Inflammation, obesity, and fatty acid metabolism: influence ofn-3 polyunsaturated fatty acids on factors contributing to metabolic syndrome

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.

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.


Lipids ◽  
1979 ◽  
Vol 14 (4) ◽  
pp. 313-317 ◽  
Author(s):  
Victor J. Moreno ◽  
Julia E. A. De Moreno ◽  
Rodolfo R. Brenner

2019 ◽  
Vol 122 (1) ◽  
pp. 4-22 ◽  
Author(s):  
Nikos Koundouros ◽  
George Poulogiannis

AbstractA common feature of cancer cells is their ability to rewire their metabolism to sustain the production of ATP and macromolecules needed for cell growth, division and survival. In particular, the importance of altered fatty acid metabolism in cancer has received renewed interest as, aside their principal role as structural components of the membrane matrix, they are important secondary messengers, and can also serve as fuel sources for energy production. In this review, we will examine the mechanisms through which cancer cells rewire their fatty acid metabolism with a focus on four main areas of research. (1) The role of de novo synthesis and exogenous uptake in the cellular pool of fatty acids. (2) The mechanisms through which molecular heterogeneity and oncogenic signal transduction pathways, such as PI3K–AKT–mTOR signalling, regulate fatty acid metabolism. (3) The role of fatty acids as essential mediators of cancer progression and metastasis, through remodelling of the tumour microenvironment. (4) Therapeutic strategies and considerations for successfully targeting fatty acid metabolism in cancer. Further research focusing on the complex interplay between oncogenic signalling and dysregulated fatty acid metabolism holds great promise to uncover novel metabolic vulnerabilities and improve the efficacy of targeted therapies.


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.


2017 ◽  
Vol 85 ◽  
pp. 372-379 ◽  
Author(s):  
Abdullah Al Mamun ◽  
Michio Hashimoto ◽  
Masanori Katakura ◽  
Yoko Tanabe ◽  
Satoru Tsuchikura ◽  
...  

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