Linked Life Data

2655471

Source:http://linkedlifedata.com/resource/pubmed/id/2655471

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5 Pt 1
pubmed:dateCreated
1989-6-16
pubmed:abstractText
To dissect the mechanisms of the prevention of hypoglycemia during fasting, eight normal humans were studied after overnight and 3-day fasts. Prolonged fasting resulted in the expected decrements in base-line glucose production and plasma glucose, insulin, and C-peptide and increments in plasma glucagon, epinephrine, norepinephrine, growth hormone, and cortisol. After the overnight and 3-day fasts, insulin restoration (0.2 mU.kg-1.min-1) alone resulted in transient decrements in glucose production and only 15 and 19% decrements in plasma glucose, respectively. Selective glucagon deficiency (somatostatin infusion with insulin and growth hormone replacement) resulted in transient decrements in glucose production and additional 24 and 29% decrements in plasma glucose, respectively. Notably, plasma glucose plateaued under both fasting conditions in both instances. Combined alpha- and beta-adrenergic blockade (phentolamine and propranolol infusions) alone had no effect on glycemia under either fasting condition. However, progressive hypoglycemia developed during adrenergic blockade coupled with glucagon deficiency after the overnight fast (85 +/- 2 to 48 +/- 4 mg/dl, P less than 0.001) and after the 3-day fast (65 +/- 2 to 33 +/- 1 mg/dl, P less than 0.001). These were the result of both decrements in glucose production and increments in glucose clearance. Thus we conclude that during fasting 1) the prevention of hypoglycemia is not due solely to decreased insulin secretion. 2) Glucagon plays a primary counterregulatory role. Sympathochromaffin catecholamines are not normally critical but compensate and become critical when glucagon is deficient. Adrenomedullary epinephrine is probably the relevant catecholamine. 3) Other hormones, neurotransmitters, or substrate effects may, or may not, be involved; if they are, they appear to stand low in the hierarchy of glucoregulatory factors.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
256
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
E651-61
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Insulin, glucagon, and catecholamines in prevention of hypoglycemia during fasting.
pubmed:affiliation
Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.