Change search
ReferencesLink to record
Permanent link

Direct link
The Ins and Outs of Adipose Tissue
Umeå University, Faculty of Medicine, Department of Medical Biosciences, Physiological chemistry.
Umeå University, Faculty of Medicine, Department of Medical Biosciences, Physiological chemistry.
2009 (English)In: Cellular Lipid Metabolism / [ed] Christian Enholm, New York: Springer Berlin/Heidelberg, 2009, 315-369 p.Chapter in book (Other academic)
Abstract [en]

The aim of this chapter is to discuss what mechanisms are available to rapidly modulate fatty acid uptake/mobilization in adipose tissue. The major pathway for net uptake is lipoprotein lipase (LPL)-mediated hydrolysis of lipoprotein lipids. There are several mechanisms for control and they all serve to suppress LPL activity on a time-scale of hours in the setting of essentially unchanged LPL mRNA and mass. A protein complex that specifically binds to LPL mRNA can block synthesis of new enzyme. The Ca2+ milieu, and perhaps other conditions in the ER, can partition more of the enzyme towards intracellular degradation and less for export. After secretion from the adipocytes, active LPL can be converted into inactive monomers through interaction with angiopoietin-like proteins. At the vascular endothelium, product control may balance LPL action. If fatty acids accumulate at sites of lipolysis they eliminate the effect of apolipoprotein CII, which is a necessary activator for LPL. Intracellular lipolysis is initiated by adipose tissue triglyceride lipase (ATGL) which hydrolyzes triglycerides to diglycerides. These can either be re-esterified by a diacylglycerol acyl transferase (DGAT) enzyme or further hydrolyzed by hormone-sensitive lipase (HSL). The system is controlled by phosphorylation mediated by protein kinase A, and perhaps other protein kinases, as well as protein phosphatases. The prime target is perilipin, a lipid droplet protein which in its unphosphorylated form suppresses the activity of both ATGL and HSL. The two lipase systems are modulated by different mechanisms and on different time-scales. Both systems seem to operate at levels that generate an excess of fatty acids. The overriding control of how Much gets deposited in the tissue as triglyceride and how much spills over into blood as albumin-bound fatty acids (NEFA) is exerted by the rate of glyceride synthesis. Recent studies show that glycerol-3-phosphate for this is generated mainly through glyceroneogenesis from citric acid cycle intermediates.

Place, publisher, year, edition, pages
New York: Springer Berlin/Heidelberg, 2009. 315-369 p.
National Category
Cell Biology
URN: urn:nbn:se:umu:diva-75764DOI: 10.1007/978-3-642-00300-4_13ISI: 000269609500013ISBN: 978-3-642-00299-1ISBN: 978-3-642-00300-4OAI: diva2:635254
Available from: 2013-07-03 Created: 2013-07-03 Last updated: 2013-07-03Bibliographically approved

Open Access in DiVA

No full text

Other links

Publisher's full text

Search in DiVA

By author/editor
Olivecrona, ThomasOlivecrona, Gunilla
By organisation
Physiological chemistry
Cell Biology

Search outside of DiVA

GoogleGoogle Scholar
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

Altmetric score

Total: 20 hits
ReferencesLink to record
Permanent link

Direct link