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Maternal obesity during pregnancy and lactation programs the development of offspring non-alcoholic fatty liver disease in mice
Abstract
Background & aims Obesity induced, non-alcoholic fatty liver disease (NAFLD), is now the major cause in affluent countries, of the spectrum of steatosis-to-cirrhosis. Obesity and NAFLD rates in reproductive age women, and adolescents, are rising worldwide. Our hypothesis was that maternal obesity and lactation transmit to the offspring a pre-disposition to dysmetabolism, obesity and NAFLD. Methods Female mice were fed standard or obesogenic chow, before, throughout pregnancy, and during lactation. The critical developmental period was studied by cross-fostering offspring of lean and obese dams. Offspring were then weaned onto standard chow and studied at 3months. Read-outs included markers of metabolic dysfunction, biochemical and histological indicators of NAFLD, induction of liver fibrogenesis, and activation of pro-fibrotic pathways. Mechanisms involved in programming a dysmetabolic and NAFLD phenotype were investigated by assaying breast milk components. Results Offspring of obese dams had a dysmetabolic, insulin resistant and NAFLD phenotype compared to offspring of lean dams. Offspring of lean dams that were suckled by obese dams showed an exaggerated dysmetabolic and NAFLD phenotype, with increased body weight, as well as increased levels of insulin, leptin, aspartate transaminase, interleukin-6, tumour necrosis factor-alpha, liver triglycerides, steatosis, hepatic fibrogenesis, renal norepinephrine, and liver alpha1-D plus beta1-adrenoceptors, indicative of sympathetic nervous system activation. Obese dams also had raised breast milk leptin levels compared to lean dams. Conclusions Maternal obesity programs development of a dysmetabolic and NAFLD phenotype, which is critically dependent on the early postnatal period and possibly involving alteration of hypothalamic appetite nuclei signalling by maternal breast milk and neonatal adipose tissue derived, leptin.
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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 [95]
In the citing paper
“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 [95]
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Self-citationZhang, W.-P., Shi, Y., Wang, Y., Liu, X., Yan, J.-C., Chen, H.-R., & Zhao, J. (2024) · Journal of Functional Foods · doi:10.1016/j.jff.2024.106398 · Cited by 1
Argentato, P. P., Pisani, L., de Rosso, V. D., Soares, G. R., Silva, M. J. D., Vilegas, W., & Ribeiro, D. (2019) · Pathophysiology · doi:10.1016/j.pathophys.2019.11.002 · Cited by 1
Developmental programming of non‐alcoholic fatty liver disease
Li, J.-W., Cordero, P., & Oben, J. (2016) · doi:10.1002/9781118924938.ch26 · Cited by 1
Self-citationApplying developmental programming to clinical obstetrics: my ward round
Painter, R. C. (2015) · Journal of Developmental Origins of Health and Disease · doi:10.1017/s2040174415001099 · Cited by 1
Current Models of Fatty Liver Disease; New Insights, Therapeutic Targets and Interventions
Jonscher, K. R., & Bruce, K. D. (2019) · Advances in experimental medicine and biology · doi:10.1007/978-3-030-12668-1_3 · Cited by 1
Han, L., Wu, Y., Li, J., Chen, Y., Li, L., Wang, T., Chen, M., Wang, S., Li, C., Ding, G., et al. (2026) · Nature Metabolism · doi:10.1038/s42255-026-01617-6
Beckett, L. M., Lichti, N. I., Teeple, K. M., Thirumalaikumar, V. P., Hernandez, L. L., Rajwa, B. P., Jannasch, A., Han-Hallett, Y., & Casey, T. (2026) · PLoS ONE · doi:10.1371/journal.pone.0346148
McCarter, S. J., Werre, S., Power, M. L., & Balogh, O. (2026) · Frontiers in Nutrition · doi:10.3389/fnut.2026.1747221
Rivera-Aguirre, J. (2023) · Revista Médicas UIS · doi:10.18273/revmed.v36n3-2023001
Effect of a Diet-Induced Obesity on the Progeny Response in a Murine Model
Paffetti, M. G., Cárcamo, J. G., Azócar-Aedo, L., & Parra, A. (2023) · Nutrients · doi:10.3390/nu15234970
Lonardo, A., & Suzuki, A. (2023) · Metabolism and Target Organ Damage · doi:10.20517/mtod.2023.17 · Cited by 10
Sympathetic blockage attenuates fasting-induced hepatic steatosis
Zheng, L., Gong, L., Cai, X., Lu, S., Zhou, Y., Duan, Z., Fang, W. Y., & Li, G. (2022) · Neuroreport · doi:10.1097/wnr.0000000000001844 · Cited by 1
“…et al., 2020; Bruinstroop et al., 2014; Edinburgh and Frampton, 2020; Guarino et al., 2017; Yi et al., 2010) or indirectly modulate hepatic steatosis through governing the release of adipokines(Miyamoto et al., 2012; Oben et al., 2010; Wang et al., 2020; Warne et al., 2011; Zeng et al., 2015).”
