lipoprotein lipase (LPL) and endothelial lipase enzymes activity. Loss of function mutation of ANGPTL3 gene has been identified in many subjects with familial combined hypolipidemia. ANGPTL4 produces irreversible inhibition of LPL activity, while ANGPTL8 enhances the activity of ANGPTL3, which highlight the interplay between the different ANGPTLs in a coordinated manner to regulate lipid metabolism during different nutritional states. This new class of lipid modulators may serve as potential novel therapeutic target for reducing plasma lipoprotein and treatment of metabolic syndrome. 

Niga-ichigoside F1 ameliorates high-fat diet-induced hepatic steatosis in male mice by Nrf2 activation

2018 ◽  
Vol 9 (2) ◽  
pp. 906-916 ◽  
Author(s):  
Shu-Fang Xia ◽  
Jing Shao ◽  
Shu-Ying Zhao ◽  
Yu-Yu Qiu ◽  
Li-Ping Teng ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Nuclear Translocation ◽  
Male Mice ◽  
High Fat ◽  
Genes Expression ◽  
Nrf2 Activation ◽  
Lipid Metabolism Genes ◽  
Regulate Lipid Metabolism

Niga-ichigoside F1 ameliorated high-fat diet-induced hepatic steatosis by increasing Nrf2 nuclear translocation to regulate lipid metabolism genes expression in livers of C57BL/6J mice.

scholarly journals Dysregulated liver lipid metabolism and innate immunity associated with hepatic steatosis in neonatal BBdp rats and NOD mice

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
D. Serrano ◽  
J. A. Crookshank ◽  
B. S. Morgan ◽  
R. W. Mueller ◽  
M.-F. Paré ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Lipid Metabolism ◽  
Hepatic Steatosis ◽  
Liver Lipid ◽  
Nod Mice ◽  
Gene Signature ◽  
Enhanced Expression ◽  
Liver Lipid Metabolism ◽  
Hepatic Innate Immunity ◽  
Lipid Metabolism Genes

Abstract In a previous study we reported that prediabetic rats have a unique gene signature that was apparent even in neonates. Several of the changes we observed, including enhanced expression of pro-inflammatory genes and dysregulated UPR and metabolism genes were first observed in the liver followed by the pancreas. In the present study we investigated further early changes in hepatic innate immunity and metabolism in two models of type 1 diabetes (T1D), the BBdp rat and NOD mouse. There was a striking increase in lipid deposits in liver, particularly in neonatal BBdp rats, with a less striking but significant increase in neonatal NOD mice in association with dysregulated expression of lipid metabolism genes. This was associated with a decreased number of extramedullary hematopoietic clusters as well as CD68+ macrophages in the liver of both models. In addition, PPARɣ and phosphorylated AMPKα protein were decreased in neonatal BBdp rats. BBdp rats displayed decreased expression of antimicrobial genes in neonates and decreased M2 genes at 30 days. This suggests hepatic steatosis could be a common early feature in development of T1D that impacts metabolic homeostasis and tolerogenic phenotype in the prediabetic liver.

scholarly journals High Fat Activates O-GlcNAcylation and Affects AMPK/ACC Pathway to Regulate Lipid Metabolism

Nutrients ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1740
Author(s):  
Yuning Pang ◽  
Xiang Xu ◽  
Xiaojun Xiang ◽  
Yongnan Li ◽  
Zengqi Zhao ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
High Fat Diet ◽  
Lipid Synthesis ◽  
Fat Deposition ◽  
Liver Fat ◽  
Lipid Homeostasis ◽  
High Fat ◽  
Dual Inhibitor ◽  
Regulate Lipid Metabolism

A high-fat diet often leads to excessive fat deposition and adversely affects the organism. However, the mechanism of liver fat deposition induced by high fat is still unclear. Therefore, this study aimed at acetyl-CoA carboxylase (ACC) to explore the mechanism of excessive liver deposition induced by high fat. In the present study, the ORF of ACC1 and ACC2 were cloned and characterized. Meanwhile, the mRNA and protein of ACC1 and ACC2 were increased in liver fed with a high-fat diet (HFD) or in hepatocytes incubated with oleic acid (OA). The phosphorylation of ACC was also decreased in hepatocytes incubated with OA. Moreover, AICAR dramatically improved the phosphorylation of ACC, and OA significantly inhibited the phosphorylation of the AMPK/ACC pathway. Further experiments showed that OA increased global O-GlcNAcylation and agonist of O-GlcNAcylation significantly inhibited the phosphorylation of AMPK and ACC. Importantly, the disorder of lipid metabolism caused by HFD or OA could be rescued by treating CP-640186, the dual inhibitor of ACC1 and ACC2. These observations suggested that high fat may activate O-GlcNAcylation and affect the AMPK/ACC pathway to regulate lipid synthesis, and also emphasized the importance of the role of ACC in lipid homeostasis.

scholarly journals Feedback looping between ChREBP and PPAR^|^alpha; in the regulation of lipid metabolism in brown adipose tissues

