Eicosapentaenoic acid upregulates VEGF-A through both GPR120 and PPARγ mediated pathways in 3T3-L1 adipocytes

Hasan, Azeem; Ohmori, Koji; Konishi, Kuniyoshi; Igarashi, Jun–ichi; Hashimoto, Takeshi; Kamitori, Kazuyo; Yamaguchi, Fuminori; Tsukamoto, Ikuko; Uyama, Toru; Ishihara, Yasuhiro; Noma, Takahisa; Tokuda, Masaaki; Kohno, Masakazu

doi:10.1016/j.mce.2015.02.012

Cited by 62 publications

(45 citation statements)

References 55 publications

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“…DHA and EPA are known to activate the genes for GPR120, and their anti-inflammatory effects are to some extent dependent on this pathway. Previous studies have shown that the antiinflammatory effects of DHA, was absent in GPR120 knockdown cells, [27] further substantiating this assertion. This implies that the inhibitory effects of DHA on NF-κB, most likely occurred via the GPR120 pathway.…”

Section: Inflammatory Proteins and The Role Of Membrane Lipidssupporting

confidence: 72%

“…They inhibit monocyte NF-κB and consequently modulate transcription of TNF-α, [22] (which plays a central role in inflammation) this influences the other factors to indirectly control fatty and triacyl glycerol metabolism. The PPARs are transcription factors which regulate gene expression by binding to retinoic-X-receptors, which are bound by the ligand; 6 cisretinoic acid [27]. The genes coding for several enzymes involved in β-oxidation are regulated by the PPAR-α isoform, predominantly found in the liver.…”

Section: Inflammatory Proteins and The Role Of Membrane Lipidsmentioning

confidence: 99%

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The Role of Lipids in Inflammation: Review of the Evolving Pathogenesis of Sickle Cell Disease

Madu

Abuknesha²,

Ghebremeskel³

2015

Biol Med (Aligarh)

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The pathologic features of sickle cell disease had been known in the past to be as a result of red cell abnormality leading to vascular occlusion, haemolysis and consequent anaemia. Recent knowledge has revealed numerous pathogenetic pathways involving leukocytes, platelets and the vascular endothelium. Complex interactions between the inflammatory cytokines and the membrane lipids in sickle cell present several pathogenetic processes affecting disease severity. The mechanisms of membrane fluidity, aggregation, adhesion and inflammation are strongly associated with membrane lipid constitution. The omega -3 fatty acids via incorporation into the lipid membrane have been found to play a central role in suppressing inflammation in several disease processes. Variations in disease severity have been shown to correspond with levels of fatty acid desaturases involved in the synthesis of these fatty acids. The genes coding for these substances can also be manipulated to achieve a favorable outcome and may provide several possible therapeutic and prophylactic access points This review aims at exploring these delicate interactions and proffering possible targets to ameliorate disease features. The information and referenced publications quoted in this review were obtained from the PubMed Central database, using the search keywords; inflammation, sickle cell, fatty acids and cytokines.

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Section: Inflammatory Proteins and The Role Of Membrane Lipidssupporting

confidence: 72%

Section: Inflammatory Proteins and The Role Of Membrane Lipidsmentioning

confidence: 99%

The Role of Lipids in Inflammation: Review of the Evolving Pathogenesis of Sickle Cell Disease

Madu

Abuknesha²,

Ghebremeskel³

2015

Biol Med (Aligarh)

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“…In summary, STRs, whose expression and function can be modulated by ambient glucose (27), regulate endocrine secretion in the gut and the pancreas as well as energy storage in the adipocyte (16,18,27,28,34,45,46,50). Taken together, these data suggest that STRs play a role in regulating energy homeostasis.…”

Section: E695 Disruption Of T1r2 Attenuates Metabolic Derangementsmentioning

confidence: 80%

“…Similar to sugars, fatty acids of various chain lengths activate GPRs on enteroendocrine cells, islets, and adipocytes to modulate gut-derived hormones (GLP-1, PYY, CCK, GIP), insulin, glucagon, and leptin secretion, respectively (50). Interestingly, T1R2/T1R3 and fatty acid receptors on adipocytes can also mediate endocrine-independent functions such as lipolysis, glucose uptake, and adipogenesis (16,18,34,45,46). The diverse tissue distribution of nutrient-sensing GPRs suggests multiple roles in delivery, processing, and storage of energy in the integration of whole body nutrient metabolism.…”

mentioning

confidence: 99%

Disruption of the sugar-sensing receptor T1R2 attenuates metabolic derangements associated with diet-induced obesity

