scholarly journals Chronic Oleoylethanolamide Treatment Decreases Hepatic Triacylglycerol Level in Rat Liver by a PPARγ/SREBP-Mediated Suppression of Fatty Acid and Triacylglycerol Synthesis

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 394
Author(s):  
Adele Romano ◽  
Marzia Friuli ◽  
Laura Del Coco ◽  
Serena Longo ◽  
Daniele Vergara ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Rat Liver ◽  
Fatty Acid Synthase ◽  
Sphingolipid Metabolism ◽  
Beneficial Effects ◽  
Triacylglycerol Synthesis ◽  
Triacylglycerol Level ◽  
Treatment Of Obesity ◽  
Induced Changes ◽  
Hepatic Triacylglycerol

Oleoylethanolamide (OEA) is a naturally occurring bioactive lipid belonging to the family of N-acylethanolamides. A variety of beneficial effects have been attributed to OEA, although the greater interest is due to its potential role in the treatment of obesity, fatty liver, and eating-related disorders. To better clarify the mechanism of the antiadipogenic effect of OEA in the liver, using a lipidomic study performed by 1H-NMR, LC-MS/MS and thin-layer chromatography analyses we evaluated the whole lipid composition of rat liver, following a two-week daily treatment of OEA (10 mg kg−1 i.p.). We found that OEA induced a significant reduction in hepatic triacylglycerol (TAG) content and significant changes in sphingolipid composition and ceramidase activity. We associated the antiadipogenic effect of OEA to decreased activity and expression of key enzymes involved in fatty acid and TAG syntheses, such as acetyl-CoA carboxylase, fatty acid synthase, diacylglycerol acyltransferase, and stearoyl-CoA desaturase 1. Moreover, we found that both SREBP-1 and PPARγ protein expression were significantly reduced in the liver of OEA-treated rats. Our findings add significant and important insights into the molecular mechanism of OEA on hepatic adipogenesis, and suggest a possible link between the OEA-induced changes in sphingolipid metabolism and suppression of hepatic TAG level.

scholarly journals Transient induction of fatty acid synthase in rat liver after removal of a peroxisome proliferator

FEBS Letters ◽  
1994 ◽  
Vol 356 (1) ◽  
pp. 122-124 ◽  
Author(s):  
Kiyoto Motojima ◽  
Masanori Isaka ◽  
Yasuko Takino ◽  
Sataro Goto
Keyword(s):  
Fatty Acid ◽  
Rat Liver ◽  
Fatty Acid Synthase ◽  
Peroxisome Proliferator

Increased fatty acid uptake, a factor in increased hepatic triacylglycerol synthesis in aging rats

1986 ◽  
Vol 37 (1) ◽  
pp. 49-54 ◽  
Author(s):  
Veeraraghavan K. Murthy ◽  
Oladipo A. Oredipe ◽  
Mark R. Stiles ◽  
Joseph C. Shipp
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Aging Rats ◽  
Triacylglycerol Synthesis ◽  
Hepatic Triacylglycerol

Nutritional Control of Rat Liver Fatty Acid Synthase and S14 mRNA Abundance

1990 ◽  
Vol 120 (2) ◽  
pp. 218-224 ◽  
Author(s):  
Steven D. Clarke ◽  
Michael K. Armstrong ◽  
Donald B. Jump
Keyword(s):  
Fatty Acid ◽  
Rat Liver ◽  
Fatty Acid Synthase ◽  
Mrna Abundance ◽  
Liver Fatty Acid

scholarly journals GosB Inhibits Triacylglycerol Synthesis and Promotes Cell Survival in Mouse Mammary Epithelial Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-12
Author(s):  
Gaoxiao Xu ◽  
Saixing Duan ◽  
Jianye Hou ◽  
Zhongxin Wei ◽  
Guangwei Zhao
Keyword(s):  
Fatty Acid ◽  
Epithelial Cells ◽  
Milk Fat ◽  
Fatty Acid Synthase ◽  
Mammary Epithelial Cells ◽  
Mammary Glands ◽  
Mammary Epithelial ◽  
Milk Fatty Acid ◽  
Fatty Acid Binding ◽  
Triacylglycerol Synthesis

