scholarly journals Fatty acids regulate the expression of lipoprotein lipase gene and activity in preadipose and adipose cells

1996 ◽  
Vol 314 (2) ◽  
pp. 541-546 ◽  
Author(s):  
Ez-Zoubir AMRI ◽  
Lydia TEBOUL ◽  
Christian VANNIER ◽  
Paul-André GRIMALDI ◽  
Gérard AILHAUD
Keyword(s):  
Gene Expression ◽  
Fatty Acids ◽  
Lipoprotein Lipase ◽  
Fine Tuning ◽  
Lipase Gene ◽  
Lpl Gene ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Adipose Cells

During fasting, a reduction in lipoprotein lipase (LPL) activity has been observed in rat fat pad with no change in enzyme mass, whereas LPL mRNA and synthesis are increased, suggesting that insulin and/or fatty acids (FA) regulate LPL activity post-translationaly [Doolittle, Ben-Zeev, Elovson, Martin and Kirchgessner (1990) J. Biol. Chem. 265, 4570–4577]. To examine the role of FA, either preadipose Ob1771 cells or Ob1771 and 3T3-F442A adipose cells were exposed to long-chain FA and to 2-bromopalmitate, a non-metabolized FA. A rapid (2–8 h) and dose-dependent increase (up to 6-fold) in LPL mRNA occurred, primarily due to increased transcription, which is accompanied by a decrease (down to 4-fold) in LPL cellular activity. Under these conditions, secretion of active LPL was nearly abolished. Removal of FA led to full recovery of LPL activity. LPL gene expression in 3T3-C2 fibroblasts was not affected by FA treatment. However fatty acid-activated receptor transfected-3T3-C2 cells, which show FA responsiveness, had increased LPL gene expression upon FA addition. LPL synthesis and cellular content appeared unaffected by FA treatment, whereas secretion of LPL was inhibited. These results indicate that FA regulate the post-translational processing of LPL. It is proposed that the regulation of LPL activity by FA is important with regard to the fine-tuning of FA entry into adipocytes during fasting/feeding periods.

Linkage and linkage disequilibrium analysis of the lipoprotein lipase gene with lipid profiles in Chinese hypertensive families

2005 ◽  
Vol 108 (2) ◽  
pp. 137-142 ◽  
Author(s):  
Wenjie YANG ◽  
Jianfeng HUANG ◽  
Cailiang YAO ◽  
Shaoyong SU ◽  
Donghai LIU ◽  
...  
Keyword(s):  
Linkage Disequilibrium ◽  
Lipoprotein Lipase ◽  
Lipid Profiles ◽  
Strong Linkage Disequilibrium ◽  
Nucleotide Polymorphisms ◽  
Linkage Disequilibrium Analysis ◽  
Lipid Levels ◽  
Lipase Gene ◽  
Significant Independent Risk Factor ◽  
Lpl Gene

Elevated TG [triacylglycerol (triglyceride)] is a significant independent risk factor for cardiovascular disease. LPL (lipoprotein lipase) is one of the key enzymes in the metabolism of the TG-rich lipoproteins which hydrolyses TG from the chylomicrons and very-LDL (low-density lipoprotein). To investigate the relationship between the LPL gene and lipid profiles, especially TG, in 148 hypertensive families, we have chosen seven flanking microsatellite markers and four internal markers of the LPL gene and conducted linkage analysis by SOLAR and S.A.G.E. (statistical analysis for genetic epidemiology)/SIBPAL 2 programs, and linkage disequilibrium analysis by QTDT (quantitative transmission/disequilibrium test) and GOLD (graphical overview of linkage disequilibrium). There were statistically significant differences in lipid levels between subjects without and with hypertension within families. A maximum LOD score of 1.3 with TG at the marker D8S261 was observed by SOLAR. Using S.A.G.E./SIBPAL 2, we identified a linkage with TG at the marker ‘ATTT’ located within intron 6 of the LPL gene (P=0.0095). Two SNPs (single nucleotide polymorphisms), HindIII and HinfI, were found in linkage disequilibrium with LDL-cholesterol levels (P=0.0178 and P=0.0088 respectively). A strong linkage disequilibrium was observed between the HindIII in intron 8 and HinfI in the exon 9 (P<0.00001, D′=0.895). Linkage disequilibrium was also found between the ‘ATTT’ polymorphism in intron 6 and two SNPs (P=0.0021 and D′=0.611 for HindIII; and P=0.00004, D′=0.459 for HinfI). The present study in the Chinese families with hypertension suggested that the LPL gene might influence lipid levels, especially TG metabolism. Replication studies both in Chinese and other populations are warranted to confirm these results.

