Effect of diet in females (F1) from prenatally undernourished mothers on metabolism and liver function in the F2 progeny is sex-specific

Cisse, Ouma; Fajardy, I.; Delahaye, Fabien; Dickes, Anne; Montel, Valérie; Moitrot, Emmanuelle; Breton, Christophe; Vieau, Didier; Laborie, Christine

doi:10.1007/s00394-018-1794-y

Cited by 9 publications

(4 citation statements)

References 62 publications

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“…Additionally, while the F1 generation trended toward lower BMIs early in development, the F2 generation had higher BMI scores. In other studies considering underweight mothers and the weight gain of their offspring, maternal undernutrition improves the metabolic health of the next generation 52 and can lead to weight gain and obesity in the next generation 53 , much like what we observed in our overweight F2 generation compared to their underweight F1 mothers.…”

Section: Discussionsupporting

confidence: 83%

Characterization of the intergenerational impact of in utero and postnatal oxycodone exposure

et al. 2020

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Prescription opioid abuse during and after pregnancy is a rising public health concern. While earlier studies have documented that offspring exposed to opioids in utero have impaired neurodevelopment, a significant knowledge gap remains in comparing the overall development between offspring exposed in utero and postnatally. Adding a layer of complexity is the role of heredity in the overall development of these exposed offspring. To fill in these important knowledge gaps, the current study uses a preclinical rat model mimicking oxycodone (oxy) exposure in utero (IUO) and postnatally (PNO) to investigate comparative and intergenerational effects in the two different treatment groups. While significant phenotypic attributes were observed with the two treatments and across the two generations, RNA sequencing revealed alterations in the expression of key synaptic genes in the two exposed groups in both generations. RNA sequencing and post validation of genes using RT-PCR highlighted the differential expression of several neuropeptides associated with the hypocretin system, a system recently implicated in addiction. Further, behavior studies revealed anxiety-like behaviors and social deficits that persisted even in the subsequent generations in the two treatment groups. To summarize, our study for the first time reveals a new line of investigation on the potential risks associated with oxy use during and after pregnancy, specifically the disruption of neurodevelopment and intergenerational impact on behavior.

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Section: Discussionsupporting

confidence: 83%

Characterization of the intergenerational impact of in utero and postnatal oxycodone exposure

et al. 2020

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“…Based on the above, we can say that there is an alteration in gene expression that results in an elevated regulation of GFAP and inflammatory mediators, in addition to adipokine receptors, due to overweight/obesity [ 34 , 36 ]. These effects are derived from the defensive response of astrocytes to inflammatory action and injury, which also causes their morphological and functional remodeling, which can cause neuronal hypertrophy [ 37 ]. Debarba et al, in studies carried out in rats that at the neonatal level, showed underfeeding as well as overfeeding, which is generally known as neonatal malnutrition, causes morphological changes in the glia in addition to metabolism alterations that lead not only to increased GFAP expression but also increased expression of T cell protein tyrosine phosphatase (TCPTP) and alterations in connexin 30 expression, molecules related to the regulation of proinflammatory cytokines in the hypothalamic astrogliosis.…”

Section: Role Of Astrocytes In the Expression Of Glial Fibrillary Aci...mentioning

confidence: 99%

Trends in Gliosis in Obesity, and the Role of Antioxidants as a Therapeutic Alternative

et al. 2022

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Obesity remains a global health problem. Chronic low-grade inflammation in this pathology has been related to comorbidities such as cognitive alterations that, in the long term, can lead to neurodegenerative diseases. Neuroinflammation or gliosis in patients with obesity and type 2 diabetes mellitus has been related to the effect of adipokines, high lipid levels and glucose, which increase the production of free radicals. Cerebral gliosis can be a risk factor for developing neurodegenerative diseases, and antioxidants could be an alternative for the prevention and treatment of neural comorbidities in obese patients. Aim: Identify the immunological and oxidative stress mechanisms that produce gliosis in patients with obesity and propose antioxidants as an alternative to reducing neuroinflammation. Method: Advanced searches were performed in scientific databases: PubMed, ProQuest, EBSCO, and the Science Citation index for research on the physiopathology of gliosis in obese patients and for the possible role of antioxidants in its management. Conclusion: Patients with obesity can develop neuroinflammation, conditioned by various adipokines, excess lipids and glucose, which results in an increase in free radicals that must be neutralized with antioxidants to reduce gliosis and the risk of long-term neurodegeneration.

