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

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

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
Open this paper in CoChat — free account

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.

Overview

Integrity signals

Registry

Crossref · 10.1152/ajpregu.00494.2004

Cites

63 of 63 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 1

  1. SAS Institute. SAS/STAT User's Guide (8th ed.). Cary, NC: SAS Institute, 1999.

Cited by

Sorted by citations

See all 154

Related

See all

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)
ORCID
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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review