scholarly journals The impact of dietary fatty acids on human adipose tissue

2019 ◽  
Vol 79 (1) ◽  
pp. 42-46 ◽  
Author(s):  
Paul Petrus ◽  
Peter Arner

Nutrition is a major variable factor in human environments. The composition of nutrients has changed markedly in recent decades which may contribute to the increased prevalence of metabolic diseases, such as obesity and type 2 diabetes. Fat is an important component of the diet which comes in various forms with fatty acids (FA) of different carbon chain lengths and saturation degrees. In addition to being an energy supply, FA function as potent signalling molecules and influence transcriptional activity. Among other tissues, dietary FA target white adipose tissue function, which is central in maintaining metabolic health. This review focuses on the possible role of dietary FA composition and its effect on human white adipose tissue expandability and transcriptional response. Altogether, the existing literature suggests that unsaturated fat has more benign effects on adipose tissue distribution when compared to long-chain saturated fat. However, the mechanisms of action remain poorly characterised.

2009 ◽  
Vol 81 (3) ◽  
pp. 453-466 ◽  
Author(s):  
Cláudia M. Oller do Nascimento ◽  
Eliane B. Ribeiro ◽  
Lila M. Oyama

Approximately 40% of the total energy consumed by western populations is represented by lipids, most of them being ingested as triacylglycerols and phospholipids. The focus of this review is to analyze the effect of the type of dietary fat on white adipose tissue metabolism and secretory function, particularly on haptoglobin, TNF-α, plasminogen activator inhibitor-1 and adiponectin secretion. Previous studies have demonstrated that the duration of the exposure to the high-fat feeding, amount of fatty acid present in the diet and the type of fatty acid may or may not have a significant effect on adipose tissue metabolism. However, the long-term or short-term high fat diets, especially rich in saturated fatty acids, probably by activation of toll-like receptors, stimulated the expression of proinflammatory adipokines and inhibited adiponectin expression. Further studies are needed to investigate the cellular mechanisms by which dietary fatty acids affect white adipose tissue metabolism and secretory functions.


2013 ◽  
Vol 98 (2) ◽  
pp. 549S-555S ◽  
Author(s):  
Hans Hauner ◽  
Stefanie Brunner ◽  
Ulrike Amann-Gassner

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 861-861
Author(s):  
Jowy Seah Yi Hoong ◽  
Wee Siong Chew ◽  
Federico Torta ◽  
Chin Meng Khoo ◽  
Markus R Wenk ◽  
...  

Abstract Objectives Sphingolipid concentrations have been associated with risk of type 2 diabetes and cardiovascular diseases. Because sphingolipids can be synthesized de novo from saturated fatty acids (SFA), dietary fatty acids may affect plasma sphingolipid concentrations. We aimed to evaluate dietary fat and protein intakes in relation to circulating sphingolipid levels. Methods We used cross-sectional data from 2860 ethnic Chinese Singaporeans collected from 2004–2007. Nutrient intakes were estimated on the basis of a validated 159-item food frequency questionnaire. We quantified 79 molecularly distinct sphingolipids in a large-scale lipidomic evaluation from plasma samples. Results Higher saturated fat intake was associated with higher concentrations of 16:1; O2 sphingolipids including ceramides, monohexosylcermides, dihexosylceramides, sphingomyelins, and sphingosine 1-phosphates. Higher polyunsaturated fat intake was associated with lower plasma long-chain ceramides and long-chain monohexosylcermide concentrations. Protein intake was inversely associated with concentrations of most subclasses of sphingolipids, with the exception of sphingolipids containing a 16:1; O2 sphingoid base. Lower intake of saturated fat and higher intake of polyunsaturated fat and protein may decrease plasma concentrations of several sphingolipid classes. Conclusions These findings may represent a novel biological mechanism for the impact of nutrient intakes on cardio-metabolic health. Funding Sources This work was supported by the National Research Foundation Investigatorship grant (NRF-NRFI2015–05, to MRW), A*STAR (I1901E0040), and the National University Health System (NUHSRO/2014/085/AF-Partner/01, DRH). FT was supported by the NRF and A*STAR IAF-ICP I1901E0040.


2018 ◽  
Vol 120 (6) ◽  
pp. 619-627 ◽  
Author(s):  
Perla P. Argentato ◽  
Helena de Cássia César ◽  
Débora Estadella ◽  
Luciana P. Pisani

AbstractBrown adipose tissue (BAT) has recently been given more attention for the part it plays in obesity. BAT can generate great amounts of heat through thermogenesis by the activation of uncoupling protein 1 (UCP-1), which can be regulated by many environmental factors such as diet. Moreover, the build-up of BAT relates to maternal nutritional changes during pregnancy and lactation. However, at present, there is a limited number of studies looking at maternal nutrition and BAT development, and it seems that the research trend in this field has been considerably declining since the 1980s. There is much to discover yet about the role of different fatty acids on the development of BAT and the activation of UCP-1 during the fetal and the postnatal periods of life. A better understanding of the impact of nutritional intervention on the epigenetic regulation of BAT could lead to new preventive care for metabolic diseases such as obesity. It is important to know in which circumstances lipids could programme BAT during pregnancy and lactation. The modification of maternal dietary fatty acids, amount and composition, during pregnancy and lactation might be a promising strategy for the prevention of obesity in the offspring and future generations.


