Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-6-26
pubmed:abstractText
The relative contributions of net hepatic glycogenolysis (NHG) and gluconeogenesis to rates of glucose production during a physiological increment in plasma epinephrine concentrations, independent of changes in plasma insulin concentrations, were determined in seven fasting, healthy young subjects. Plasma insulin concentrations were kept constant by infusing somatostatin (0.1 microg.kg(-1).min(-1)) and replacing basal insulin (24 pmol.m(-2).min(-1)). Epinephrine (1.2 microg.m(-2).min(-1)) was infused for 90 min while NHG was assessed directly by (13)C magnetic resonance spectroscopy. The rate of glucose production was assessed using [6,6-(2)H(2)]glucose, and gluconeogenesis was calculated as the difference between the rate of glucose production and NHG. Plasma epinephrine concentrations increased rapidly from approximately 100 to approximately 2,000 pmol/l (P < 0.00001) accompanied by an increase in plasma glucose concentrations from 4.3 +/- 0.2 to 13.3 +/- 0.3 mmol/l at 90 min (P = 0.00001). This increase in plasma epinephrine concentration resulted in a 2.5-fold increase in glucose production (from 14.4 +/- 1.0 micromol.kg(-1).min(-1) to 35.7 +/- 2.0 micromol.kg(-1).min(-1), P < 0.0001), which lasted for approximately 60 min (phase 1), after which glucose production decreased to 31.2 +/- 1.9 micromol.kg(-1).min(-1) (P < 0.0001 vs. basal) during the last 30 min of the epinephrine infusion (phase 2). Hepatic glycogen concentrations decreased almost linearly during phase 1, and rates of NHG were 19.9 +/- 3.0 micromol.kg(-1).min(-1) (P = 0.005 vs. basal), which could account for approximately 60% of glucose production. During phase 2, NHG decreased to 7.3 +/- 2.8 micromol.kg(-1).min(-1) (P = 0.02 vs. peak), accounting for only approximately 20% of glucose production. In conclusion, in the presence of basal plasma insulin and glucagon concentrations, a physiological increase in plasma epinephrine concentrations stimulates glucose production with an initial, 60-min transient phase caused by stimulation of NHG and a second phase that can mostly be attributed to a twofold increase in rates of gluconeogenesis.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/19458062-11812757, http://linkedlifedata.com/resource/pubmed/commentcorrection/19458062-11872682, http://linkedlifedata.com/resource/pubmed/commentcorrection/19458062-12959935, http://linkedlifedata.com/resource/pubmed/commentcorrection/19458062-15356077, http://linkedlifedata.com/resource/pubmed/commentcorrection/19458062-15671906, http://linkedlifedata.com/resource/pubmed/commentcorrection/19458062-17731092, http://linkedlifedata.com/resource/pubmed/commentcorrection/19458062-1948033, http://linkedlifedata.com/resource/pubmed/commentcorrection/19458062-4357612, http://linkedlifedata.com/resource/pubmed/commentcorrection/19458062-670404, http://linkedlifedata.com/resource/pubmed/commentcorrection/19458062-6833886, http://linkedlifedata.com/resource/pubmed/commentcorrection/19458062-7859939, http://linkedlifedata.com/resource/pubmed/commentcorrection/19458062-8456, http://linkedlifedata.com/resource/pubmed/commentcorrection/19458062-9502760, http://linkedlifedata.com/resource/pubmed/commentcorrection/19458062-9927497
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1522-1555
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
297
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
E231-5
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Regulation of net hepatic glycogenolysis and gluconeogenesis by epinephrine in humans.
pubmed:affiliation
Department of Internal Medicine, Yale University School of Medicine, The Anlyan Center, S263, New Haven, CT 06520-8020, USA.
pubmed:publicationType
Journal Article, Clinical Trial, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural