Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2010 Winter;7(3-4):e213-e218.
doi: 10.1016/j.ddmec.2011.01.003.

The Role of Phospholipase A(2)-derived Mediators in Obesity

Marcia J Abbott  1 , Tianyi Tang, Hei Sook Sul
Affiliations

The Role of Phospholipase A(2)-derived Mediators in Obesity

Marcia J Abbott et al. Drug Discov Today Dis Mech. 2010 Winter.

Abstract

Obesity has become an epidemic and its prevalence is increasing exponentially. A great deal of focus has been given to understanding the molecular processes that regulate obesity. The characterization of phospholipase A(2)s, especially adipose-specific PLA(2), have lead to a proposed role of their downstream products in the progression of obesity and obesity related disorders. This review summarizes recent developments in the role of PLA(2) and their downstream effects in the development of metabolic disorders.

PubMed Disclaimer

Figures

Figure 1
Figure 1. Phospholipase A2 and its downstream products
Phospholipase A2 (PLA2) cleaves sn-2 fatty acids from phospholipids. Arachidonic acid is an important fatty acid produced by PLA2 activity, since it can be converted into many bioactive molecules, prostaglandins and leukotrienes. Numerous enzymes are involved in the generation of bioactive molecules, and cylclooxygenase-1 and -2, prostaglandin E synthase, and 5-lipoxygenase are key players in the production of prostaglandins and luekotrienes.
Figure 2
Figure 2. The role of AdPLA-PGE2-EP3 signaling in the regulation of lipolysis
AdPLA is an adipose specific PLA2 that can produce arachidonic acid (AA) from the sn-2 position of membrane phospholipids. Subsequently, prostaglandin E2 (PGE2) is produced via cyclooxygenase (COX) pathway and acts to suppress lipolysis through Giα-coupled prostaglandin E3 (EP3) to inhibit adenylate cyclase (AC). This model suggests an autocrine-paracrine role of PGE2 in the regulation of lipolysis in adipose tissue.
Figure 3
Figure 3. Potential role of cyclooxygenase-2s in obesity
Cyclooxyganse-2 (COX-2) may contribute to increased inflammation and insulin resistance associated with obesity, possibly through increasing cytokine secretion or by increasing prostaglandin production from the macrophage. On the other hand, COX-2 may also act to increase brown adipocyte generation in white adipose tissue thus ameliorating obesity.
See this image and copyright information in PMC

References

    1. Flegal KM, Carroll MD, Ogden CL, Curtin LR. Prevalence and Trends in Obesity Among US Adults, 1999–2008. JAMA: The Journal of the American Medical Association. 2010;303:235–241. - PubMed
    1. Bray GA. Medical Consequences of Obesity. J Clin Endocrinol Metab. 2004;89:2583–2589. - PubMed
    1. Foreyt JP, Goodrick GK. Evidence for Success of Behavior Modification in Weight Loss and Control. Annals of Internal Medicine. 1993;119:698–701. - PubMed
    1. Sjostrom L, Lindroos AK, Peltonen M, Torgerson J, Bouchard C, Carlsson Br, Dahlgren S, Larsson B, Narbro K, Sjostrom CD, Sullivan M, Wedel H. Lifestyle, Diabetes, and Cardiovascular Risk Factors 10 Years after Bariatric Surgery. New England Journal of Medicine. 2004;351:2683–2693. - PubMed
    1. Elangbam CS. Review Paper: Current Strategies in the Development of Anti-obesity Drugs and Their Safety Concerns. Veterinary Pathology Online. 2009;46:10–24. - PubMed

LinkOut - more resources