Document Detail


Hepatic glucose production during exercise.
MedLine Citation:
PMID:  9781319     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Hepatic glucose production increases during exercise as a sum of liver glycogenolysis and gluconeogenesis. Whereas the former dominates during intense exercise, the latter contributes substantially with prolonged exercise and the concomitant decline in liver glycogen stores and with increased gluconeogenic precursor supply. Afferent neural feedback signals from contracting muscle and feedback signals mediated via the blood stream, can stimulate glucose production to maintain euglycemia. A rise in blood glucose directly inhibits hepatic glucose production, whereas a decline in blood glucose enhances liver glucose production via release of glucoregulatory hormones. In addition to this, central mechanisms coupled to the degree of motor center activity can be responsible for part of the increase in glucose mobilization, especially during intense exercise where hepatic glucose release exceeds peripheral glucose uptake and plasma glucose rises. A decline in plasma insulin is important for the rise in glucose production during exercise in a variety of species, whereas an increase in plasma glucagon is probably more important in other species than man, where glucagon plays a role only in prolonged exercise. Sympathetic nervous activity to the liver and circulating norepinephrine has been demonstrated to be without any role in glucose production, whereas epinephrine has a minor stimulating effect on hepatic glucose mobilization during intense exercise. Growth hormone and cortisol contribute only minimally to the exercise induced rise in liver glucose output.
Authors:
M Kjaer
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Advances in experimental medicine and biology     Volume:  441     ISSN:  0065-2598     ISO Abbreviation:  Adv. Exp. Med. Biol.     Publication Date:  1998  
Date Detail:
Created Date:  1998-12-01     Completed Date:  1998-12-01     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0121103     Medline TA:  Adv Exp Med Biol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  117-27     Citation Subset:  IM    
Affiliation:
Copenhagen Muscle Research Centre, Rigshospitalet, University of Copenhagen, Denmark. mkjaer@mfi.ku.dk
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Glucose / metabolism
Exercise / physiology*
Glucose / biosynthesis*
Humans
Liver / innervation,  physiology*
Physical Conditioning, Animal / physiology
Sympathetic Nervous System / physiology
Chemical
Reg. No./Substance:
0/Blood Glucose; 50-99-7/Glucose

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


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