Document Detail


Corticosteroid-mediated programming and the pathogenesis of obesity and diabetes.
MedLine Citation:
PMID:  20117209     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Epidemiological studies have shown that low birthweight is associated with increased risk of development of diabetes and obesity in later life. Over-exposure of the developing fetus to glucocorticoids is one of the major hypotheses that has been proposed to explain this association. In animal models, a range of manipulations that increase fetal glucocorticoid load, 'programme' permanent changes in glucose and insulin metabolism and adiposity. This may be mediated by alterations in regulation of the hypothalamic-pituitary-adrenal (HPA) axis. In humans, low birthweight is associated with increased circulating glucocorticoid levels, and an increased cortisol response to physiological and psychosocial stressors, in child- and adulthood. This activation of the HPA axis is also associated with increased risk of development of diabetes and obesity in later life.
Authors:
Rebecca M Reynolds
Related Documents :
21868779 - Effects of exenatide on measures of β-cell function after 3 years in metformin-treated...
19020139 - The extended mallampati score and a diagnosis of diabetes mellitus are predictors of di...
10624789 - Intracellular hyperinsulinism: a metabolic characteristic of obesity with and without t...
8964829 - Abnormalities of insulin pulsatility and glucose oscillations during meals in obese non...
1604959 - From obesity to type 2 diabetes.
3512339 - Effects of obesity, hyperinsulinemia, and glucose intolerance on insulin action in adip...
1622729 - Esophageal clearance scintigraphy, in diabetic patients--a preliminary study.
9068299 - Metabolic cataracts in newly diagnosed diabetes.
25290109 - A case for immune response genes?
Publication Detail:
Type:  Journal Article; Review     Date:  2010-02-01
Journal Detail:
Title:  The Journal of steroid biochemistry and molecular biology     Volume:  122     ISSN:  1879-1220     ISO Abbreviation:  J. Steroid Biochem. Mol. Biol.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-09-13     Completed Date:  2010-10-15     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9015483     Medline TA:  J Steroid Biochem Mol Biol     Country:  England    
Other Details:
Languages:  eng     Pagination:  3-9     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Ltd. All rights reserved.
Affiliation:
Endocrinology Unit, Centre for Cardiovascular Science, University of Edinburgh, Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, United Kingdom. R.Reynolds@ed.ac.uk
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Diabetes Mellitus / chemically induced*
Female
Fetal Development / physiology
Fetus
Glucocorticoids / metabolism*,  poisoning*
Glucose / metabolism
Humans
Hypothalamo-Hypophyseal System / embryology*,  physiology
Infant, Low Birth Weight / physiology
Infant, Newborn
Insulin / metabolism
Obesity / chemically induced*
Pituitary-Adrenal System / physiology*
Pregnancy
Chemical
Reg. No./Substance:
0/Glucocorticoids; 11061-68-0/Insulin; 50-99-7/Glucose

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


Previous Document:  Gender-associated modulation of inducible CYP1A1 expression by andrographolide in mouse liver.
Next Document:  Erythropoietin promotes hippocampal neurogenesis in in vitro models of neonatal stroke.