ArticleOxidative medicine and cellular longevity2019
Label-Free Proteomics of the Fetal Pancreas Identifies Deficits in the Peroxisome in Rats with Intrauterine Growth Restriction.
Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- The peroxisome: an update on mysteries 3.0.Histochemistry and cell biology · 2024Review
- Fetal Cardiac Lipid Sensing Triggers an Early and Sex-related Metabolic Energy Switch in Intrauterine Growth Restriction.The Journal of clinical endocrinology and metabolism · 2021Article
- Comparative Proteomic Analysis to Investigate the Pathogenesis of Oral Adenoid Cystic Carcinoma.ACS omega · 2021Article
- Peroxisome Deficiency Dysregulates Fatty Acid Oxidization and Exacerbates Lipotoxicity inOxidative medicine and cellular longevity · 2021Article
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
aimThe objective of the present study was to identify differentially expressed proteins (DEPs) in the pancreas of a fetus with intrauterine growth restriction (IUGR) and to investigate the molecular mechanisms leading to adulthood diabetes in IUGR.
methodsThe IUGR rat model was induced by maternal protein malnutrition. The fetal pancreas was collected at embryonic day 20 (E20). Protein was extracted, pooled, and subjected to label-free quantitative proteomic analysis. Bioinformatics analysis (GO and IPA) was performed to define the pathways and networks associated with DEPs. LC-MS results were confirmed by western blotting and/or quantitative PCR (q-PCR). The principal parameters of oxidative stress-superoxide dismutase (Sod) were determined in blood samples of fetal rats.
resultsA total of 57 DEPs (27 upregulated, 30 downregulated) were identified with a 1.5-fold change threshold and a
conclusionThe present study identified DEPs in the fetal pancreas of IUGR rats by proteomic analysis. Downregulation of pancreas peroxins and dysregulation of enzymes involved in peroxisomal FAO may impair the biogenesis and function of the peroxisome and may underlie the development of T2 diabetes mellitus in adult IUGR rats. Disorders of cell cycle regulators may induce cell division arrest and lead to smaller islets. The present data provide new insight into the role of the peroxisome in the development of the pancreas and may be valuable in furthering our understanding of the pathogenesis of IUGR-induced diabetes.
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