Fatty acid metabolism in young oysters,Crassostrea gigas: Polyunsaturated fatty acids

Lipids ◽  
1984 ◽  
Vol 19 (5) ◽  
pp. 332-336 ◽  
Author(s):  
M. J. Waldock ◽  
D. L. Holland
Lipids ◽  
1979 ◽  
Vol 14 (4) ◽  
pp. 313-317 ◽  
Author(s):  
Victor J. Moreno ◽  
Julia E. A. De Moreno ◽  
Rodolfo R. Brenner

2007 ◽  
Vol 32 (6) ◽  
pp. 1008-1024 ◽  
Author(s):  
Lindsay E. Robinson ◽  
Andrea C. Buchholz ◽  
Vera C. Mazurak

Metabolic syndrome (MetS) comprises an array of metabolic risk factors including abdominal obesity, dyslipidemia, hypertension, and glucose intolerance. Individuals with MetS are at elevated risk for diabetes and cardiovascular disease. Central to the etiology of MetS is an interrelated triad comprising inflammation, abdominal obesity, and aberrations in fatty acid metabolism, coupled with the more recently recognized changes in metabolism during the postprandial period. We review herein preliminary evidence regarding the role of dietary n-3 polyunsaturated fatty acids in modulating each of the components of the triad of adiposity, inflammation, and fatty acid metabolism, with particular attention to the role of the postprandial period as a contributor to the pathophysiology of MetS.


2020 ◽  
Author(s):  
Qiting Qing ◽  
Lili Huang ◽  
Mei Zhao

Abstract Maternal lipopolysaccharide(LPS)exposure during pregnancy induced metabolic abnormalities in male offspring, but the underlying mechanisms are still unclear. The aims of this study were to elucidate the underlying etiologies by characterizing the metabolic alterations in maternal serum and male fetal liver. Pregnant mice were intraperitoneally injected with LPS (50ug/kg/d) from gestational period (GD 15 to GD 17). In the GD18, maternal serum and male fetal liver were collected. The metabolic profiles were analyzed using liquid Chromatograph Mass Spectrometer (LC-MS) techniques. After LPS exposure, glycerophospholipids containing saturated fatty acids were up-regulated, and glycerophospholipids containing polyunsaturated fatty acids were down-regulated in both pregnant mice and male offspring. In addition, we observed that LPS-exposed dams also had increased saturated fatty acids levels and decreased polyunsaturated fatty acids levels. Because these abnormal glycerophospholipids and fatty acid metabolism have been identified as possibly associated with the risk of type 2 diabetes, our study has therefore identified two pathways (glycerophospholipids and fatty acid metabolism) that potentially underlie LPS induced fetal metabolic disease.


2007 ◽  
Vol 98 (S1) ◽  
pp. S46-S53 ◽  
Author(s):  
Laurence S. Harbige ◽  
Mohammad K. Sharief

Epidemiological, biochemical, animal model and clinical trial data described in this overview strongly suggest that polyunsaturated fatty acids, particularly n-6 fatty acids, have a role in the pathogenesis and treatment of multiple sclerosis (MS). Data presented provides further evidence for a disturbance in n-6 fatty acid metabolism in MS. Disturbance of n-6 fatty acid metabolism and dysregulation of cytokines are shown to be linked and a “proof of concept clinical trial” further supports such a hypothesis. In a randomised double-blind, placebo controlled trial of a high dose and low dose selected GLA (18 : 3n-6)-rich oil and placebo control, the high dose had a marked clinical effect in relapsing-remitting MS, significantly decreasing the relapse rate and the progression of disease. Laboratory findings paralleled clinical changes in the placebo group in that production of mononuclear cell pro-inflammatory cytokines (TNF-α, IL-1β) was increased and anti-inflammatory TGF-β markedly decreased with loss of membrane n-6 fatty acids linoleic (18 : 2n-6) and arachidonic acids (20 : 4n-6). In contrast there were no such changes in the high dose group. The improvement in disability (Expanded Disability Status Scale) in the high dose suggests there maybe a beneficial effect on neuronal lipids and neural function in MS. Thus disturbed n-6 fatty acid metabolism in MS gives rise to loss of membrane long chain n-6 fatty acids and loss of the anti-inflammatory regulatory cytokine TGF-β, particularly during the relapse phase, as well as loss of these important neural fatty acids for CNS structure and function and consequent long term neurological deficit in MS.


2009 ◽  
Vol 34 (3) ◽  
pp. 315-322 ◽  
Author(s):  
Gregory R. Steinberg

During moderate-intensity exercise, fatty acids are the predominant substrate for working skeletal muscle. The release of fatty acids from adipose tissue stores, combined with the ability of skeletal muscle to actively fine tune the gradient between fatty acid and carbohydrate metabolism, depending on substrate availability and energetic demands, requires a coordinated system of metabolic control. Over the past decade, since the discovery that AMP-activated protein kinase (AMPK) was increased in accordance with exercise intensity, there has been significant interest in the proposed role of this ancient stress-sensing kinase as a critical integrative switch controlling metabolic responses during exercise. In this review, studies examining the role of AMPK as a regulator of fatty acid metabolism in both adipose tissue and skeletal muscle during exercise will be discussed. Exercise induces activation of AMPK in adipocytes and regulates triglyceride hydrolysis and esterfication through phosphorylation of hormone sensitive lipase (HSL) and glycerol-3-phosphate acyl-transferase, respectively. In skeletal muscle, exercise-induced activation of AMPK is associated with increases in fatty acid uptake, phosphorylation of HSL, and increased fatty acid oxidation, which is thought to occur via the acetyl-CoA carboxylase-malony-CoA-CPT-1 signalling axis. Despite the importance of AMPK in regulating fatty acid metabolism under resting conditions, recent evidence from transgenic models of AMPK deficiency suggest that alternative signalling pathways may also be important for the control of fatty acid metabolism during exercise.


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