Lipid signaling in adipose tissue: Connecting inflammation &amp; metabolism

Masoodi, Mojgan; Kuda, Ondřej; Rossmeisl, Martin; Flachs, Pavel; Kopecký, Jan

doi:10.1016/j.bbalip.2014.09.023

Cited by 195 publications

(171 citation statements)

References 226 publications

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“…In contrast to acute inflammation, in chronic inflammation the initiation phase is not followed by a resolution, and failure of resolution may be responsible for low-grade inflammation in obesity (3)(4)(5). During the unresolved inflammation, proinflammatory cytokines released by the adipose tissue act in a paracrine and systemic manner, promoting the development of insulin resistance in metabolic tissues (6,7). However, the mechanisms by which inflammation causes metabolic alterations have not been fully elucidated.…”

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confidence: 99%

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ALOX5AP Overexpression in Adipose Tissue Leads to LXA4 Production and Protection Against Diet-Induced Obesity and Insulin Resistance

et al. 2016

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Eicosanoids, such as leukotriene B4 (LTB4) and lipoxin A4 (LXA4), may play a key role during obesity. While LTB4 is involved in adipose tissue inflammation and insulin resistance, LXA4 may exert anti-inflammatory effects and alleviate hepatic steatosis. Both lipid mediators derive from the same pathway, in which arachidonate 5-lipoxygenase (ALOX5) and its partner, arachidonate 5-lipoxygenase–activating protein (ALOX5AP), are involved. ALOX5 and ALOX5AP expression is increased in humans and rodents with obesity and insulin resistance. We found that transgenic mice overexpressing ALOX5AP in adipose tissue had higher LXA4 rather than higher LTB4 levels, were leaner, and showed increased energy expenditure, partly due to browning of white adipose tissue (WAT). Upregulation of hepatic LXR and Cyp7a1 led to higher bile acid synthesis, which may have contributed to increased thermogenesis. In addition, transgenic mice were protected against diet-induced obesity, insulin resistance, and inflammation. Finally, treatment of C57BL/6J mice with LXA4, which showed browning of WAT, strongly suggests that LXA4 is responsible for the transgenic mice phenotype. Thus, our data support that LXA4 may hold great potential for the future development of therapeutic strategies for obesity and related diseases.

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confidence: 99%

“…Lipid mediators, such as eicosanoids produced from arachidonic acid, play critical roles in inflammation and its resolution (5,6,8). Among them, leukotrienes are wellknown proinflammatory molecules (9).…”

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confidence: 99%

ALOX5AP Overexpression in Adipose Tissue Leads to LXA4 Production and Protection Against Diet-Induced Obesity and Insulin Resistance

et al. 2016

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“…Eosinophils contributes to M2 polarization [11][12][13], while neutrophils and mast cells in obese conditions are associated with inflammation possibly ATM recruitment [6]. Macrophage infiltration increase lipolysis in WAT and impairs the liver's carbohydrate and lipid metabolism in several ways [14].…”

Section: Introductionmentioning

confidence: 99%

“…For example, Omega-3 PUFA drives the cellular phenotype towards M2 ATMs [5,6]. Resolvin 1 (DHA derived lipid mediators) reduces ATM accumulation, and induces a shift towards M2 polarization in obese mice [6,7].…”

Section: Introductionmentioning

confidence: 99%

Macrophages Switch: The Fate of Adipose Tissue in Obesity

Wankhade¹

2016

MOJI

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The development of Insulin resistance in obesity is associated with infiltration of immune cells in white adipose tissue (WAT). Especially macrophage infiltration in WAT is known to produce several proinflmmatory cytokines which induces the state of inflammation and impairs the insulin signaling and related pathways. Several animal and human studies have been conducted to unravel the mystery of metabolic dysregulation in adipose tissue because of chronic inflammation. A new and promising explanation is the switching of macrophages within WAT between M1 and M2 phenotype. In this short review, we addressed the recent advances in macrophage switch concept to explain the dysregulation of adipose tissue.

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“…Some of the excess energy is stored as triglyceride in adipose tissue without deleterious effects, but the capacity to store energy is limited and regulated by poorly understood mechanisms. The subsequent excessive accumulation of lipids and other metabolites in tissues that are not designed to manage this condition (e.g., liver, muscle, and pancreas) commonly ensues in an unhealthy course of metabolic events [2,3]. Detection and treatment of subclinical metabolic derangements are challenging.…”

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confidence: 99%

Exploring the Process of Energy Generation in Pathophysiology by Targeted Metabolomics: Performance of a Simple and Quantitative Method

Riera-Borrull

Rodríguez-Gallego

Hernández-Aguilera

et al. 2015

J. Am. Soc. Mass Spectrom.

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Abstract. Abnormalities in mitochondrial metabolism and regulation of energy balance contribute to human diseases. The consequences of high fat and other nutrient intake, and the resulting acquired mitochondrial dysfunction, are essential to fully understand common disorders, including obesity, cancer, and atherosclerosis. To simultaneously and noninvasively measure and quantify indirect markers of mitochondrial function, we have developed a method based on gas chromatography coupled to quadrupole-time of flight mass spectrometry and an electron ionization interface, and validated the system using plasma from patients with peripheral artery disease, human cancer cells, and mouse tissues. This approach was used to increase sensibility in the measurement of a wide dynamic range and chemical diversity of multiple intermediate metabolites used in energy metabolism. We demonstrate that our targeted metabolomics method allows for quick and accurate identification and quantification of molecules, including the measurement of small yet significant biological changes in experimental samples. The apparently low process variability required for its performance in plasma, cell lysates, and tissues allowed a rapid identification of correlations between interconnected pathways. Our results suggest that delineating the process of energy generation by targeted metabolomics can be a valid surrogate for predicting mitochondrial dysfunction in biological samples. Importantly, when used in plasma, targeted metabolomics should be viewed as a robust and noninvasive source of biomarkers in specific pathophysiological scenarios.

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Lipid signaling in adipose tissue: Connecting inflammation & metabolism

Cited by 195 publications

References 226 publications

ALOX5AP Overexpression in Adipose Tissue Leads to LXA4 Production and Protection Against Diet-Induced Obesity and Insulin Resistance

ALOX5AP Overexpression in Adipose Tissue Leads to LXA4 Production and Protection Against Diet-Induced Obesity and Insulin Resistance

Macrophages Switch: The Fate of Adipose Tissue in Obesity

Exploring the Process of Energy Generation in Pathophysiology by Targeted Metabolomics: Performance of a Simple and Quantitative Method

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