The Role of Fatty Acids in Gene Expression: Health Implications

1996 ◽  
Vol 40 (6) ◽  
pp. 303-311 ◽  
Author(s):  
Artemis P. Simopoulos
Keyword(s):  
Gene Expression ◽  
Fatty Acids ◽  
Health Implications

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.

scholarly journals The role of n-3 polyunsaturated fatty acids in brain: Modulation of rat brain gene expression by dietary n-3 fatty acids

2002 ◽  
Vol 99 (5) ◽  
pp. 2619-2624 ◽  
Author(s):  
K. Kitajka ◽  
L. G. Puskas ◽  
A. Zvara ◽  
L. Hackler ◽  
G. Barcelo-Coblijn ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Rat Brain ◽  
Brain Gene Expression

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.

scholarly journals Activation of Adipocyte mTORC1 Increases Milk Lipids in a Mouse Model of Lactation

2021 ◽  
Author(s):  
Noura El-Habbal ◽  
Allison C. Meyer ◽  
Hannah Hafner ◽  
JeAnna R. Redd ◽  
Zach Carlson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fatty Acids ◽  
Mammary Gland ◽  
Milk Fat ◽  
Saturated Fatty Acids ◽  
Milk Composition ◽  
Nutrient Sensing ◽  
Lower Percentage ◽  
Milk Lipids

Human milk is the recommended nutrient source for newborns. The mammary gland comprises multiple cell types including epithelial cells and adipocytes. The contributions of mammary adipocytes to breast milk composition and the intersections between mammary nutrient sensing and milk lipids are not fully understood. A major nutrient sensor in most tissues is the mechanistic target of rapamycin 1 (mTORC1). To assess the role of excess nutrient sensing on mammary gland structure, function, milk composition, and offspring weights, we used an Adiponectin-Cre driven Tsc1 knockout model of adipocyte mTORC1 hyperactivation. Our results show that the knockout dams have higher milk fat contributing to higher milk caloric density and heavier offspring weight during lactation. Additionally, milk of knockout dams displayed a lower percentage of saturated fatty acids, higher percentage of monounsaturated fatty acids, and a lower milk ω6: ω3 ratio driven by increases in Docosahexaenoic acid (DHA). Mammary gland gene expression analyses identified changes in eicosanoid metabolism, adaptive immune function and contractile gene expression. Together, these results suggest a novel role of adipocyte mTORC1 in mammary gland function and morphology, milk composition, and offspring growth.

scholarly journals PPARα Gene Expression in the Developing Rat Kidney: Role of Glucocorticoids

2001 ◽  
Vol 12 (6) ◽  
pp. 1197-1203
Author(s):  
FATIMA DJOUADI ◽  
JEAN BASTIN
Keyword(s):  
Gene Expression ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Culture Media ◽  
Rat Kidney ◽  
Fold Increase ◽  
Kidney Cortex ◽  
Peroxisome Proliferator ◽  
Rat Kidney Cortex

Abstract. The α isoform of peroxisome proliferator-activated receptor (PPARα), which is highly expressed in the kidney, can stimulate the expression of genes that are involved in fatty acid catabolism and therefore might be involved in the control of renal fatty acid β-oxidation. PPARα expression and its regulation in the immature kidney are not well documented. This study delineated the developmental pattern of PPARα expression in the rat kidney cortex and the medulla between postnatal days 10 and 30 and investigated the role of glucocorticoids in regulating PPARα expression. In the cortex, PPARα mRNA and protein increased 2- and 1.8-fold, respectively, from 10 to 21 d and then decreased 1.5- and 2.4-fold from 21 to 30 d. In the medulla, PPARα mRNA and protein increased continuously 3.3- and 2.4-fold, respectively. It is shown here that acute treatment by dexamethasone of 10-d-old rats precociously induced a 4- to 6-fold increase in PPARα mRNA and a 1.8-fold increase in protein within 6 h in each part of the kidney. Chronic injection of dexamethasone for 3 d also increased PPARα mRNA 3.8- and 2.2-fold in the cortex and the medulla, respectively, with a 1.5- and 2-fold increase in protein. Furthermore, adrenalectomy prevented the increases in PPARα mRNA and protein in both the cortex and the medulla between postnatal days 16 and 21, and these could be restored by dexamethasone treatment. Finally, with the use of an established renal cell line, it was shown that glucocorticoids stimulate gene expression of PPARα and of medium chain acyl-CoA dehydrogenase (MCAD, a PPARα target gene) 2- to 4-fold and 1.5-fold, respectively, and that addition of fatty acids in the culture media led to a 2.2-fold increase in MCAD mRNA. Altogether, these results demonstrated that glucocorticoids are potent regulators of PPARα development in the immature kidney and that these hormones act in concert with fatty acids to regulate MCAD gene expression in renal cells.

scholarly journals Nutrigenomics of Dietary Lipids

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 994
Author(s):  
Laura Bordoni ◽  
Irene Petracci ◽  
Fanrui Zhao ◽  
Weihong Min ◽  
Elisa Pierella ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fatty Acids ◽  
Lipid Metabolism ◽  
Current Knowledge ◽  
Scientific Evidence ◽  
Biological Properties ◽  
Dietary Lipids ◽  
Dietary Fats ◽  
Current Evidence

Dietary lipids have a major role in nutrition, not only for their fuel value, but also as essential and bioactive nutrients. This narrative review aims to describe the current evidence on nutrigenomic effects of dietary lipids. Firstly, the different chemical and biological properties of fatty acids contained both in plant- and animal-based food are illustrated. A description of lipid bioavailability, bioaccessibility, and lipotoxicity is provided, together with an overview of the modulatory role of lipids as pro- or anti-inflammatory agents. Current findings concerning the metabolic impact of lipids on gene expression, epigenome, and gut microbiome in animal and human studies are summarized. Finally, the effect of the individual’s genetic make-up on lipid metabolism is described. The main goal is to provide an overview about the interaction between dietary lipids and the genome, by identifying and discussing recent scientific evidence, recognizing strengths and weaknesses, to address future investigations and fill the gaps in the current knowledge on metabolic impact of dietary fats on health.

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