scholarly journals Fatty acids, epigenetic mechanisms and chronic diseases: a systematic review

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
K. González-Becerra ◽  
O. Ramos-Lopez ◽  
E. Barrón-Cabrera ◽  
J. I. Riezu-Boj ◽  
F. I. Milagro ◽  
...  
Keyword(s):  
Gene Expression ◽  
Systematic Review ◽  
Fatty Acids ◽  
Chronic Diseases ◽  
Gene Expression Regulation ◽  
Saturated Fatty Acids ◽  
Dietary Fatty Acids ◽  
Epigenetic Mechanisms ◽  
Metabolic Alterations

Abstract Background Chronic illnesses like obesity, type 2 diabetes (T2D) and cardiovascular diseases, are worldwide major causes of morbidity and mortality. These pathological conditions involve interactions between environmental, genetic, and epigenetic factors. Recent advances in nutriepigenomics are contributing to clarify the role of some nutritional factors, including dietary fatty acids in gene expression regulation. This systematic review assesses currently available information concerning the role of the different fatty acids on epigenetic mechanisms that affect the development of chronic diseases or induce protective effects on metabolic alterations. Methods A targeted search was conducted in the PubMed/Medline databases using the keywords “fatty acids and epigenetic”. The data were analyzed according to the PRISMA-P guidelines. Results Consumption fatty acids like n-3 PUFA: EPA and DHA, and MUFA: oleic and palmitoleic acid was associated with an improvement of metabolic alterations. On the other hand, fatty acids that have been associated with the presence or development of obesity, T2D, pro-inflammatory profile, atherosclerosis and IR were n-6 PUFA, saturated fatty acids (stearic and palmitic), and trans fatty acids (elaidic), have been also linked with epigenetic changes. Conclusions Fatty acids can regulate gene expression by modifying epigenetic mechanisms and consequently result in positive or negative impacts on metabolic outcomes.

Role of glutamine and arginase in protection against ammonia-induced cell death in gastric epithelial cells

2002 ◽  
Vol 283 (6) ◽  
pp. G1264-G1275 ◽  
Author(s):  
Eiji Nakamura ◽  
Susan J. Hagen
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Ammonium Chloride ◽  
Gastric Epithelial Cells ◽  
Cytotoxic Factor ◽  
Ammonia Detoxification ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Detoxification Pathways

Ammonia is a cytotoxic factor produced during Helicobacter pylori infection that may reduce the survival of surface epithelial cells. Here we examine whether ammonia kills cells and whether l-glutamine (l-Gln) protects against cell death by stimulating ammonia detoxification pathways. Cell viability and vacuolation were quantified in rat gastric epithelial (RGM1) cells incubated with ammonium chloride at pH 7.4 in the presence or absence of l-Gln. Incubation of RGM1 cells with ammonium chloride caused a dose-dependent increase in cell death and vacuolation, which were both inhibited byl-Gln. We show that RGM1 cells metabolize ammonia to urea via arginase, a process that is stimulated by l-Gln and results in reduced ammonia cytotoxicity. l-Gln also inhibits the uptake and facilitates the extrusion of ammonia from cells. Blockade of glutamine synthetase did not reduce the survival of RGM1 cells, demonstrating that the conversion ofl-glutamate and ammonia to l-Gln is not involved in ammonia detoxification. Thus our data support a role forl-Gln and arginase in protection against ammonia-induced cell death in gastric epithelial cells.

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