It has been demonstrated that the activator protein related transcription factor Finkel-Biskis-Jinkins murine osteosarcoma B (GosB) is involved in preadipocyte differentiation and triacylglycerol synthesis. However, the role of GosB in regulating the synthesis of milk fatty acid in mouse mammary glands remains unclear. This research uncovered potentially new roles of GosB in suppressing milk fatty acid synthesis. Results revealed that GosB had the highest expression in lung tissue and showed a higher expression level during nonlactation than during lactation. GosB inhibited the expression of fatty acid synthase (FASN), stearoyl-CoA desaturase (SCD), fatty acid binding protein 4 (FABP4), diacylglycerol acyltransferase 1 (DGAT1), perilipin 2 (PLIN2), perilipin 3 (PLIN3), and C/EBPα in mouse mammary gland epithelial cells (MEC). In addition, GosB reduced cellular triglyceride content and the accumulation of lipid droplets; in particular, GosB enhanced saturated fatty acid concentration (C16:0 and C18:0). The PPARγ agonist, rosiglitazone (ROSI), promoted apoptosis and inhibited cell proliferation. GosB increased the expression of Bcl-2 and protected MEC from ROSI-induced apoptosis. Furthermore, MECs were protected from apoptosis through the GosB regulation of intracellular calcium concentrations. These findings suggest that GosB may regulate mammary epithelial cells milk fat synthesis and apoptosis via PPARγ in mouse mammary glands.

Regulation of fatty acid synthase at transcriptional and post-transcriptional levels in rat liver

1992 ◽  
Vol 33 (3) ◽  
pp. 199 ◽  
Author(s):  
Kyung Sup Kim ◽  
Sahng Wook Park ◽  
Yoon Soo Kim
Keyword(s):  
Fatty Acid ◽  
Rat Liver ◽  
Fatty Acid Synthase

PPARγ2 regulates lipogenesis and lipid accumulation in steatotic hepatocytes

2005 ◽  
Vol 288 (6) ◽  
pp. E1195-E1205 ◽  
Author(s):  
Susan E. Schadinger ◽  
Nancy L. R. Bucher ◽  
Barbara M. Schreiber ◽  
Stephen R. Farmer
Keyword(s):  
Fatty Acid ◽  
Cell Line ◽  
Lipid Accumulation ◽  
Fatty Acid Synthase ◽  
Molecular Mechanisms ◽  
De Novo ◽  
Binding Protein ◽  
Regulatory Element ◽  
Fatty Acid Binding ◽  
Triacylglycerol Synthesis

Peroxisome proliferator-activated receptor-γ (PPARγ) is considered to be one of the master regulators of adipocyte differentiation. PPARγ2 is abundantly expressed in mature adipocytes and is elevated in the livers of animals that develop fatty livers. The aim of this study was to determine the ability of PPARγ2 to induce lipid accumulation in hepatocytes and to delineate molecular mechanisms driving this process. The hepatic cell line AML-12 was used to generate a cell line stably expressing PPARγ2. Oil Red O staining revealed that PPARγ2 induces lipid accumulation in hepatocytes. This phenotype is accompanied by a selective upregulation of several adipogenic and lipogenic genes including adipose differentiation-related protein (ADRP), adipocyte fatty acid-binding protein 4, sterol regulatory element-binding protein-1 (SREBP-1), fatty acid synthase (FAS), and acetyl-CoA carboxylase, genes whose expression levels are known to increase in steatotic livers of ob/ob mice. Furthermore, the PPARγ2-regulated induction of both SREBP-1 and FAS parallels an increase in de novo triacylglycerol synthesis in hepatocytes. Triacylglycerol synthesis and lipid accumulation are further enhanced by culturing hepatocytes with troglitazone in the absence of exogenous lipids. These results correspond with an increase in the lipid droplet protein, ADRP, and the data demonstrate that ADRP functions to coat lipid droplets in hepatocytes as observed by confocal microscopy. Taken together, these observations propose a role for PPARγ2 as an inducer of steatosis in hepatocytes and suggest that this phenomenon occurs through an induction of pathways regulating de novo lipid synthesis.

Sign in / Sign up

Export Citation Format

Share Document