AdPLA ablation increases lipolysis and prevents obesity induced by high-fat feeding or leptin deficiency (Nat Med, 2009, doi:1038/nm.1904)

報告日期: 2009/04/28
報告時間: 15:10/16:00
報告學生: 陳立仁(英文報告)
講評老師: 蔡曜聲
附件下載:

http://basicmed.med.ncku.edu.tw/admin/up_img/980428-1.pdf

AdPLA ablation increases lipolysis and prevents obesity induced by high-fat feeding or leptin deficiency

Abstract

Speaker: Li-Jen Chen

Commentator: Dr. Yau-Sheng Tsai

Date: 2009.04.28 15:00 pm.

Room: 602

 

 

Triacylglycerol in adipose tissue is the major energy storage form in mammals. An imbalance between energy intake and expenditure can result in excess triacylglycerol accumulation in this tissue, resulting in obesity. In morbid obesity increased adipocyte number (hyperplasia) may occur through adipocyte differentiation of precursor cells present in adipose tissue2. However, obesity is largely attributed to adipocyte hypertrophy that occurs when triacylglycerol synthesis exceeds breakdown (lipolysis), resulting in elevated triacylglycerol storage. Adipose-specific PLA2, named AdPLA (adipose-specific phospholipase A2). AdPLA was highly expressed specifically in white adipose tissue and was induced during preadipocyte differentiation into adipocytes. PLA2 enzymes catalyze the initial rate-limiting step in the production of eicosanoids. Eicosanoids, including prostaglandins, are potent local mediators of signal transduction. PGE2 is a product of the arachidonic acid cascade that is initiated by breakdown of phospholipids in most cells. However, in adipocytes arachidonic acid can also be derived from the breakdown of triacyglycerols. AdPLA is the major PLA2 enzyme in adipose tissue and that it regulates lipolysis in an autocrine and paracrine manner through PGE2. This study reported that ablation of AdPLA prevents obesity from high fat feeding or leptin deficiency by regulating lipolysis through the PGE2-EP3-cAMP pathway.

 

Reference:

1. Duncan, R.E., Ahmadian, M., Jaworski, K., Sarkadi-Nagy, E. & Sul, H.S. Regulation of lipolysis in adipocytes. Annu. Rev. Nutr. 27, 79–101 (2007).

2. Savage, D.B., Petersen, K.F. & Shulman, G.I. Disordered lipid metabolism and the pathogenesis of insulin resistance. Physiol. Rev. 87, 507–520 (2007).