Document Detail


Fatty acid transport proteins, implications in physiology and disease.
MedLine Citation:
PMID:  21979150     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Uptake of long-chain fatty acids plays pivotal roles in metabolic homeostasis and human physiology. Uptake rates must be controlled in an organ-specific fashion to balance storage with metabolic needs during transitions between fasted and fed states. Many obesity-associated diseases, such as insulin resistance in skeletal muscle, cardiac lipotoxicity, and hepatic steatosis, are thought to be driven by the overflow of fatty acids from adipose stores and the subsequent ectopic accumulation of lipids resulting in apoptosis, ER stress, and inactivation of the insulin receptor signaling cascade. Thus, it is of critical importance to understand the components that regulate the flux of fatty acid between the different organ systems. Cellular uptake of fatty acids by key metabolic organs, including the intestine, adipose tissue, muscle, heart, and liver, has been shown to be protein mediated and various unique combinations of fatty acid transport proteins (FATPs/SLC27A1-6) are expressed by all of these tissues. Here we review our current understanding of how FATPs can contribute to normal physiology and how FATP mutations as well as hypo- and hypermorphic changes contribute to disorders ranging from cardiac lipotoxicity to hepatosteatosis and ichthyosis. Ultimately, our increasing knowledge of FATP biology has the potential to lead to the development of new diagnostic tools and treatment options for some of the most pervasive chronic human disorders. This article is part of a Special Issue entitled Triglyceride Metabolism and Disease.
Authors:
Melissa Kazantzis; Andreas Stahl
Publication Detail:
Type:  Journal Article; Review     Date:  2011-09-25
Journal Detail:
Title:  Biochimica et biophysica acta     Volume:  1821     ISSN:  0006-3002     ISO Abbreviation:  Biochim. Biophys. Acta     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-04-02     Completed Date:  2012-11-13     Revised Date:  2013-09-23    
Medline Journal Info:
Nlm Unique ID:  0217513     Medline TA:  Biochim Biophys Acta     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  852-7     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier B.V. All rights reserved.
Affiliation:
Metabolic Biology, NST, UC Berkeley, Berkeley, CA 94720, USA.
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MeSH Terms
Descriptor/Qualifier:
Adipose Tissue / metabolism
Energy Metabolism
Fatty Acid Transport Proteins* / genetics,  metabolism
Fatty Acids / metabolism*
Fatty Liver / complications,  metabolism,  physiopathology
Humans
Insulin Resistance / physiology
Liver* / metabolism,  physiopathology
Muscle, Skeletal / metabolism,  physiology
Obesity / complications,  metabolism*,  physiopathology
Polymorphism, Genetic
Grant Support
ID/Acronym/Agency:
R01 DK066336/DK/NIDDK NIH HHS; R01 DK066336-09/DK/NIDDK NIH HHS; R01 DK089202/DK/NIDDK NIH HHS; R01 DK089202-01A1/DK/NIDDK NIH HHS; R56 DK066336/DK/NIDDK NIH HHS; R56 DK066336-07/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Fatty Acid Transport Proteins; 0/Fatty Acids
Comments/Corrections

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