The ontogeny of the endocrine pancreas in the fetal/newborn baboon.
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.
Neonatology Division, Department of Pediatrics, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229, USA.
Amy R
AR
Quinn
Cynthia L
CL
Blanco
Carla
C
Perego
Giovanna
G
Finzi
Stefano
S
La Rosa
Carlo
C
Capella
Rodolfo
R
Guardado-Mendoza
Francesca
F
Casiraghi
Amalia
A
Gastaldelli
Marney
M
Johnson
Edward J
EJ
Dick
Franco
F
Folli
D061354:Acinar Cells / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D000821:Animal Feed; D000818:Animals; D000831:Animals, Newborn; D003922:Diabetes Mellitus, Type 1 / Q000209:etiology; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology; D004750:Enteral Nutrition; D005260:Female; D005865:Gestational Age; D050416:Glucagon-Secreting Cells / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D005947:Glucose / Q000378:metabolism; D006943:Hyperglycemia / Q000378:metabolism / Q000473:pathology*; D050417:Insulin-Secreting Cells / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D007515:Islets of Langerhans / Q000196:embryology* / Q000378:metabolism / Q000473:pathology*; D008297:Male; D016253:Microscopy, Immunoelectron; D010183:Pancreatic Ducts / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D010215:Papio; D011247:Pregnancy; D047928:Premature Birth / Q000378:metabolism / Q000473:pathology*
D005947:Glucose