Molecular Mechanism of Betaine on Hepatic Lipid Metabolism: Inhibition of Forkhead Box O1 (FoxO1) Binding to Peroxisome Proliferator-Activated Receptor Gamma (PPARγ)

2016 ◽  
Vol 64 (36) ◽  
pp. 6819-6825 ◽  
Author(s):  
Dae Hyun Kim ◽  
Bonggi Lee ◽  
Min Jo Kim ◽  
Min Hi Park ◽  
Hye Jin An ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Molecular Mechanism ◽  
Peroxisome Proliferator ◽  
Hepatic Lipid Metabolism ◽  
Peroxisome Proliferator Activated Receptor ◽  
Hepatic Lipid ◽  
Forkhead Box ◽  
Metabolism Inhibition

scholarly journals Impact of Dietary Crude Protein Level on Hepatic Lipid Metabolism in Weaned Female Piglets

Animals ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1829
Author(s):  
Ning Liu ◽  
Yun Ji ◽  
Ying Yang ◽  
Hai Jia ◽  
Xuemeng Si ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Crude Protein ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Fatty Acid Synthase ◽  
Mrna Level ◽  
Building Blocks ◽  
Peroxisome Proliferator ◽  
Hepatic Lipid Metabolism ◽  
Peroxisome Proliferator Activated Receptor ◽  
Hepatic Lipid

Amino acids serve not only as building blocks for proteins, but also as substrates for the synthesis of low-molecular-weight substances involved in hepatic lipid metabolism. In the present study, eighteen weaned female piglets at 35 days of age were fed a corn- and soybean meal-based diet containing 20%, 17%, or 14% crude protein (CP), respectively. We found that 17% or 20% CP administration reduced the triglyceride and cholesterol concentrations, while enhanced high-density lipoprotein cholesterol (HDL-C) concentration in serum. Western blot analysis showed that piglets in the 20% CP group had higher protein abundance of hormone-sensitive triglyceride lipase (HSL) and peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α), as compared with other groups. Moreover, the mRNA expression of sterol regulatory element binding transcription factor 1 (SREBPF1), fatty acid synthase (FASN), and stearoyl-CoA desaturase (SCD) were lower in the 17% or 20% CP group, compared with those of the piglets administered with 14% CP. Of note, the mRNA level of acetyl-CoA carboxylase alpha (ACACα) was lower in the 17% CP group, compared with other groups. Additionally, the mRNA level of lipoprotein lipase (LPL), peroxisome proliferator-activated receptor alpha α (PPARα), glucose-6-phosphatase catalytic subunit (G6PC), and phosphoenolpyruvate carboxykinase 1 (PKC1) in the liver of piglets in the 20% CP group were higher than those of the 14% CP group. Collectively, our results demonstrated that dietary CP could regulate hepatic lipid metabolism through altering hepatic lipid lipogenesis, lipolysis, oxidation, and gluconeogenesis.

scholarly journals Lysine Acetylation of CREBH Regulates Fasting-Induced Hepatic Lipid Metabolism

2015 ◽  
Vol 35 (24) ◽  
pp. 4121-4134 ◽  
Author(s):  
Hyunbae Kim ◽  
Roberto Mendez ◽  
Xuequn Chen ◽  
Deyu Fang ◽  
Kezhong Zhang
Keyword(s):  
Lipid Metabolism ◽  
Transcriptional Activity ◽  
Target Genes ◽  
Sirtuin 1 ◽  
Site Directed Mutagenesis ◽  
Lipid Homeostasis ◽  
Peroxisome Proliferator ◽  
Dependent Manner ◽  
Hepatic Lipid Metabolism ◽  
Hepatic Lipid

