Document Detail

Mechanisms of the free fatty acid-induced increase in hepatic glucose production.
MedLine Citation:
PMID:  12676648     Owner:  NLM     Status:  MEDLINE    
The associations between obesity, insulin resistance, and type 2 diabetes mellitus are well documented. Free fatty acids (FFA), which are often elevated in obesity, have been implicated as an important link in these associations. Contrary to muscle glucose metabolism, the effects of FFA on hepatic glucose metabolism and the associated mechanisms have not been extensively investigated. It is still controversial whether FFA have substantial effects on hepatic glucose production, and the mechanisms responsible for these putative effects remain unknown. We review recent progress in this area and try to clarify controversial issues regarding the mechanisms responsible for the FFA-induced increase in hepatic glucose production in the postabsorptive state and during hyperinsulinemia.
Tony K T Lam; André Carpentier; Gary F Lewis; Gérald van de Werve; I George Fantus; Adria Giacca
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  284     ISSN:  0193-1849     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2003 May 
Date Detail:
Created Date:  2003-04-04     Completed Date:  2003-05-21     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E863-73     Citation Subset:  IM    
Department of Physiology and Medicine, Medical Science Building, University of Toronto, 1 King's College Circle, Toronto, Ontario M5S 1A8, Canada.
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MeSH Terms
Fatty Acids, Nonesterified / metabolism*
Gluconeogenesis / physiology*
Insulin / metabolism
Lipid Metabolism
Liver / metabolism*
Time Factors
Reg. No./Substance:
0/Fatty Acids, Nonesterified; 11061-68-0/Insulin

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

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