Smith

Hussain

Azari

et al. 2016

American Journal of Physiology-Endocrinology and Metabolism

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Pratley RE, Kyriazis GA. Disruption of the sugar-sensing receptor T1R2 attenuates metabolic derangements associated with diet-induced obesity. Am J Physiol Endocrinol Metab 310: E688 -E698, 2016. First published February 16, 2016 doi:10.1152/ajpendo.00484.2015.-Sweet taste receptors (STRs) on the tongue mediate gustatory sweet sensing, but their expression in the gut, pancreas, and adipose tissue suggests a physiological contribution to whole body nutrient sensing and metabolism. However, little is known about the function and contribution of these sugar sensors during metabolic stress induced by overnutrition and subsequent obesity. Here, we investigated the effects of high-fat/low-carbohydrate (HF/LC) diet on glucose homeostasis and energy balance in mice with global disruption of the sweet taste receptor protein T1R2. We assessed body composition, energy balance, glucose homeostasis, and tissue-specific nutrient metabolism in T1R2 knockout (T1R2-KO) mice fed a HF/LC diet for 12 wk. HF/LC diet-fed T1R2-KO mice gained a similar amount of body mass as did WT mice, but had reduced fat mass and increased lean mass relative to WT mice. T1R2-KO mice were also hyperphagic and hyperactive. Ablation of the T1R2 sugar sensor protected mice from HF/LC diet-induced hyperinsulinemia and altered substrate utilization, including increased rates of glucose oxidation and decreased liver triglyceride (TG) accumulation, despite normal intestinal fat absorption. Finally, STRs (T1r2/T1r3) were upregulated in the adipose tissue of WT mice in response to HF/LC diet, and their expression positively correlated with fat mass and glucose intolerance. The chemosensory receptor T1R2, plays an important role in glucose homeostasis during diet-induced obesity through the regulation of yet to be identified molecular mechanisms that alter energy disposal and utilization in peripheral tissues. sweet taste receptors; obesity; hyperinsulinemia; body composition; diabetes OBESITY AND ITS COMORBIDITIES have become a global epidemic (37). In the United States alone, about two thirds of all adults are overweight and one third are classified as obese (12). Obesity is associated with an increased risk for the development of insulin resistance and type 2 diabetes (T2D) (21,38). Although the etiology of obesity is a complex interplay of environmental and genetic components, it is largely linked to excessive caloric intake and decreased physical activity (13). Disturbances in energy balance induce the activation of cellular biochemical sensors that attempt to restore homeostasis by the activation of metabolic, hormonal, and neuronal pathways. For instance, glucose influx and metabolism causes the accumulation of malonyl coenzyme A (CoA), which inhibits lipid oxidation in favor of triglyceride synthesis and glucose oxidation (35,44). Nevertheless, the range and nature of nutrientsensing pathways that regulate adaptive responses to nutrient surplus and their role in the development of obesity are not completely understood.A series of G protein-coupled rec...

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“…The role of 3-PUFAs in angiogenesis is poorly documented; however, one recent report indicates that 3-PUFA dietary supplementation prevents microvascular rarefaction in a hind-limb ischemia model ( 41 ). Further, another report indicates that EPA induces VEGF-A expression through activation of FFAR4 in adipocytes ( 42 ). Therefore, prevention of microvascular rarefaction might, through EPAmediated angiogenesis, represent another mechanism to improve outcomes in HFpEF .…”

Section: Ffar4 Was Required To Prevent Tgf ␤ 1-induced Fi Brosis In Pmentioning

confidence: 99%

EPA, not DHA, prevents fibrosis in pressure overload-induced heart failure: potential role of free fatty acid receptor 4

Eclov

Qian

Redetzke

et al. 2015

Journal of Lipid Research

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Eicosapentaenoic acid upregulates VEGF-A through both GPR120 and PPARγ mediated pathways in 3T3-L1 adipocytes

Cited by 62 publications

References 55 publications

The Role of Lipids in Inflammation: Review of the Evolving Pathogenesis of Sickle Cell Disease

The Role of Lipids in Inflammation: Review of the Evolving Pathogenesis of Sickle Cell Disease

Disruption of the sugar-sensing receptor T1R2 attenuates metabolic derangements associated with diet-induced obesity

EPA, not DHA, prevents fibrosis in pressure overload-induced heart failure: potential role of free fatty acid receptor 4

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