Cited by 154Pancreatic function and diabetesBirth, Development, and HealthDiabetes and associated disorders

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Diminished β-cell replication contributes to reduced β-cell mass in fetal sheep with intrauterine growth restriction

Limesand, Sean W., Jensen, Jan, Hutton, John C., Hay, William W.·2005·American Journal of Physiology-Regulatory, Integrative and Comparative Physiology

DOI 10.1152/ajpregu.00494.2004

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Abstract

Human fetuses with severe intrauterine growth restriction (IUGR) have less pancreatic endocrine tissue and exhibit β-cell dysfunction, which may limit β-cell function in later life and contribute to their increased incidence of noninsulin-dependent diabetes mellitus. Three factors, replication, apoptosis, and neoformation, contribute to fetal β-cell mass. We studied an ovine model of IUGR to understand whether nutrient deficits lead to decreased rates of fetal pancreatic β-cell replication, increased rates of apoptosis, or lower rates of differentiation. At 90% of term gestation, IUGR fetal and pancreatic weights were 58% and 59% less than pair-fed control, respectively. We identified a selective impairment of β-cell mass compared with other pancreatic cell types in IUGR fetuses. Insulin and insulin mRNA contents were less than other pancreatic endocrine hormones in IUGR fetuses, as were pancreatic insulin positive area (42%) and β-cell mass (76%). Pancreatic β-cell apoptosis was not different between treatments. β-cell capacity for cell cycling, determined by proliferating cell nuclear antigen (PCNA) immunostaining, was not different between treatment groups. However, the percentage of β-cells actually undergoing mitosis was 72% lower in IUGR fetuses. These results indicate that in utero nutrient deficits decrease the population of pancreatic β-cells by lengthening G1, S, and G2 stages of interphase and decreasing mitosis near term. Diminished β-cell mass in IUGR infants at birth, if not adequately compensated for after birth, may contribute to insufficient insulin production in later life and, thus, a predisposition to noninsulin-dependent diabetes.

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Authors: Limesand, S. W., Jensen, J., Hutton, J. C., & Hay, W. W.
Affiliations: University of Colorado Health (US)
University of Colorado Denver (US)
University of Colorado Anschutz (US)
ORCID: Limesand, Sean W.
Jensen, Jan
Hay, William W.
Venue: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
Publisher: American Physiological Society
Published: 2005-05
Volume: 288
Issue: 5
Pages: R1297-R1305
ISSN: 0363-6119 (ISSN-L)
1522-1490
DOI: 10.1152/ajpregu.00494.2004
OpenAlex: W2105434442
Cited by: 153
References: 62
Citations by year: 2026: 4 · 2025: 5 · 2024: 4 · 2023: 3 · 2022: 4 · 2021: 8 · 2020: 6 · 2019: 3 · 2018: 9 · 2017: 7 · 2016: 13 · 2015: 6 · 2014: 6 · 2013: 10 · 2012: 11
FWCI: 7.00
Type: journal article
Language: en
Open access: closed
Locations: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute of Diabetes and Digestive and Kidney Diseases (DK-60300, F32DK060300, P30DK057516, P30 DK 57516, K01DK067393, DK-067393)
Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD-42815, HD20761)
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
Keywords: fetal growth restriction, beta-cell proliferation, beta-cell mass, fetal sheep, pancreatic beta cells, beta-cell apoptosis, cell cycle, mitosis, proliferating cell nuclear antigen, insulin, type 2 diabetes risk, nutritional deficiency, pancreatic development
MeSH terms: Animals, Cell Differentiation, Female, Fetal Growth Retardation, Fetus, Islets of Langerhans, Mitosis, Organ Size, Placental Insufficiency, Pregnancy, Sheep, Apoptosis

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Diminished β-cell replication contributes to reduced β-cell mass in fetal sheep with intrauterine growth restriction

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