The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.
Oxidative stress and altered lipid homeostasis in the programming of offspring fatty liver by maternal obesity
Open accessAbstract
Changes in the maternal nutritional environment during fetal development can influence offspring's metabolic risk in later life. Animal models have demonstrated that offspring of diet-induced obese dams develop metabolic complications, including nonalcoholic fatty liver disease. In this study we investigated the mechanisms in young offspring that lead to the development of nonalcoholic fatty liver disease (NAFLD). Female offspring of C57BL/6J dams fed either a control or obesogenic diet were studied at 8 wk of age. We investigated the roles of oxidative stress and lipid metabolism in contributing to fatty liver in offspring. There were no differences in body weight or adiposity at 8 wk of age; however, offspring of obese dams were hyperinsulinemic. Oxidative damage markers were significantly increased in their livers, with reduced levels of the antioxidant enzyme glutathione peroxidase-1. Mitochondrial complex I and II activities were elevated, while levels of mitochondrial cytochrome c were significantly reduced and glutamate dehydrogenase was significantly increased, suggesting mitochondrial dysfunction. Offspring of obese dams also had significantly greater hepatic lipid content, associated with increased levels of PPARγ and reduced triglyceride lipase. Liver glycogen and protein content were concomitantly reduced in offspring of obese dams. In conclusion, offspring of diet-induced obese dams have disrupted liver metabolism and develop NAFLD prior to any differences in body weight or body composition. Oxidative stress may play a mechanistic role in the progression of fatty liver in these offspring.
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“It is evident that the distribution of adipose tissue depends on sex and environmental factors, such as exposure to maternal obesity in utero, which can modify its programming as it does for all other tissues [80,81].”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [80]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“The results of this study highlight how maternal obesity led to profound changes in the offspring’s liver histology and physiology; histological analysis shows an increase in hepatic lipid content compared to control subjects. Plasma analysis showed a decrease in HDL cholesterol, an increase in fasting insulin, TNF-α and DNA oxidative damage markers and hepatic protein oxidation.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [80]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“Also, variations in protein expression involved in oxidative stress homeostasis were found, including reduced expression of NADPH oxidase and glutathione peroxidase, an increase in catalase and a decrease in protein levels involved in lipogenesis and lipolysis; in particular, an increase in PPARγ expression was discovered.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [80]
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“Regarding mitochondrial damage, there was an increase in the activity of complexes I and II and a significant reduction in cytochrome C expression [80,81].”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [80]
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“a number of studies showed that maternal obesity induced greater adiposity and obesity [95,96,97,98] as well as hepatic steatosis [95,96,99] in the offspring.”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [99]
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“at birth, fat mass accounts for approximately 15% of neonatal body weight, and sexually dimorphic differences in body composition are already present.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [80]
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“Adipose tissue develops prenatally, with marked expansion during the third trimester of pregnancy; at birth, fat mass accounts for approximately 15% of neonatal body weight, and sexually dimorphic differences in body composition are already present.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [80]
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Citations
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Kunz, R. I., Brancalhão, R. M. C., Ribeiro, L. D. F. C., & Natali, M. R. M. (2016) · BioMed Research International · doi:10.1155/2016/8175701 · Cited by 480
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Metadata
- Authors
- Alfaradhi, M. Z., Fernandez-Twinn, D. S., Martin-Gronert, M. S., Musial, B., Fowden, A., & Ozanne, S. E.
- Affiliations
- University of Cambridge (GB)
- University of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge, United Kingdom; and
- Department of Physiology, Development and Neuroscience, Centre for Trophoblast Research, University of Cambridge, Cambridge, United Kingdom
- Corresponding author
- Alfaradhi, Maria Z.
- Venue
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
- Publisher
- American Physiological Society
- Published
- 2014-07-01
- Volume
- 307
- Issue
- 1
- Pages
- R26-R34
- ISSN
- 0363-6119 (ISSN-L)
- 1522-1490
- PMC
- PMC4080277
- OpenAlex
- W2128764301
- Cited by
- 136
- References
- 42
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 10 · 2023: 13 · 2022: 13 · 2021: 14 · 2020: 13 · 2019: 7 · 2018: 11 · 2017: 10 · 2016: 16 · 2015: 15 · 2014: 3
- FWCI
- 13.80
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by
- Locations
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- British Heart Foundation (FS/09/029/27902)
- Biotechnology and Biological Sciences Research Council (BB/F015364/1)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Keywords
- non-alcoholic fatty liver disease, maternal obesity, developmental programming, oxidative stress, lipid homeostasis, hyperinsulinemia, glutathione peroxidase 1, mitochondrial dysfunction, PPARγ, hepatic lipase, liver glycogen, obesogenic diet
- MeSH terms
- Glutathione Peroxidase GPX1, Age Factors, Animals, Animal Nutritional Physiological Phenomena, Body Weight, Fatty Liver, Female, Glutamate Dehydrogenase, Glutathione Peroxidase, Glycogen, Homeostasis, Insulin, Lipase, Liver, Mice, Inbred C57BL, Obesity, Phenotype, Pregnancy, Prenatal Exposure Delayed Effects, Risk Factors, Signal Transduction, Oxidative Stress, Prenatal Nutritional Physiological Phenomena, Electron Transport Complex II, Electron Transport Complex I, Cytochromes c, PPAR gamma, Adiposity, Lipid Metabolism, Mice, Non-alcoholic Fatty Liver Disease
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