ArticleWorld journal of diabetes2011
Alteration of mitochondrial function in adult rat offspring of malnourished dams.
Article in World journal of diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- Developmental regulation of fetal mitochondrial respiratory function towards term: the role of glucocorticoid and thyroid hormones.The Journal of endocrinology · 2025Review
- Impact of Obesity and Hyperglycemia on Placental Mitochondria.Oxidative medicine and cellular longevity · 2018Article
- Implication of Oxidative Stress in Fetal Programming of Cardiovascular Disease.Frontiers in physiology · 2018Review
- Influence of maternal obesity, diet and exercise on epigenetic regulation of adipocytes.Molecular aspects of medicine · 2017Review
- Protein malnutrition potentiates the amplifying pathway of insulin secretion in adult obese mice.Scientific reports · 2016Article
- MicroRNAs with Specific Roles in Diabetes and Psychiatric Diseases.Clujul medical (1957) · 2014Review
- Impaired hypothalamic mTOR activation in the adult rat offspring born to mothers fed a low-protein diet.PloS one · 2013Article
- Beta cell dysfunction and insulin resistance.Frontiers in endocrinology · 2013Article
- Perinatal nutritional programming of health and metabolic adult disease.World journal of diabetes · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Under-nutrition as well as over-nutrition during pregnancy has been associated with the development of adult diseases such as diabetes and obesity. Both epigenetic modifications and programming of the mitochondrial function have been recently proposed to explain how altered intrauterine metabolic environment may produce such a phenotype. This review aims to report data reported in several animal models of fetal malnutrition due to maternal low protein or low calorie diet, high fat diet as well as reduction in placental blood flow. We focus our overview on the β cell. We highlight that, notwithstanding early nutritional events, mitochondrial dysfunctions resulting from different alteration by diet or gender are programmed. This may explain the higher propensity to develop obesity and diabetes in later life.
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Registered trials
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