Cyclic AMP-responsive element-binding protein 3-like 3, hepatocyte specific (CREBH), is a hepatic transcription factor that functions as a key regulator of energy homeostasis. Here, we defined a regulatory CREBH posttranslational modification process, namely, lysine-specific acetylation, and its functional involvement in fasting-induced hepatic lipid metabolism. Fasting induces CREBH acetylation in mouse livers in a time-dependent manner, and this event is critical for CREBH transcriptional activity in regulating hepatic lipid homeostasis. The histone acetyltransferase PCAF-mediated acetylation and the deacetylase sirtuin-1-mediated deacetylation coexist to maintain CREBH acetylation states under fasting conditions. Site-directed mutagenesis and functional analyses revealed that the lysine (K) residue at position 294 (K294) within the bZIP domain of the CREBH protein is the site where fasting-induced acetylation/deacetylation occurs. Introduction of the acetylation-deficient (K294R) or acetylation-mimicking (K294Q) mutation inhibited or enhanced CREBH transcriptional activity, respectively. Importantly, CREBH acetylation at lysine 294 was required for the interaction and synergy between CREBH and peroxisome proliferator-activated receptor α (PPARα) in activating their target genes upon fasting or glucagon stimulation. Introduction of the CREBH lysine 294 mutation in the liver leads to hepatic steatosis and hyperlipidemia in animals under prolonged fasting. In summary, our study reveals a molecular mechanism by which fasting or glucagon stimulation modulates lipid homeostasis through acetylation of CREBH.

scholarly journals Genistein Regulates Lipid Metabolism via Estrogen Receptor β and Its Downstream Signal Akt/mTOR in HepG2 Cells

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 4015
Author(s):  
Hong Qin ◽  
Ziyu Song ◽  
Horia Shaukat ◽  
Wenya Zheng
Keyword(s):  
Estrogen Receptor ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Hepg2 Cells ◽  
Fatty Acid Synthase ◽  
Regulatory Element ◽  
Estrogen Receptor Β ◽  
Peroxisome Proliferator ◽  
Hepatic Lipid Metabolism ◽  
Hepatic Lipid

Genistein (GEN) has been shown to significantly inhibit hepatic triglyceride accretion triggered by estrogen deficiency. The main purpose of this in vitro study was to investigate the function and molecular mechanism of estrogen receptor β (ERβ) in regulating hepatic lipid metabolism induced by GEN. Different doses of GEN or GEN with an ERβ antagonist were treated with HepG2 cells. Results showed that 25 μM GEN significantly diminished triglyceride levels. Meanwhile, GEN downregulated the levels of genes and proteins involved in lipogenesis, such as sterol-regulatory element-binding protein-1c (SREBP-1c), fatty acid synthase (FASN), and stearoyl-coenzyme A desaturase 1 (SCD1), and upregulated the gene and protein levels of the regulation factors responsible for fatty acid β-oxidation, such as carnitine palmitoyltransferase 1α (CPT-1α) and peroxisome proliferator-activated receptor α (PPARα). Furthermore, 25 μM GEN reduced the levels of phosphorylation of protein kinase B (Akt) and mechanistic target of rapamycin (mTOR). Moreover, most of these effects from GEN were reverted by pretreatment with the antagonist of ERβ. In conclusion, GEN improved hepatic lipid metabolism by activating ERβ and further modulation of Akt/mTOR signals. The results provide novel aspects of the regulatory mechanism of ERβ on hepatic lipid metabolism and might help to profoundly understand the functions of food-derived phytoestrogens in preventing and treating hepatic steatosis in postmenopausal women.

Altered hepatic lipid metabolism in leptin-deficlent mice

2001 ◽  
Vol 120 (5) ◽  
pp. A546-A546
Author(s):  
D SWARTZBASILE ◽  
M GOLDBLATT ◽  
C SVATEK ◽  
M WALTERS ◽  
S CHOI ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Hepatic Lipid Metabolism ◽  
Hepatic Lipid

Prenatal programming of hepatic lipid metabolism: Sex, hormones and lifelong health

2020 ◽  
Author(s):  
Katarzyna Siemienowicz ◽  
Panagiotis Filis ◽  
Chiara Talia ◽  
Jennifer Thomas ◽  
Paul Fowler ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Sex Hormones ◽  
Prenatal Programming ◽  
Hepatic Lipid Metabolism ◽  
Hepatic Lipid
Sign in / Sign up

Export Citation Format

Share Document