scholarly journals Peroxisome proliferator–activated receptor α genetic variation interacts with n−6 and long-chain n−3 fatty acid intake to affect total cholesterol and LDL-cholesterol concentrations in the Atherosclerosis Risk in Communities Study

2008 ◽  
Vol 87 (6) ◽  
pp. 1926-1931 ◽  
Author(s):  
Kelly A Volcik ◽  
Jennifer A Nettleton ◽  
Christie M Ballantyne ◽  
Eric Boerwinkle
Keyword(s):  
Genetic Variation ◽  
Fatty Acid ◽  
Total Cholesterol ◽  
Ldl Cholesterol ◽  
Peroxisome Proliferator ◽  
Fatty Acid Intake ◽  
Peroxisome Proliferator Activated Receptor ◽  
Atherosclerosis Risk In Communities ◽  
Atherosclerosis Risk ◽  
Long Chain

scholarly journals Effects of Paramylon Extracted from Euglena gracilis EOD-1 on Parameters Related to Metabolic Syndrome in Diet-Induced Obese Mice

Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1674 ◽  
Author(s):  
Seiichiro Aoe ◽  
Chiemi Yamanaka ◽  
Kotone Koketsu ◽  
Machiko Nishioka ◽  
Nobuteru Onaka ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Mrna Expression ◽  
Euglena Gracilis ◽  
Ldl Cholesterol ◽  
Growth Parameters ◽  
Postprandial Glucose ◽  
Abdominal Fat ◽  
Fatty Acid Transport ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor

Paramylon (PM), a type of β-glucan, functions like dietary fiber, which has been suggested to exert a protective effect against obesity. We evaluated the potential beneficial effects of PM powder on obesity in mice. Male C57BL/6J mice were fed a high-fat diet supplemented with either 2.5 or 5% PM powder, extracted from Euglena gracilis, for 74 days. Growth parameters, abdominal fat content, serum biochemical markers, hepatic lipid accumulation and hepatic mRNA expression were measured. Dietary supplementation with PM resulted in decreased food efficiency ratios and abdominal fat accumulation. Dose-dependent decreases were observed in postprandial glucose levels, serum low-density lipoprotein (LDL)-cholesterol, and serum secretary immunoglobulin A (sIgA) concentrations. PM supplementation increased peroxisome proliferator-activated receptor α (PPARα) mRNA expression in the liver which is suggested to induce β-oxidation through activation of acyl-coenzyme A oxidase (ACOX), carnitine palmitoyltransferase (CPT) and fatty acid transport protein 2 (FATP2) mRNA expression. Changes in fatty acid metabolism may improve lipid and glucose metabolism. In conclusion, a preventive effect against obesity was observed in mice given a PM-enriched diet. The mechanism is suggested to involve a reduction in both serum LDL-cholesterol levels and the accumulation of abdominal fat, in addition to an improvement in postprandial glucose concentration.

scholarly journals n–3 Fatty acids, hypertension and risk of cognitive decline among older adults in the Atherosclerosis Risk in Communities (ARIC) study

2008 ◽  
Vol 11 (1) ◽  
pp. 17-29 ◽  
Author(s):  
May A Beydoun ◽  
Jay S Kaufman ◽  
Philip D Sloane ◽  
Gerardo Heiss ◽  
Joseph Ibrahim
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Cognitive Decline ◽  
Screening Tools ◽  
Word Recall ◽  
Plasma Fatty Acid ◽  
Men And Women ◽  
Atherosclerosis Risk In Communities ◽  
Atherosclerosis Risk ◽  
Long Chain

AbstractObjectiveRecent research indicates that n–3 fatty acids can inhibit cognitive decline, perhaps differentially by hypertensive status.DesignWe tested these hypotheses in a prospective cohort study (the Atherosclerosis Risk in Communities). Dietary assessment using a food-frequency questionnaire and plasma fatty acid exposure by gas chromatography were completed in 1987–1989 (visit 1), while cognitive assessment with three screening tools – the Delayed Word Recall Test, the Digit Symbol Substitution Test of the Wechsler Adult Intelligence Scale–Revised and the Word Fluency Test (WFT) – was completed in 1990–1992 (visit 2) and 1996–1998 (visit 4). Regression calibration and simulation extrapolation were used to control for measurement error in dietary exposures.SettingFour US communities – Forsyth County (North Carolina), Jackson (Mississippi), suburbs of Minneapolis (Minnesota) and Washington County (Maryland).SubjectsMen and women aged 50–65 years at visit 1 with complete dietary data (n = 7814); white men and women in same age group in the Minnesota field centre with complete plasma fatty acid data (n = 2251).ResultsFindings indicated that an increase of one standard deviation in dietary long-chain n–3 fatty acids (% of energy intake) and balancing long-chain n−3/n–6 decreased the risk of 6-year cognitive decline in verbal fluency with an odds ratio (95% confidence interval) of 0.79 (0.66–0.95) and 0.81 (0.68–0.96), respectively, among hypertensives. An interaction with hypertensive status was found for dietary long-chain n–3 fatty acids (g day−1) and WFT decline (likelihood ratio test, P = 0.06). This exposure in plasma cholesteryl esters was also protective against WFT decline, particularly among hypertensives (OR = 0.51, P < 0.05).ConclusionOne implication from our study is that diets rich in fatty acids of marine origin should be considered for middle-aged hypertensive subjects. To this end, randomised clinical trials are needed.

