Document Detail


The ontogeny of the endocrine pancreas in the fetal/newborn baboon.
MedLine Citation:
PMID:  22723715     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Erratic regulation of glucose metabolism including hyperglycemia is a common condition in premature infants and is associated with increased morbidity and mortality. The objective of this study was to examine histological and ultrastructural differences in the endocrine pancreas in fetal (throughout gestation) and neonatal baboons. Twelve fetal baboons were delivered at 125 days (d) gestational age (GA), 140d GA, or 175d GA. Eight animals were delivered at term (185d GA); half were fed for 5 days. Seventy-three nondiabetic adult baboons were used for comparison. Pancreatic tissue was studied using light microscopy, confocal imaging, and electron microscopy. The fetal and neonatal endocrine pancreas islet architecture became more organized as GA advanced. The percent areas of α-β-δ-cell type were similar within each fetal and newborn GA (NS) but were higher than the adults (P<0.05) regardless of GA. The ratio of β cells within the islet (whole and core) increased with gestation (P<0.01). Neonatal baboons, which survived for 5 days (feeding), had a 2.5-fold increase in pancreas weight compared with their counterparts killed at birth (P=0.01). Endocrine cells were also found in exocrine ductal and acinar cells in 125, 140 and 175d GA fetuses. Subpopulation of tissue that coexpressed trypsin and glucagon/insulin shows the presence of cells with mixed endo-exocrine lineage in fetuses. In summary, the fetal endocrine pancreas has no prevalence of a α-β-δ-cell type with larger endocrine cell percent areas than adults. Cells with mixed endocrine/exocrine phenotype occur during fetal development. Developmental differences may play a role in glucose homeostasis during the neonatal period and may have long-term implications.
Authors:
Amy R Quinn; Cynthia L Blanco; Carla Perego; Giovanna Finzi; Stefano La Rosa; Carlo Capella; Rodolfo Guardado-Mendoza; Francesca Casiraghi; Amalia Gastaldelli; Marney Johnson; Edward J Dick; Franco Folli
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-06-21
Journal Detail:
Title:  The Journal of endocrinology     Volume:  214     ISSN:  1479-6805     ISO Abbreviation:  J. Endocrinol.     Publication Date:  2012 Sep 
Date Detail:
Created Date:  2012-08-27     Completed Date:  2012-12-10     Revised Date:  2013-07-12    
Medline Journal Info:
Nlm Unique ID:  0375363     Medline TA:  J Endocrinol     Country:  England    
Other Details:
Languages:  eng     Pagination:  289-99     Citation Subset:  IM    
Affiliation:
Neonatology Division, Department of Pediatrics, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229, USA.
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MeSH Terms
Descriptor/Qualifier:
Acinar Cells / metabolism,  pathology,  ultrastructure
Animal Feed
Animals
Animals, Newborn
Diabetes Mellitus, Type 1 / etiology
Diabetes Mellitus, Type 2 / etiology
Enteral Nutrition
Female
Gestational Age
Glucagon-Secreting Cells / metabolism,  pathology,  ultrastructure
Glucose / metabolism
Hyperglycemia / metabolism,  pathology*
Insulin-Secreting Cells / metabolism,  pathology,  ultrastructure
Islets of Langerhans / embryology*,  metabolism,  pathology*
Male
Microscopy, Immunoelectron
Pancreatic Ducts / metabolism,  pathology,  ultrastructure
Papio
Pregnancy
Premature Birth / metabolism,  pathology*
Grant Support
ID/Acronym/Agency:
HL52636/HL/NHLBI NIH HHS; P51 RR013986/RR/NCRR NIH HHS; P51 RR013986/RR/NCRR NIH HHS; R0-1 DK080148/DK/NIDDK NIH HHS; R01 DK080148/DK/NIDDK NIH HHS; U01 HL052636/HL/NHLBI NIH HHS; UL1 RR025767/RR/NCRR NIH HHS; UL1 TR000149/TR/NCATS NIH HHS; UL1RR025767/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
50-99-7/Glucose
Comments/Corrections

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