2009 ◽  
Vol 54 (2) ◽  
pp. 97-103 ◽  
Author(s):  
H. Hauner ◽  
C. Vollhardt ◽  
K.T.M. Schneider ◽  
A. Zimmermann ◽  
T. Schuster ◽  
...  

1998 ◽  
Vol 80 (6) ◽  
pp. 495-502 ◽  
Author(s):  
Barbara A. Fielding ◽  
Keith N. Frayn

Lipoprotein lipase (EC 3.1.1.34; LPL) is a key enzyme regulating the disposal of lipid fuels in the body. It is expressed in a number of peripheral tissues including adipose tissue, skeletal and cardiac muscle and mammary gland. Its role is to hydrolyse triacylglycerol (TG) circulating in the TG-rich lipoprotein particles in order to deliver fatty acids to the tissue. It appears to act preferentially on chylomicron-TG, and therefore may play a particularly important role in regulating the disposition of dietary fatty acids. LPL activity is regulated according to nutritional state in a tissue-specific manner according to the needs of the tissue for fatty acids. For instance, it is highly active in lactating mammary gland; in white adipose tissue it is activated in the fed state and suppressed during fasting, whereas the reverse is true in muscle. Such observations have led to the view of LPL as a metabolic gatekeeper, especially for dietary fatty acids. However, closer inspection of its action in white adipose tissue reveals that this picture is only partially true. Normal fat deposition in adipose tissue can occur in the complete absence of LPL, and conversely, if LPL activity is increased by pharmacological means, increased fat storage does not necessarily follow. LPL appears to act as one member of a series of metabolic steps which are regulated in a highly coordinated manner. In white adipose tissue, it is clear that there is a major locus of control of fatty acid disposition downstream from LPL. This involves regulation of the pathway of fatty acid uptake and esterification, and appears to be regulated by a number of factors including insulin, acylation-stimulating protein and possibly leptin.


2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Rebecca Dewhurst-Trigg ◽  
Rachel M. Woods ◽  
Carl J. Hulston ◽  
Oonagh Markey

AbstractWhite adipose tissue (WAT) inflammation is linked to the development of cardiometabolic disease. A high intake of saturated fatty acids (SFA) may promote a more pro-inflammatory WAT gene expression profile, compared to monounsaturated fatty acids(1,2). This is concerning as the UK adult population currently exceeds the SFA intake target of < 10% total energy (TE), at 11.9%TE(3). However, further research is needed to understand how SFA ingestion impacts the protein content and phosphorylation of key targets involved in WAT inflammatory signalling. Therefore, this study investigated the effect of short-term, high-fat overfeeding on WAT and systemic metabolic and inflammatory responses in healthy, non-obese individuals.Fifteen (9 men, 6 women) apparently healthy participants (mean (SE) age; 26.6 (1.2) y, BMI; 24.4 (0.6) kg/m2) consumed a high-fat (dietary target: 65.0%TE total fat; 32.5%TE SFA), high-calorie (+ 50% estimated energy requirements) diet for 7 days. Fasted venous blood and WAT samples were collected pre- and post-intervention.Body mass increased following the intervention (pre-intervention vs. post-intervention: 75.2 (2.9) kg vs. 76.4 (2.9) kg; P < 0.0001). The intervention also led to increases in glucose (4.4 (0.1) vs. 4.6 (0.1) mmol/L; P = 0.022) and lipopolysaccharide-binding protein (12.9 (1.3) vs. 17.7 (3.0) μg/mL; P = 0.038), and a decrease in triacylglycerol (0.91 (0.08) vs. 0.72 (0.05) mmol/L; P = 0.007). Insulin, IL-6 and soluble CD14 concentrations remained unchanged (all P > 0.05). At the WAT level, total protein (TLR4; NF-κB; IKβα; P38; MCP-1) and phosphorylation (p) of proteins (p-NF-κB; p-IKβα; p-P38) involved in inflammatory signalling were unchanged following the intervention (all P > 0.05).In conclusion, although short-term, high-fat overfeeding led to an increase in body mass as well as systemic metabolic alterations, the content and phosphorylation of proteins involved in WAT inflammatory signalling were unaltered in healthy, non-obese individuals. Further analysis will reveal the impact of high-fat overfeeding on peripheral blood monocyte populations, which are involved in mediating pro- and anti-inflammatory responses.This research was supported by a Society for Endocrinology Early Career Grant.


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