The DOI matches its Crossref record; 63 of the 63 references it cites were found in a registry or an index.
Diminished β-cell replication contributes to reduced β-cell mass in fetal sheep with intrauterine growth restriction
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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“In addition, the pancreas has fewer insulin-producing beta cells and reduced vascularization (159, 340, 473), and the structure and maturation of the brain (142), lungs (358, 359, 424, 460) and liver (209, 474) are compromised.”
From Placental Origins of Chronic Disease (2016) · cites this paper as [340]
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Cites
Fetal and infant growth and impaired glucose tolerance at age 64
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Cyclin/PCNA is the auxiliary protein of DNA polymerase-δ
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Intrauterine growth restriction
Resnik, R. (2002) · Obstetrics & Gynecology · doi:10.1016/s0029-7844(01)01780-x · Cited by 1,022
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Early-onset type-ll diabetes mellitus (MODY4) linked to IPF1
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Phosphorylation of Histone H3 Is Required for Proper Chromosome Condensation and Segregation
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Effect of a Low Protein Diet during Pregnancy on the Fetal Rat Endocrine Pancreas
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Intrauterine Growth Retardation Leads to the Development of Type 2 Diabetes in the Rat
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“In rat models of fetal growth restriction, deficits in insulin secretion capacity, as well as decreased -cell mass, have been observed in the adult animal (14, 52), although such long-term consequences also were dependent on early postnatal nutritional experiences (18).”
BackgroundBanting lecture 1990. Beta-cells in type II diabetes mellitus
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Placental Origins of Chronic Disease
Burton, G. J., Fowden, A. L., & Thornburg, K. L. (2016) · Physiological Reviews · doi:10.1152/physrev.00029.2015 · Cited by 717
The fetal brain sparing response to hypoxia: physiological mechanisms
Giussani, D. A. (2015) · The Journal of Physiology · doi:10.1113/jp271099 · Cited by 402
Invited review: Heat stress effects during late gestation on dry cows and their calves
Tao, S., & Dahl, G. E. (2013) · Journal of Dairy Science · doi:10.3168/jds.2012-6278 · Cited by 342
Placental-fetal glucose exchange and fetal glucose metabolism.
(2006) · Europe PMC (PubMed Central) · Cited by 226
Self-citationLimesand, S. W., Rozance, P. J., Zerbe, G. O., Hutton, J. C., & Hay, W. W. (2005) · Endocrinology · doi:10.1210/en.2005-0900 · Cited by 214
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Metadata
- 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)
- 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
- 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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