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Cited by 297Birth, Development, and HealthPancreatic function and diabetesGestational Diabetes Research and Management

The DOI matches its Crossref record; 37 of the 37 references it cites were found in a registry or an index.

Impaired glucose homeostasis and mitochondrial abnormalities in offspring of rats fed a fat-rich diet in pregnancy

Taylor, Paul D., McConnell, Josie, Khan, Imran Y., Holemans, Kathleen, Lawrence, Kevin M., Asare-Anane, Henry, Persaud, Shanta J., Jones, Peter M., Petrie, Linda, Hanson, Mark A., Poston, Lucilla·2005·American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
DOI 10.1152/ajpregu.00355.2004
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Abstract

We previously reported that prenatal and suckling exposure to a maternal diet rich in animal fat leads to cardiovascular dysfunction in young adult rat offspring with subsequent development of dyslipidemia and hyperglycemia. We have further investigated glucose homeostasis in adult female offspring by euglycemic-hyperinsulinemic clamp and by dynamic assessment of glucose-stimulated insulin secretion in isolated, perifused pancreatic islet cells. Additionally, given the link between reduced mitochondrial DNA (mtDNA) content and the development of type 2 diabetes mellitus, we have measured mtDNA in organs from young adult animals. Sprague-Dawley rats were fed a diet rich in animal fat or normal chow throughout pregnancy and weaning. Infusion of insulin (5 mU·kg−1·min−1) resulted in a higher steady-state plasma insulin concentration in 1-year-old offspring of fat-fed dams (OHF, n = 4) vs. offspring of control dams (OC, n = 4, P < 0.01). Glucose-stimulated insulin secretion in isolated islets from 9-mo-old OHF was significantly reduced compared with OC ( n = 4, P < 0.05). Transmission electron micrography showed altered insulin secretory granule morphology in OHF pancreatic β-cells. Kidney mtDNA was reduced in 3-mo-old OHF [16S-to-18S gene ratio: OC ( n = 10) 1.05 ± 0.19 vs. OHF ( n = 10) 0.66 ± 0.06, P < 0.05]. At 6 mo, gene chip microarray of OHF aorta showed reduced expression of the mitochondrial genome. Prenatal and suckling exposure to a diet rich in animal fat leads to whole body insulin resistance and pancreatic β-cell dysfunction in adulthood, which is preceded by reduced tissue mtDNA content and altered mitochondrial gene expression.

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Crossref · 10.1152/ajpregu.00355.2004

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Metadata

Authors
Taylor, P. D., McConnell, J., Khan, I. Y., Holemans, K., Lawrence, K. M., Asare-Anane, H., Persaud, S. J., Jones, P. M., Petrie, L., Hanson, M. A., & Poston, L.
Affiliations
King's College London (GB)
ORCID
Venue
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
Publisher
American Physiological Society
Published
2005-01
Volume
288
Issue
1
Pages
R134-R139
ISSN
  • 0363-6119 (ISSN-L)
  • 1522-1490
DOI
10.1152/ajpregu.00355.2004
OpenAlex
W2135070381
Cited by
297
References
37
Citations by year
2025: 1 · 2024: 2 · 2023: 2 · 2022: 6 · 2021: 7 · 2020: 10 · 2019: 14 · 2018: 13 · 2017: 13 · 2016: 20 · 2015: 11 · 2014: 29 · 2013: 14 · 2012: 18
FWCI
13.07
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion)
  • PubMed (publishedVersion)
  • Digital Access to Libraries (Université catholique de Louvain (UCL), l'Université de Namur (UNamur) and the Université Saint-Louis (USL-B)) (submittedVersion)
  • ePrints Soton (University of Southampton) (submittedVersion)
  • UCL Discovery (University College London) (submittedVersion)
  • Research Portal (King's College London) (submittedVersion)
Funders
British Heart Foundation
Topics
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
  • Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
Keywords
maternal high-fat diet, prenatal exposure, offspring, glucose homeostasis, insulin resistance, glucose-stimulated insulin secretion, beta-cell dysfunction, insulin secretory granules, mitochondrial DNA, mitochondrial gene expression, kidney mitochondria, aorta, type 2 diabetes, dyslipidemia, hyperglycemia, cardiovascular dysfunction
MeSH terms
Adipose Tissue, Animals, Blood Glucose, Body Weight, Dietary Fats, Female, Homeostasis, Insulin, Insulin Resistance, Islets of Langerhans, Lipids, Mitochondria, Pregnancy, Prenatal Exposure Delayed Effects, Gene Expression, Rats, Sprague-Dawley, Leptin, Metabolic Syndrome, Prenatal Nutritional Physiological Phenomena, Rats

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