Intrauterine metabolic programming alteration increased susceptibility to non-alcoholic adult fatty liver disease in prenatal caffeine-exposed rat offspring

Wang, Linlong; Shen, Lang; Ping, Jie; Zhang, Li; Liu, Zhongfen; Wu, Yong; Liu, Yansong; Huang, Hegui; Chen, Liaobin; Wang, Hui

doi:10.1016/j.toxlet.2013.11.006

Cited by 64 publications

(31 citation statements)

References 28 publications

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“…Moreover, other studies and our results indicated that female rat offspring with IUGR were more susceptible to diet-induced dyslipidaemia (37)(38)(39) . Therefore, we chose female rats as the research subjects in this study.…”

supporting

confidence: 76%

Prenatal food restriction induces poor-quality articular cartilage in female rat offspring fed a post-weaning high-fat diet and its intra-uterine programming mechanisms

Tan

et al. 2016

Br J Nutr

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Epidemiological data show that osteoarthritis (OA) is significantly associated with lower birth weight, and that OA may be a type of fetaloriginated adult disease. The present study aimed to investigate the prenatal food-restriction (PFR) effect on the quality of articular cartilage in female offspring to explore the underlying mechanisms of fetal-originated OA. Maternal rats were fed a restricted diet from gestational day (GD) 11 to 20 to induce intra-uterine growth retardation. Female fetuses and female adult offspring fed a post-weaning high-fat diet were killed at GD20 and postnatal week 24, respectively. Serum and knee cartilage samples from fetuses and adult female offspring were collected and examined for cholesterol metabolism and histology. Fetal serum corticosterone and insulin-like growth factor-1 (IGF-1) in the PFR group were lower than those of the control, but the serum cholesterol level was not changed. The lower expression of IGF-1 in the PFR group lasted into adulthood. The expression of extracellular matrix (ECM) genes, including type II collagen, aggrecan and cholesterol efflux genes including liver X receptor, were significantly induced, but the ATP-binding-cassette transporter A1 was unchanged. PFR could induce a reduction in ECM synthesis and impaired cholesterol efflux in female offspring, and eventually led to poor quality of articular cartilage and OA.

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supporting

confidence: 76%

Prenatal food restriction induces poor-quality articular cartilage in female rat offspring fed a post-weaning high-fat diet and its intra-uterine programming mechanisms

Tan

et al. 2016

Br J Nutr

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“…Using the dose conversion between humans and rats (human:rat 1:6.17) (Reagan-Shaw et al, 2008), the dose of 120 mg/kg·d in the present study is about 4 times higher than the reported data (Boylan et al, 2008;Fenster et al, 1991). Furthermore, the caffeine concentration in maternal blood was 254 ± 11 μM (49 ± 2 μg/ml) after intake of 120 mg/kg·d caffeine in our studies (Wang et al, 2013), which is only 1.6 times higher than the clinical signs of intoxication (~30 μg/ml), but did not reach the dose with fatalities (~80 μg/ml). In our previous studies (Xu et al, 2012b), we had used 20, 60 and 180 mg/kg·d of caffeine and observed some multi-index changes in 20 mg/kg·d and a clear dose-effect relationship.…”

Section: Contents Lists Available At Sciencedirectcontrasting

confidence: 57%

Prenatal caffeine ingestion induces transgenerational neuroendocrine metabolic programming alteration in second generation rats

Luo¹,

Deng²,

Liu³

et al. 2014

Toxicology and Applied Pharmacology

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“…Prenatal caffeine exposure :. Prenatal caffeine (120 mg/kg) administration in rats on gestational days 11–20 resulted in low birth weight and increased susceptibility to non-alcoholic fatty liver disease as adults when introduced to a high fat diet (Wang et al, 2014). Prenatal benzodiazepine exposure : Prenatal exposure to benzodiazepine ligands over gestational days 14–20 resulted in increased levels of thiobarbituric acid-reactive material, decreased intracellular pH, and significant change in phosphocreatine utilization in the brain when compared with controls; these changes were undetectable until early adulthood.…”

Section: Advancements In the Dohad Fieldmentioning

confidence: 99%

Alcohol-Induced Developmental Origins of Adult-Onset Diseases

Lunde

Washburn

Golding

et al. 2016

Alcohol Clin Exp Res

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Fetal alcohol exposure may impair growth, development, and function of multiple organ systems, and is encompassed by the term Fetal Alcohol Spectrum Disorders (FASD). Research has so far focused on the mechanisms, prevention, and diagnosis of FASD, while the risk for adult-onset chronic diseases in individuals exposed to alcohol in utero is not well explored. David Barker’s hypothesis on Developmental Origins of Health and Disease (DOHaD) suggests that insults to the milieu of the developing fetus program it for adult-development of chronic diseases. In the 25 years since the introduction of this hypothesis, epidemiological and animal model studies have made significant advancements in identifying in utero developmental origins of chronic adult-onset diseases affecting cardiovascular, endocrine, musculoskeletal, and psycho-behavioral systems. Teratogen exposure is an established programming agent for adult diseases, and recent studies suggest that prenatal alcohol exposure correlates with adult-onset of neuro-behavioral deficits, cardiovascular disease, endocrine dysfunction, nutrient homeostasis instability, warranting additional investigation of alcohol-induced DOHaD, as well as patient follow-up well into adulthood for affected individuals. In utero epigenetic alterations during critical periods of methylation is a key potential mechanism for programming and susceptibility of adult-onset chronic diseases, with imprinted genes affecting metabolism being critical targets. Additional studies in epidemiology, phenotypic characterization in response to timing, dose and duration of exposure, as well as elucidation of mechanisms underlying FASD-DOHaD inter-relation are thus needed to clinically define chronic disease associated with prenatal alcohol exposure. These studies are critical to establish interventional strategies that decrease incidence of these adult-onset diseases and promote healthier aging among individuals affected with FASD.

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Intrauterine metabolic programming alteration increased susceptibility to non-alcoholic adult fatty liver disease in prenatal caffeine-exposed rat offspring

Cited by 64 publications

References 28 publications

Prenatal food restriction induces poor-quality articular cartilage in female rat offspring fed a post-weaning high-fat diet and its intra-uterine programming mechanisms

Prenatal food restriction induces poor-quality articular cartilage in female rat offspring fed a post-weaning high-fat diet and its intra-uterine programming mechanisms

Prenatal caffeine ingestion induces transgenerational neuroendocrine metabolic programming alteration in second generation rats

Alcohol-Induced Developmental Origins of Adult-Onset Diseases

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