Long-term disruption of maternal glucose homeostasis induced by prenatal glucocorticoid treatment correlates with miR-29 upregulation
Abstract
Excess of glucocorticoids (GCs) during pregnancy is strongly associated with the programming of glucose intolerance in the offspring. However, the impact of high GC levels on maternal metabolism is not clearly documented. This study aimed to test the hypothesis that mothers exposed to elevated levels of GCs might also display long-term disturbances in glucose homeostasis. Dexamethasone (DEX) was administered noninvasively to the mothers via drinking water between the 14th and the 19th days of pregnancy. Mothers were subjected to glucose and insulin tolerance tests at 1, 2, 3, 6, and 12 mo postweaning. Pregnant rats not treated with DEX and age-matched virgin rats were used as controls. Pancreatic islets were isolated at the 20th day of pregnancy and 12 mo postweaning in order to evaluate glucose-stimulated insulin secretion. The expression of the miR-29 family was also studied due to its responsiveness to GCs and its well-documented role in the regulation of pancreatic β-cell function. Rats treated with DEX during pregnancy presented long-term glucose intolerance and impaired insulin secretion. These changes correlated with 1) increased expression of miR-29 and its regulator p53, 2) reduced expression of syntaxin-1a, a direct target of miR-29, and 3) altered expression of genes related to cellular senescence. Our data demonstrate that the use of DEX during pregnancy results in deleterious outcomes to the maternal metabolism, hallmarked by reduced insulin secretion and glucose…
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The increase in miR-29 in β-cells exposed to elevated glucose mediates the reduction of glucose-stimulated insulin secretion caused by long-term hypoglycemia via reduced expression of syntaxin-1.
“MiR-29 is increased in β-cells exposed to elevated glucose and it was proposed that this mediates the reduction of glucose-stimulated insulin secretion caused by long-term hypoglycemia via reduced expression of syntaxin-1 (186, 218).”
From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [218]
MiR-29 is increased in β-cells exposed to elevated glucose.
“MiR-29 is increased in β-cells exposed to elevated glucose and it was proposed that this mediates the reduction of glucose-stimulated insulin secretion caused by long-term hypoglycemia via reduced expression of syntaxin-1 (186, 218).”
From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [218]
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References 73 · Cited by 27
- Authors
- Gomes, P. R., Graciano, M. F., Pantaleão, L. C., Rennó, A. L., Rodrigues, S. C., Velloso, L. A., Latorraca, M. Q., Carpinelli, A. R., Anhê, G. F., & Bordin, S.
- Affiliations
- Universidade de São Paulo (BR)
- Universidade Estadual de Campinas (UNICAMP) (BR)
- Universidade Federal de Mato Grosso (BR)
- Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil;
- ORCID
- Venue
- American Journal of Physiology-Endocrinology and Metabolism
- Publisher
- American Physiological Society
- Published
- 2014-01-01
- Volume
- 306
- Issue
- 1
- Pages
- E109-E120
- ISSN
- 0193-1849 (ISSN-L)
- 1522-1555
- OpenAlex
- W2099464549
- Cited by
- 27
- References
- 73
- Citations by year
- 2024: 1 · 2023: 3 · 2022: 4 · 2021: 2 · 2020: 3 · 2019: 4 · 2018: 3 · 2017: 2 · 2016: 3 · 2015: 2
- FWCI
- 1.64
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (publishedVersion)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
- Keywords
- prenatal glucocorticoid exposure, dexamethasone, impaired glucose tolerance, insulin secretion, pancreatic beta cells, miR-29, p53, syntaxin 1A, cellular senescence, developmental origins of health and disease
- MeSH terms
- Insulin Secretion, Animals, Blood Glucose, Dexamethasone, Female, Gestational Age, Glucocorticoids, Glucose Tolerance Test, Homeostasis, Insulin, Pregnancy, Prenatal Care, RNA, Messenger, Up-Regulation, Tumor Suppressor Protein p53, Cellular Senescence, Rats, Wistar, Glucose Intolerance, MicroRNAs, Syntaxin 1, Rats
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