scholarly journals Postprandial inhibition of gastric ghrelin secretion by long-chain fatty acid through GPR120 in isolated gastric ghrelin cells and mice

2012 ◽  
Vol 303 (3) ◽  
pp. G367-G376 ◽  
Author(s):  
Xinping Lu ◽  
Xilin Zhao ◽  
Jianying Feng ◽  
Alice P. Liou ◽  
Shari Anthony ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Gastric Mucosa ◽  
Lipoprotein Lipase ◽  
Chain Fatty Acid ◽  
Peroxisome Proliferator ◽  
Rt Pcr ◽  
Long Chain Fatty Acid ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ghrelin Secretion ◽  
Long Chain

Ghrelin is a gastric peptide hormone that controls appetite and energy homeostasis. Plasma ghrelin levels rise before a meal and fall quickly thereafter. Elucidation of the regulation of ghrelin secretion has been hampered by the difficulty of directly interrogating ghrelin cells diffusely scattered within the complex gastric mucosa. Therefore, we generated transgenic mice with ghrelin cell expression of green fluorescent protein (GFP) to enable characterization of ghrelin secretion in a pure population of isolated gastric ghrelin-expressing GFP (Ghr-GFP) cells. Using quantitative RT-PCR and immunofluorescence staining, we detected a high level of expression of the long-chain fatty acid (LCFA) receptor GPR120, while the other LCFA receptor, GPR40, was undetectable. In short-term-cultured pure Ghr-GFP cells, the LCFAs docosadienoic acid, linolenic acid, and palmitoleic acid significantly suppressed ghrelin secretion. The physiological mechanism of LCFA inhibition on ghrelin secretion was studied in mice. Serum ghrelin levels were transiently suppressed after gastric gavage of LCFA-rich lipid in mice with pylorus ligation, indicating that the ghrelin cell may directly sense increased gastric LCFA derived from ingested intraluminal lipids. Meal-induced increase in gastric mucosal LCFA was assessed by measuring the transcripts of markers for tissue uptake of LCFA, lipoprotein lipase (LPL), fatty acid translocase (CD36), glycosylphosphatidylinositol-anchored HDL-binding protein 1, and nuclear fatty acid receptor peroxisome proliferator-activated receptor-γ. Quantitative RT-PCR studies indicate significantly increased mRNA levels of lipoprotein lipase, glycosylphosphatidylinositol-anchored HDL-binding protein 1, and peroxisome proliferator-activated receptor-γ in postprandial gastric mucosa. These results suggest that meal-related increases in gastric mucosal LCFA interact with GPR120 on ghrelin cells to inhibit ghrelin secretion.

scholarly journals Impact of L-FABP and glucose on polyunsaturated fatty acid induction of PPARα-regulated β-oxidative enzymes

2013 ◽  
Vol 304 (3) ◽  
pp. G241-G256 ◽  
Author(s):  
Anca D. Petrescu ◽  
Huan Huang ◽  
Gregory G. Martin ◽  
Avery L. McIntosh ◽  
Stephen M. Storey ◽  
...  
Keyword(s):  
Fatty Acid ◽  
High Glucose ◽  
Target Genes ◽  
De Novo ◽  
Oxidative Enzymes ◽  
Enhancement Effect ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Fatty Acid Binding ◽  
Long Chain

Liver fatty acid binding protein (L-FABP) is the major soluble protein that binds very-long-chain n-3 polyunsaturated fatty acids (n-3 PUFAs) in hepatocytes. However, nothing is known about L-FABP's role in n-3 PUFA-mediated peroxisome proliferator activated receptor-α (PPARα) transcription of proteins involved in long-chain fatty acid (LCFA) β-oxidation. This issue was addressed in cultured primary hepatocytes from wild-type, L-FABP-null, and PPARα-null mice with these major findings: 1) PUFA-mediated increase in the expression of PPARα-regulated LCFA β-oxidative enzymes, LCFA/LCFA-CoA binding proteins (L-FABP, ACBP), and PPARα itself was L-FABP dependent; 2) PPARα transcription, robustly potentiated by high glucose but not maltose, a sugar not taken up, correlated with higher protein levels of these LCFA β-oxidative enzymes and with increased LCFA β-oxidation; and 3) high glucose altered the potency of n-3 relative to n-6 PUFA. This was not due to a direct effect of glucose on PPARα transcriptional activity nor indirectly through de novo fatty acid synthesis from glucose. Synergism was also not due to glucose impacting other signaling pathways, since it was observed only in hepatocytes expressing both L-FABP and PPARα. Ablation of L-FABP or PPARα as well as treatment with MK886 (PPARα inhibitor) abolished/reduced PUFA-mediated PPARα transcription of these genes, especially at high glucose. Finally, the PUFA-enhanced L-FABP distribution into nuclei with high glucose augmentation of the L-FABP/PPARα interaction reveals not only the importance of L-FABP for PUFA induction of PPARα target genes in fatty acid β-oxidation but also the significance of a high glucose enhancement effect in diabetes.

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