Document Detail


Different mechanisms operating during different critical time-windows reduce rat fetal beta cell mass due to a maternal low-protein or low-energy diet.
MedLine Citation:
PMID:  17882398     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
AIMS/HYPOTHESIS: Adverse events during intra-uterine life may programme organ growth and favour disease later in life. In animals, protein or energy restriction during gestation alters the development of the endocrine pancreas, even though the duration of malnutrition is different. Here, we evaluate the specific effects of both diets during different periods of gestation and the mechanisms underlying the decreased beta cell mass. METHODS: Pregnant Wistar rats were fed either a low-protein or a low-energy diet during the last week of gestation or throughout gestation. Fetuses and their pancreases were analysed at days 15 and 21 of gestation. RESULTS: The low-energy diet reduced the beta cell mass from 21-day-old fetuses by 33 or 56% when administered during the last week or throughout gestation, respectively. Fetal corticosterone levels were increased. At 15 days of fetal age, the number of cells producing neurogenin 3 (NEUROG3) or pancreatic and duodenal homeobox gene 1 (PDX-1) was reduced. Neither islet vascularisation nor beta cell proliferation was affected. The low-protein diet, in contrast, was more efficient in decreasing the fetal beta cell mass when given during the last week of gestation (-53%) rather than throughout gestation (-33%). Beta cell proliferation was decreased by 50% by the low-protein diet, independently of its duration, and islet vascularisation was reduced. This diet did not affect NEUROG3- or PDX-1-positive cell numbers. CONCLUSION/INTERPRETATION: Although both diets reduced the fetal beta cell mass, the cellular mechanisms and the sensitivity windows were different. Early alteration of neogenesis due to elevated corticosterone levels is likely to be responsible for the decreased beta cell mass in low-energy fetuses, whereas impaired beta cell proliferation and islet vascularisation at later stages are implicated in low-protein fetuses.
Authors:
O Dumortier; B Blondeau; B Duvillié; B Reusens; B Bréant; C Remacle
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-09-19
Journal Detail:
Title:  Diabetologia     Volume:  50     ISSN:  0012-186X     ISO Abbreviation:  Diabetologia     Publication Date:  2007 Dec 
Date Detail:
Created Date:  2007-11-06     Completed Date:  2008-03-27     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0006777     Medline TA:  Diabetologia     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  2495-503     Citation Subset:  IM    
Affiliation:
Laboratoire de Biologie Cellulaire, Université Catholique de Louvain, 5, place Croix du Sud, 1348, Louvain-la-Neuve, Belgium.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Glucose / analysis
Caloric Restriction
Corticosterone / analysis
Diet, Protein-Restricted / adverse effects*
Diet, Reducing / adverse effects*
Energy Intake / physiology
Female
Fetal Weight
Gestational Age*
Insulin / analysis
Insulin-Secreting Cells / cytology*
Islets of Langerhans / anatomy & histology*,  blood supply,  chemistry,  embryology*
Maternal-Fetal Exchange / physiology
Organ Size
Pancreas, Exocrine / anatomy & histology,  embryology
Pregnancy
Protein-Energy Malnutrition / embryology
Rats
Rats, Wistar
Signal Transduction / physiology
Time Factors
Chemical
Reg. No./Substance:
0/Blood Glucose; 11061-68-0/Insulin; 50-22-6/Corticosterone

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


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