Document Detail

Role of AMP-activated protein kinase in adipose tissue metabolism and inflammation.
MedLine Citation:
PMID:  23298225     Owner:  NLM     Status:  MEDLINE    
AMPK (AMP-activated protein kinase) is a key regulator of cellular and whole-body energy balance. AMPK phosphorylates and regulates many proteins concerned with nutrient metabolism, largely acting to suppress anabolic ATP-consuming pathways while stimulating catabolic ATP-generating pathways. This has led to considerable interest in AMPK as a therapeutic target for the metabolic dysfunction observed in obesity and insulin resistance. The role of AMPK in skeletal muscle and the liver has been extensively studied, such that AMPK has been demonstrated to inhibit synthesis of fatty acids, cholesterol and isoprenoids, hepatic gluconeogenesis and translation while increasing fatty acid oxidation, muscle glucose transport, mitochondrial biogenesis and caloric intake. The role of AMPK in the other principal metabolic and insulin-sensitive tissue, adipose, remains poorly characterized in comparison, yet increasing evidence supports an important role for AMPK in adipose tissue function. Obesity is characterized by hypertrophy of adipocytes and the development of a chronic sub-clinical pro-inflammatory environment in adipose tissue, leading to increased infiltration of immune cells. This combination of dysfunctional hypertrophic adipocytes and a pro-inflammatory environment contributes to insulin resistance and the development of Type 2 diabetes. Exciting recent studies indicate that AMPK may not only influence metabolism in adipocytes, but also act to suppress this pro-inflammatory environment, such that targeting AMPK in adipose tissue may be desirable to normalize adipose dysfunction and inflammation. In the present review, we discuss the role of AMPK in adipose tissue, focussing on the regulation of carbohydrate and lipid metabolism, adipogenesis and pro-inflammatory pathways in physiological and pathophysiological conditions.
Silvia Bijland; Sarah J Mancini; Ian P Salt
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Clinical science (London, England : 1979)     Volume:  124     ISSN:  1470-8736     ISO Abbreviation:  Clin. Sci.     Publication Date:  2013 Apr 
Date Detail:
Created Date:  2013-01-09     Completed Date:  2013-03-12     Revised Date:  2014-11-05    
Medline Journal Info:
Nlm Unique ID:  7905731     Medline TA:  Clin Sci (Lond)     Country:  England    
Other Details:
Languages:  eng     Pagination:  491-507     Citation Subset:  IM    
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MeSH Terms
AMP-Activated Protein Kinases / genetics,  metabolism*
Adipose Tissue / cytology,  enzymology*,  immunology,  metabolism
Diabetes Mellitus, Type 2 / enzymology*,  genetics,  immunology,  metabolism
Inflammation / enzymology,  genetics
Obesity / enzymology*,  immunology,  metabolism
Grant Support
09/0003904//Diabetes UK; 09/0003948//Diabetes UK; //British Heart Foundation
Reg. No./Substance:
EC Protein Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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