Adipose Tissue Fatty Acid Metabolism during Pregnancy in Swine

1985 ◽  
Vol 61 (2) ◽  
pp. 410-415 ◽  
Author(s):  
J. P. McNamara ◽  
M. H. Dehoff ◽  
R. J. Collier ◽  
F. W. Bazer
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Adipose Tissue Fatty Acid ◽  
Tissue Fatty Acid

100th Anniversary of the discovery of insulin Perspective: Insulin and Adipose Tissue Fatty Acid Metabolism

2021 ◽  
Author(s):  
André C. Carpentier
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Dietary Fatty Acids ◽  
Nonesterified Fatty Acid ◽  
Adipose Tissue Fatty Acid ◽  
Tissue Fatty Acid

Insulin inhibits systemic nonesterified fatty acid (NEFA) flux to a greater degree than glucose or any other metabolite. This remarkable effect is mainly due to insulin-mediated inhibition of intracellular triglyceride (TG) lipolysis in adipose tissues and is essential to prevent diabetic ketoacidosis, but also to limit the potential lipotoxic effects of NEFA in lean tissues that contributes to the development of diabetes complications. Insulin also regulates adipose tissue fatty acid esterification, glycerol and TG synthesis, lipogenesis and possibly oxidation, contributing to the trapping of dietary fatty acids in the postprandial state. Excess NEFA flux at a given insulin level has been used to define in vivo adipose tissue insulin resistance. Adipose tissue insulin resistance defined in this fashion has been associated with several dysmetabolic features and complications of diabetes, but the mechanistic significance of this concept is not fully understood. This review focusses on the in vivo regulation of adipose tissue fatty acid metabolism by insulin and the mechanistic significance of the current definition of adipose tissue insulin resistance. One hundred years after the discovery of insulin and despite decades of investigations, much is still to be understood about the multifaceted in vivo actions of this hormone on adipose tissue fatty acid metabolism.

scholarly journals Adipose tissue fatty acid metabolism in insulin-resistant men

Diabetologia ◽  
2008 ◽  
Vol 51 (10) ◽  
pp. 1936-1936 ◽  
Author(s):  
A. S. T. Bickerton ◽  
R. Roberts ◽  
B. A. Fielding ◽  
H. Tornqvist ◽  
E. E. Blaak ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Insulin Resistant ◽  
Adipose Tissue Fatty Acid ◽  
Tissue Fatty Acid

scholarly journals Adipose tissue fatty acid metabolism in insulin-resistant men

Diabetologia ◽  
2008 ◽  
Vol 51 (8) ◽  
pp. 1466-1474 ◽  
Author(s):  
A. S. T. Bickerton ◽  
R. Roberts ◽  
B. A. Fielding ◽  
H. Tornqvist ◽  
E. E. Blaak ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Insulin Resistant ◽  
Adipose Tissue Fatty Acid ◽  
Tissue Fatty Acid

Gestational age dependent changes of the fetal brain, liver and adipose tissue fatty acid compositions in a population with high fish intakes

2012 ◽  
Vol 86 (4-5) ◽  
pp. 189-199 ◽  
Author(s):  
Remko S. Kuipers ◽  
Martine F. Luxwolda ◽  
Pieter J. Offringa ◽  
E. Rudy Boersma ◽  
D.A. Janneke Dijck-Brouwer ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Gestational Age ◽  
Fetal Brain ◽  
Adipose Tissue Fatty Acid ◽  
Tissue Fatty Acid ◽  
Age Dependent ◽  
High Fish ◽  
Fatty Acid Compositions

Role of the AMP-activated protein kinase in regulating fatty acid metabolism during exerciseThis paper is one of a selection of papers published in this Special Issue, entitled 14th International Biochemistry of Exercise Conference – Muscles as Molecular and Metabolic Machines, and has undergone the Journal’s usual peer review process.

2009 ◽  
Vol 34 (3) ◽  
pp. 315-322 ◽  
Author(s):  
Gregory R. Steinberg
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Protein Kinase ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Moderate Intensity ◽  
Amp Activated Protein Kinase

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.

Adipose tissue fatty acid composition and cognitive impairment

Nutrition ◽  
2018 ◽  
Vol 54 ◽  
pp. 153-157 ◽  
Author(s):  
Frej Stilling ◽  
Alicja Wolk ◽  
Dorota Religa ◽  
Jerzy Leppert ◽  
Leif Bergkvist ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid Composition ◽  
Cognitive Impairment ◽  
Fatty Acid ◽  
Acid Composition ◽  
Tissue Fatty Acid Composition ◽  
Adipose Tissue Fatty Acid ◽  
Tissue Fatty Acid

scholarly journals Role of Arginase 2 in Systemic Metabolic Activity and Adipose Tissue Fatty Acid Metabolism in Diet-Induced Obese Mice

2019 ◽  
Vol 20 (6) ◽  
pp. 1462 ◽  
Author(s):  
Reem Atawia ◽  
Haroldo Toque ◽  
Mohamed Meghil ◽  
Tyler Benson ◽  
Nicole Yiew ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Normal Diet ◽  
Metabolic Dysfunction ◽  
Ppar Γ ◽  
Obesity And Diabetes ◽  
Visceral Adipose ◽  
Upregulated Genes

Visceral adipose tissue (VAT) inflammation and metabolic dysregulation are key components of obesity-induced metabolic disease. Upregulated arginase, a ureahydrolase enzyme with two isoforms (A1-cytosolic and A2-mitochondrial), is implicated in pathologies associated with obesity and diabetes. This study examined A2 involvement in obesity-associated metabolic and vascular disorders. WT and globally deleted A2(−/−) or A1(+/−) mice were fed either a high fat/high sucrose (HFHS) diet or normal diet (ND) for 16 weeks. Increases in body and VAT weight of HFHS-fed WT mice were abrogated in A2−/−, but not A1+/−, mice. Additionally, A2−/− HFHS-fed mice exhibited higher energy expenditure, lower blood glucose, and insulin levels compared to WT HFHS mice. VAT and adipocytes from WT HFHS fed mice showed greater A2 expression and adipocyte size and reduced expression of PGC-1α, PPAR-γ, and adiponectin. A2 deletion blunted these effects, increased levels of active AMPK-α, and upregulated genes involved in fatty acid metabolism. A2 deletion prevented HFHS-induced VAT collagen deposition and inflammation, which are involved in adipocyte metabolic dysfunction. Endothelium-dependent vasorelaxation, impaired by HFHS diet, was significantly preserved in A2−/− mice, but more prominently maintained in A1+/− mice. In summary, A2 is critically involved in HFHS-induced VAT inflammation and metabolic dysfunction.

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