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“…A relationship between malnutrition and chronic diseases has been observed worldwide ( 1 ). Exponential evidence indicates that perinatal environmental factors, such as maternal malnutrition status, promote long-term effects on the metabolic phenotype of offspring ( 2 , 3 ); this process is known as metabolic programming. Epidemiological and experimental studies suggest that early life nutritional programming is associated with a higher risk for the development of cardiometabolic syndrome ( 4 – 6 ); an impaired capacity to maintain energy balance is not only limited to exposed individuals but also subsequent generations, even though nutritional conditions are favorable ( 7 ).…”

Section: Introductionmentioning

confidence: 99%

“…Lactation is a window of susceptibility due to the development and maturation of major organs and tissues, which determine the offspring’s metabolic phenotype ( 2 , 15 ). Thus, exposure to undernutrition during this period can affect metabolism and pancreatic function.…”

Section: Introductionmentioning

confidence: 99%

Protein restriction during lactation causes transgenerational metabolic dysfunction in adult rat offspring

Vargas

Martins²,

Matiusso³

et al. 2023

Front. Nutr.

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IntroductionProtein restriction during lactation can induce metabolic dysfunctions and has a huge impact on the offspring’s phenotype later in its life. We tested whether the effects of a maternal low-protein diet (LP) in rats can be transmitted to the F2 generation and increase their vulnerability to dietary insults in adulthood.MethodsFemale Wistar rats (F0) were fed either a low-protein diet (LP; 4% protein) during the first 2 weeks of lactation or a normal-protein diet (NP; 23% protein). The female offspring (F1 generation) were maintained on a standard diet throughout the experiment. Once adulthood was reached, female F1 offspring from both groups (i.e., NP-F1 and LP-F1) were bred to proven males, outside the experiment, to produce the F2 generation. Male F2 offspring from both groups (NP-F2 and LP-F2 groups) received a standard diet until 60 days old, at which point they received either a normal fat (NF; 4.5% fat) or a high fat diet (HF; 35% fat) for 30 days.ResultsAt 90 days old, LPNF-F2 offspring had increased lipogenesis and fasting insulinemia compared to NPNF-F2, without alteration in insulin sensitivity. HF diet caused increased gluconeogenesis and displayed glucose intolerance in LPHF-F2 offspring compared to LPNF-F2 offspring. Additionally, the HF diet led to damage to lipid metabolism (such as steatosis grade 3), higher body weight, fat pad stores, and hepatic lipid content.DiscussionWe concluded that an F0 maternal protein restricted diet during lactation can induce a transgenerational effect on glucose and liver metabolism in the F2 generation, making the offspring’s liver more vulnerable to nutritional injury later in life.

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Effect of diet in females (F1) from prenatally undernourished mothers on metabolism and liver function in the F2 progeny is sex-specific

Abstract: Maternal undernutrition during gestation (F0) improves the metabolic health of second-generation offspring with more beneficial effects in females.

Cited by 9 publications

References 62 publications

Characterization of the intergenerational impact of in utero and postnatal oxycodone exposure

Characterization of the intergenerational impact of in utero and postnatal oxycodone exposure

Trends in Gliosis in Obesity, and the Role of Antioxidants as a Therapeutic Alternative

Protein restriction during lactation causes transgenerational metabolic dysfunction in adult rat offspring

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