Protein malnutrition during fetal programming induces fatty liver in adult male offspring rats

Campisano, Sabrina; Echarte, Stella Maris; Podaza, Enrique; Chisari, Andrea N.

doi:10.1007/s13105-017-0549-1

Cited by 10 publications

(4 citation statements)

References 45 publications

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“…Increased ALT levels reveal hepatocellular damage and are strongly correlated with liver fat content [81], being commonly used as a marker of NAFLD (non-alcoholic fatty liver disease). Low protein diet in rats showed a similar pattern with increased hepatic enzyme levels in offspring adult male rats [82]. Then, our results suggest that altered metabolic parameters found in fetuses could be reverted to physiological levels when progeny is fed ad libitum after birth, although some hepatic changes persist.…”

Section: Discussionsupporting

confidence: 67%

Gestation Food Restriction and Refeeding Compensate Maternal Energy Status and Alleviate Metabolic Consequences in Juvenile Offspring in a Rabbit Model

et al. 2021

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Nutritional status during gestation can influence mother and offspring metabolism. Undernutrition in pregnancy affects women in both western and developing countries, and it is associated with a high prevalence of chronic diseases in later life. The present work was conducted in the rabbit model, as a longitudinal study, to examine the effect of food restriction during early and mid-gestation, and re-feeding ad libitum until the end of pregnancy on metabolic status and body reserves of mother and, its association with development and metabolism of fetuses and female offspring to the juvenile stage. Little changes in live body weight (LBW), compensatory feed intake, similar body reserves, and metabolism were observed in dams. Placenta biometry and efficiency were slightly affected, but fetal BW and phenotype were not modified. However, hyperinsulinemia, insulin resistance, and hypertriglyceridemia were demonstrated in pre-term fetuses. In the juvenile period, these changes were not evidenced, and a similar pattern of growth and serum metabolic parameters in offspring of food-restricted mothers were found, except in serum aminotransferases levels, which increased. These were associated with higher liver fibrosis. Maternal food restriction in the early and mid-pregnancy followed by re-feeding in our rabbit model established a compensatory energy status in dams and alleviated potential long-term consequences in growth and metabolism in the offspring, even if fetal metabolism was altered.

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Section: Discussionsupporting

confidence: 67%

Gestation Food Restriction and Refeeding Compensate Maternal Energy Status and Alleviate Metabolic Consequences in Juvenile Offspring in a Rabbit Model

et al. 2021

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“…There are also reductions in the abundance of AKT proteins (total and activated/phosphorylated) in the liver of offspring exposed to hypoxia during gestation that are exposed by feeding a high-fat diet postnatally [122,124]. The levels of the INSR and phosphorylated AKT are instead elevated in the liver of offspring exposed to maternal protein restriction [76,80], even though these offspring are insulin resistant [80]. Together, these findings illustrate that there can be a disconnect between hepatic and body insulin sensitivity.…”

Section: Hepatic Insulin Sensitivitymentioning

confidence: 99%

“…In offspring exposed to suboptimal maternal environments including undernutrition, protein restriction, high-fat diet, hypoxia and dexamethasone treatment, hepatic and circulating lipids, such as cholesterol are increased [ 61 , 68 , 69 , 73 , 74 , 76 , 86 , 89 , 99 , 108 , 109 , 111 , 122 , 124 ]. Dysregulated hepatic lipid metabolism and an increase in circulating lipids are associated in the development of metabolic disease.…”

Section: Hepatic Lipid Metabolismmentioning

confidence: 99%

Molecular mechanisms governing offspring metabolic programming in rodent models of in utero stress

Christoforou

Sferruzzi‐Perri

2020

Cell. Mol. Life Sci.

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The results of different human epidemiological datasets provided the impetus to introduce the now commonly accepted theory coined as 'developmental programming', whereby the presence of a stressor during gestation predisposes the growing fetus to develop diseases, such as metabolic dysfunction in later postnatal life. However, in a clinical setting, human lifespan and inaccessibility to tissue for analysis are major limitations to study the molecular mechanisms governing developmental programming. Subsequently, studies using animal models have proved indispensable to the identification of key molecular pathways and epigenetic mechanisms that are dysregulated in metabolic organs of the fetus and adult programmed due to an adverse gestational environment. Rodents such as mice and rats are the most used experimental animals in the study of developmental programming. This review summarises the molecular pathways and epigenetic mechanisms influencing alterations in metabolic tissues of rodent offspring exposed to in utero stress and subsequently programmed for metabolic dysfunction. By comparing molecular mechanisms in a variety of rodent models of in utero stress, we hope to summarise common themes and pathways governing later metabolic dysfunction in the offspring whilst identifying reasons for incongruencies between models so to inform future work. With the continued use and refinement of such models of developmental programming, the scientific community may gain the knowledge required for the targeted treatment of metabolic diseases that have intrauterine origins.

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“…Hypertension is not the only cardiovascular risk factor that has been observed in offspring exposed to severe protein restriction in utero: insulin resistance [73], reduced insulin secretion [74] and insulin signaling deregulation [75], reduced pulmonary compliance and higher tissue elastance [76], altered lipid metabolism [77], fatty liver disease [78], cardiac fibrosis [79] and cardiac oxidative stress [80], muscle fiber and neuromuscular junction changes [81], metabolic syndrome [82], altered fat distribution [83], increased susceptibility to vascular injury [84], and alteration of coagulation factors [85] have all been described.…”

Section: Models Of Protein Deprivation During Pregnancy In Rodents Anmentioning

confidence: 99%

Of Mice and Men: The Effect of Maternal Protein Restriction on Offspring’s Kidney Health. Are Studies on Rodents Applicable to Chronic Kidney Disease Patients? A Narrative Review

et al. 2020

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In the almost 30 years that have passed since the postulation of the “Developmental Origins of Health and Disease” theory, it has been clearly demonstrated that a mother’s dietary habits during pregnancy have potential consequences for her offspring that go far beyond in utero development. Protein malnutrition during pregnancy, for instance, can cause severe alterations ranging from intrauterine growth retardation to organ damage and increased susceptibility to hypertension, diabetes mellitus, cardiovascular diseases and chronic kidney disease (CKD) later in life both in experimental animals and humans. Conversely, a balanced mild protein restriction in patients affected by CKD has been shown to mitigate the biochemical derangements associated with kidney disease and even slow its progression. The first reports on the management of pregnant CKD women with a moderately protein-restricted plant-based diet appeared in the literature a few years ago. Today, this approach is still being debated, as is the optimal source of protein during gestation in CKD. The aim of this report is to critically review the available literature on the topic, focusing on the similarities and differences between animal and clinical studies.

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Protein malnutrition during fetal programming induces fatty liver in adult male offspring rats

Cited by 10 publications

References 45 publications

Gestation Food Restriction and Refeeding Compensate Maternal Energy Status and Alleviate Metabolic Consequences in Juvenile Offspring in a Rabbit Model

Gestation Food Restriction and Refeeding Compensate Maternal Energy Status and Alleviate Metabolic Consequences in Juvenile Offspring in a Rabbit Model

Molecular mechanisms governing offspring metabolic programming in rodent models of in utero stress

Of Mice and Men: The Effect of Maternal Protein Restriction on Offspring’s Kidney Health. Are Studies on Rodents Applicable to Chronic Kidney Disease Patients? A Narrative Review

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