Maternal high-fat intake predisposes nonalcoholic fatty liver disease in C57BL/6 offspring

Gregório, Bianca Martins; Souza-Mello, Vanessa; Carvalho, Jorge José de; Mandarim-de-Lacerda, Carlos Alberto; Águila, Márcia Barbosa

doi:10.1016/j.ajog.2010.06.042

Cited by 100 publications

(98 citation statements)

References 31 publications

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“…Another study of chronic administration a HF diet both before and during pregnancy resulted in decreased fetal birth weight in rodents, which suggests some degree of placental insufficiency (Howie et al). The present findings are in agreement with previous results of our laboratory as offspring from HF-fed mothers were smaller at birth but has a catch-up growth, showing overweight at weaning (Gregorio et al;Bringhenti et al;Graus-Nunes et al, 2015).…”

Section: Discussionsupporting

confidence: 94%

“…A high fat (HF) fed mothers favors the early onset of obesity and its comorbidities in the offspring even when there is balanced nutrition in their postweaning life (Gregorio et al, 2010). Hyperinsulinemia seems to mediate this metabolic disruption as it is able to transpose placenta and the liver, as a central organ of metabolism, has emerged as a potent target to excessive lipids during intrauterine life (Yessoufou & Moutairou, 2011).…”

Section: Introductionmentioning

confidence: 99%

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Both Hepatic Lipogenesis and Beta-Oxidation are Altered in Offspring of Mothers Fed a High-Fat Diet in the First Two Generations (F1 and F2)

et al. 2015

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SUMMARY:The high fat (HF) fed mothers may program susceptibility in offspring to chronic diseases and affect subsequent generations. The present study evaluated the liver structure in adulthood, focusing on the F1 and F2 generations. Females C57BL/6 (F0) were fed standard chow (SC) or HF diet (8 weeks) prior to mating and during the gestation and lactation to provide the F1 generation (SC-F1 and HF-F1). All other mothers and offspring fed SC. At 3 months old, F1 females were mated to produce the F2 generation (SC-F2 and HF-F2). The liver was kept in several fragments and prepared for histological analysis or frozen for biochemical and molecular analyzes. The F1 and F2 offspring were studied at 3 months old. HF-F1 had higher body mass (BM) compared to SC-F1 (P= 0.001), but not HF-F2 compared to SC-F2. HF-F1 had glucose intolerance when compared to SC-F1, but not HF-F2 compared to SC-F2. HF-F1 (P= 0.009) and HF-F2 (P= 0.03) showed hyperinsulinemia compared to their counterparts. Both groups HF-F1 and HF-F2 showed more steatosis than the SC counterparts (F1 and F2, P<0.0001). HF-F1 showed increased expression of PPAR-gamma and SREBP1-c compared to SC-F1 (P= 0.01). HF-F2 showed increased PPAR-gamma expression compared to SC-F2 (P= 0.04). In conclusion, HF-fed mother impairs both lipogenesis and beta-oxidation pathways in F1 through upregulation of PPAR-gamma and downregulation of PPAR-alpha. In F2, the only lipogenesis is enhanced, but it causes a disrupted PPAR balance, favoring the hepatic lipid accumulation and impaired metabolism in these animals that were not directly exposed to the maternal HF intake.

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Section: Discussionsupporting

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Both Hepatic Lipogenesis and Beta-Oxidation are Altered in Offspring of Mothers Fed a High-Fat Diet in the First Two Generations (F1 and F2)

et al. 2015

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“…69 Mice offspring of dams with high fat intake during pregnancy show insulin resistance, reduced glucose transporter-2 expression and hepatic steatosis. 70,71 Consistently, in utero exposure to high fat diet programs the expression and epigenetics of hepatic phosphoenolpyruvate carboxykinase gene in offspring rats 72 and affects hepatic energy sensing pathways in a porcine model. 73 Finally, in heterozygous leptin receptor-deficient mice, the exposure to maternal gestational diabetes mellitus induces hepatic insulin resistance in the adult offspring.…”

Section: Evidence For Liver Programmingmentioning

confidence: 96%

Effect of intrauterine growth retardation on liver and long-term metabolic risk

Cianfarani

Agostoni

Bedogni³

et al. 2012

Int J Obes

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Intrauterine growth retardation predisposes toward long-term morbidity from type 2 diabetes and cardiovascular disease. To explain this association, the concept of programming was introduced to indicate a process whereby a stimulus or insult at a critical period of development has lasting or lifelong consequences on key endocrine and metabolic pathways. Subtle changes in cell composition of tissues, induced by suboptimal conditions in utero, can influence postnatal physiological functions. There is increasing evidence, suggesting that liver may represent one of the candidate organs targeted by programming, undergoing structural, functional and epigenetic changes following exposure to an unfavorable intrauterine environment. The aim of this review is to provide insights into the molecular mechanisms underlying liver programming that contribute to increase the cardiometabolic risk in subjects with intrauterine growth restriction.

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“…Several obesogenic models, primarily in the rodent, show a relatively common phenotype of metabolic disorders in offspring, although the magnitude of effects differs with the timing of the nutritional challenge and diet composition [84] . A maternal cafeteria or high fat diet has been shown to induce obesity, insulin and leptin resistance [58,85,86] , hypertension [87][88][89] , hepatic steatosis and non-alcoholic fatty liver disease in offspring [90][91][92] . Even mild maternal overnutrition has been shown to induce increased adiposity, glucose intolerance and altered brain appetite regulators in offspring [93] .…”

Section: Maternal Obesitymentioning

confidence: 99%

Developmental programming of the metabolic syndrome - critical windows for intervention

Vickers

2011

WJG

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Metabolic disease results from a complex interaction of many factors, including genetic, physiological, behavioral and environmental influences. The recent rate at which these diseases have increased suggests that environmental and behavioral influences, rather than genetic causes, are fuelling the present epidemic. In this context, the developmental origins of health and disease hypothesis has highlighted the link between the periconceptual, fetal and early infant phases of life and the subsequent development of adult obesity and the metabolic syndrome. Although the mechanisms are yet to be fully elucidated, this programming was generally considered an irreversible change in developmental trajectory. Recent work in animal models suggests that developmental programming of metabolic disorders is potentially reversible by nutritional or targeted therapeutic interventions during the period of developmental plasticity. This review will discuss critical windows of developmental plasticity and possible avenues to ameliorate the development of postnatal metabolic disorders following an adverse early life environment.

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Maternal high-fat intake predisposes nonalcoholic fatty liver disease in C57BL/6 offspring

Cited by 100 publications

References 31 publications

Both Hepatic Lipogenesis and Beta-Oxidation are Altered in Offspring of Mothers Fed a High-Fat Diet in the First Two Generations (F1 and F2)

Both Hepatic Lipogenesis and Beta-Oxidation are Altered in Offspring of Mothers Fed a High-Fat Diet in the First Two Generations (F1 and F2)

Effect of intrauterine growth retardation on liver and long-term metabolic risk

Developmental programming of the metabolic syndrome - critical windows for intervention

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