2013 ◽  
Vol 60 (10) ◽  
pp. 1145-1153 ◽  
Author(s):  
Katsumi Iizuka ◽  
Wudelehu Wu ◽  
Yukio Horikawa ◽  
Masayuki Saito ◽  
Jun Takeda
Keyword(s):  
Lipid Metabolism ◽  
Ppar Alpha ◽  
Adipose Tissues ◽  
Brown Adipose

scholarly journals Hepatocyte-specific Sirt6 deficiency impairs ketogenesis

2018 ◽  
Vol 294 (5) ◽  
pp. 1579-1589 ◽  
Author(s):  
Lei Chen ◽  
Qinhui Liu ◽  
Qin Tang ◽  
Jiangying Kuang ◽  
Hong Li ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Metabolic Diseases ◽  
Critical Role ◽  
Gene Promoter ◽  
Camp Response Element Binding ◽  
Hepatic Lipid Metabolism ◽  
Camp Response Element ◽  
Hepatic Lipid ◽  
Element Binding Protein ◽  
Regulate Lipid Metabolism

Sirt6 is an NADH (NAD+)-dependent deacetylase with a critical role in hepatic lipid metabolism. Ketogenesis is controlled by a signaling network of hepatic lipid metabolism. However, how Sirt6 functions in ketogenesis remains unclear. Here, we demonstrated that Sirt6 functions as a mediator of ketogenesis in response to a fasting and ketogenic diet (KD). The KD-fed hepatocyte-specific Sirt6 deficiency (HKO) mice exhibited impaired ketogenesis, which was due to enhanced Fsp27 (fat-specific induction of protein 27), a protein known to regulate lipid metabolism. In contrast, overexpression of Sirt6 in mouse primary hepatocytes promoted ketogenesis. Mechanistically, Sirt6 repressed Fsp27β expression by interacting with Crebh (cAMP response element–binding protein H) and preventing its recruitment to the Fsp27β gene promoter. The KD-fed HKO mice also showed exacerbated hepatic steatosis and inflammation. Finally, Fsp27 silencing rescued hypoketonemia and other metabolic phenotypes in KD-fed HKO mice. Our data suggest that the Sirt6–Crebh–Fsp27 axis is pivotal for hepatic lipid metabolism and inflammation. Sirt6 may be a pharmacological target to remedy metabolic diseases.

scholarly journals The changes of chemerin and chemerin receptor to regulate lipid metabolism in liver and pituitary gland

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Sanggun Roh ◽  
Shun Kitayama ◽  
Astrid Ardiyanti ◽  
Yutaka Suzuki ◽  
Eri Yamauchi ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Pituitary Gland ◽  
Regulate Lipid Metabolism

scholarly journals Effects of an alpha‐linolenic acid enriched diet on mRNA expression of lipid metabolism genes in bovine milk somatic cells

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Katherine M Hunt ◽  
Kevin G Carnahan ◽  
Brent P Hatch ◽  
Kelleen O Parnell ◽  
Janet E Williams ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Mrna Expression ◽  
Linolenic Acid ◽  
Somatic Cells ◽  
Bovine Milk ◽  
Alpha Linolenic Acid ◽  
Milk Somatic Cells ◽  
Lipid Metabolism Genes

scholarly journals Glial Hedgehog and lipid metabolism regulate neural stem cell proliferation in Drosophila

2020 ◽  
Author(s):  
Qian Dong ◽  
Michael Zavortink ◽  
Francesca Froldi ◽  
Sofya Golenkina ◽  
Tammy Lam ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Cell Cycle Progression ◽  
De Novo ◽  
De Novo Lipogenesis ◽  
Post Translational Modification ◽  
Final Size ◽  
Neural Lineage ◽  
Signalling Molecule ◽  
Lipid Metabolism Genes ◽  
And Function

AbstractThe final size and function of the adult central nervous system (CNS) is determined by neuronal lineages generated by neural stem cells (NSCs) in the developing brain. In Drosophila, NSCs called neuroblasts (NBs) reside within a specialised microenvironment called the glial niche. Here, we explore non-autonomous glial regulation of NB proliferation. We show that lipid droplets (LDs) which reside within the glial niche are closely associated with the signalling molecule Hedgehog (Hh). Under physiological conditions, cortex glial Hh is autonomously required to sustain niche chamber formation, and non-autonomously restrained to prevent ectopic Hh signalling in the NBs. In the context of cortex glial overgrowth, induced by Fibroblast Growth Factor (FGF) activation, Hh and lipid storage regulators Lsd-2 and Fasn1 were upregulated, resulting in activation of Hh signalling in the NBs; which in turn disrupted NB cell cycle progression and reduced neuronal production. We show that the LD regulator Lsd-2 modulates Hh’s ability to signal to NBs, and de novo lipogenesis gene Fasn1 regulates Hh post-translational modification via palmitoylation. Together, our data suggest that the glial niche non-autonomously regulates NB proliferation and neural lineage size via Hh signaling that is modulated by lipid metabolism genes.

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