Resolution of Adipose Tissue Inflammation. (2010)
- Record Type:
- Journal Article
- Title:
- Resolution of Adipose Tissue Inflammation. (2010)
- Main Title:
- Resolution of Adipose Tissue Inflammation
- Authors:
- González-Périz, Ana
Clària, Joan - Other Names:
- Serhan Charles N. Academic Editor.
- Abstract:
- Abstract : The presence of the so-called "low-grade" inflammatory state is recognized as a critical event in adipose tissue dysfunction in obesity. This chronic "low-grade" inflammation in white adipose tissue is powerfully augmented through the infiltration of macrophages, which, together with adipocytes, perpetuate a vicious cycle of macrophage recruitment and secretion of free fatty acids and deleterious adipokines that predispose the development of obesity-related comorbidities, such as insulin resistance and nonalcoholic fatty liver disease. In the last decade, many factors have been identified that contribute to mounting uncontrolled inflammation in obese adipose tissue. Among them, bioactive lipid mediators derived from the cyclooxygenase and 5-lipoxygenase pathways, which convert the ω-6-polyunsaturated fatty acid (PUFA) arachidonic acid into potent proinflammatory eicosanoids (i.e., prostaglandins [PGs] and leukotrienes), have emerged. Interestingly, the same lipid mediators that initially trigger the inflammatory response also signal the termination of inflammation by stimulating the biosynthesis of anti-inflammatory and proresolving lipid autacoids. This review discusses the current status, characteristics, and progress in this class of "stop signals", including the lipoxins, which were the first identified ω-6 PUFA–derived lipid mediators with potent anti-inflammatory properties; the recently described ω-3 PUFA–derived lipid mediators resolvins and protectins;Abstract : The presence of the so-called "low-grade" inflammatory state is recognized as a critical event in adipose tissue dysfunction in obesity. This chronic "low-grade" inflammation in white adipose tissue is powerfully augmented through the infiltration of macrophages, which, together with adipocytes, perpetuate a vicious cycle of macrophage recruitment and secretion of free fatty acids and deleterious adipokines that predispose the development of obesity-related comorbidities, such as insulin resistance and nonalcoholic fatty liver disease. In the last decade, many factors have been identified that contribute to mounting uncontrolled inflammation in obese adipose tissue. Among them, bioactive lipid mediators derived from the cyclooxygenase and 5-lipoxygenase pathways, which convert the ω-6-polyunsaturated fatty acid (PUFA) arachidonic acid into potent proinflammatory eicosanoids (i.e., prostaglandins [PGs] and leukotrienes), have emerged. Interestingly, the same lipid mediators that initially trigger the inflammatory response also signal the termination of inflammation by stimulating the biosynthesis of anti-inflammatory and proresolving lipid autacoids. This review discusses the current status, characteristics, and progress in this class of "stop signals", including the lipoxins, which were the first identified ω-6 PUFA–derived lipid mediators with potent anti-inflammatory properties; the recently described ω-3 PUFA–derived lipid mediators resolvins and protectins; and the cyclopentenone PGs of the D series. Special emphasis is given to the participation of these bioactive lipid autacoids in the resolution of adipose tissue inflammation and in preventing the development of obesity-related complications. … (more)
- Is Part Of:
- TheScientificWorldjournal. Volume 10(2010)
- Journal:
- TheScientificWorldjournal
- Issue:
- Volume 10(2010)
- Issue Display:
- Volume 10, Issue 2010 (2010)
- Year:
- 2010
- Volume:
- 10
- Issue:
- 2010
- Issue Sort Value:
- 2010-0010-2010-0000
- Page Start:
- 832
- Page End:
- 856
- Publication Date:
- 2010
- Subjects:
- adipose tissue -- adipocytes -- macrophages -- inflammation -- insulin signaling -- adiponectin -- AMPK -- omega-3 PUFA -- omega-3 PUFA–derived lipid autacoids -- resolvins -- protectins
Science -- Periodicals
Technology -- Periodicals
Medicine -- Periodicals
505 - Journal URLs:
- https://www.hindawi.com/journals/tswj/biblio/ ↗
- DOI:
- 10.1100/tsw.2010.77 ↗
- Languages:
- English
- ISSNs:
- 2356-6140
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library HMNTS - ELD Digital store
- Ingest File:
- 15810.xml