BackgroundNonalcoholic Fatty Liver Disease
Fitzpatrick, E. (2015) · Springer eBooks · doi:10.1007/978-3-319-17169-2_66 · Cited by 3
The Effect of Maternal Pre-pregnancy Body Mass Index on Very Low Birth Weight Infants
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Developmental Programming of Nonalcoholic Fatty Liver Disease (NAFLD)
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Obesidad en el embarazo: razones para volver a preocuparse de la nutrición materna
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Metadata
- Authors
- Oben, J. A., Mouralidarane, A., Samuelsson, A.-M., Matthews, P. J., Morgan, M. L., Mckee, C., Soeda, J., Fernandez-Twinn, D. S., Martin-Gronert, M. S., Ozanne, S. E., Sigala, B., Novelli, M., Poston, L., & Taylor, P. D.
- Affiliations
- St Thomas' Hospital (GB)
- King's College London (GB)
- The Royal Free Hospital (GB)
- University of Cambridge (GB)
- University College London (GB)
- Corresponding author
- Oben, Jude A.
- ORCID
- Venue
- Journal of Hepatology
- Publisher
- Elsevier BV
- Published
- 2010-06
- Volume
- 52
- Issue
- 6
- Pages
- 913-920
- ISSN
- 0168-8278 (ISSN-L)
- OpenAlex
- W2034714209
- Cited by
- 314
- References
- 0
- Citations by year
- 2026: 4 · 2025: 12 · 2024: 8 · 2023: 28 · 2022: 24 · 2021: 10 · 2020: 21 · 2019: 31 · 2018: 22 · 2017: 20 · 2016: 28 · 2015: 21 · 2014: 27 · 2013: 25 · 2012: 14
- FWCI
- 13.26
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Hepatology (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Research Portal (King's College London) (submittedVersion)
- Funders
- British Heart Foundation (FS/10/003/28163, FS/09/029/27902)
- Biotechnology and Biological Sciences Research Council (BB/F015364/1)
- Topics
- Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Keywords
- maternal obesity, non-alcoholic fatty liver disease, developmental programming, lactation, cross-fostering, insulin resistance, leptin, breast milk, liver fibrosis, sympathetic nervous system, adrenergic receptors, leptin resistance, dysmetabolism, offspring phenotype, obesogenic diet
- MeSH terms
- Actins, Adipose Tissue, Animals, Collagen, Fatty Liver, Female, Lactation, Mice, Inbred C57BL, Milk, Obesity, Pregnancy, Pregnancy Complications, Prenatal Exposure Delayed Effects, Tumor Necrosis Factor-alpha, Signal Transduction, Interleukin-6, Gene Expression, Receptors, Adrenergic, alpha-1, Leptin, Collagen Type I, Metabolic Syndrome, Mice
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