Early weaning induces programmed obesity in rats at adulthood through impairing fatty acid β-oxidation and cholesterol metabolism, which can be mitigated by leucine supplementation
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE203486 | GEO | 2024/01/01
REPOSITORIES: GEO
Similar Datasets
Project description:Early weaning induces programmed obesity in rats at adulthood through impairing fatty acid β-oxidation and cholesterol metabolism, which can be mitigated by leucine supplementation
| PRJNA840933 | ENA
Project description:Extracorporeal membrane oxygenation (ECMO) provides a rescue for children with severe cardiac failure. It has previously been shown that triiodothyronine (T3) improves cardiac function by modulating pyruvate oxidation during weaning. This study focused on fatty acid (FA) metabolism modulated by T3 for weaning from ECMO after cardiac injury. METHODS AND RESULTS: Nineteen immature piglets (9.1-15.3 kg) were separated into 3 groups with ECMO (6.5 h) and wean: normal circulation (Group-C); transient coronary occlusion (10 min) for ischemia-reperfusion (IR) followed by ECMO (Group-IR); and IR with T3 supplementation (Group-IR-T3). 13-Carbon ((13)C)-labeled lactate, medium-chain and long-chain FAs, was infused as oxidative substrates. Substrate fractional contribution (FC) to the citric acid cycle was analyzed by(13)C-nuclear magnetic resonance. ECMO depressed circulating T3 levels to 40% of the baseline at 4 h and were restored in Group-IR-T3. Group-IR decreased cardiac power, which was not fully restorable and 2 pigs were lost because of weaning failure. Group-IR also depressed FC-lactate, while the excellent contractile function and energy efficiency in Group-IR-T3 occurred along with a marked FC-lactate increase and [adenosine triphosphate]/[adenosine diphosphate] without either decreasing FC-FAs or elevating myocardial oxygen consumption over Group-C or -IR.T3 releases inhibition of lactate oxidation following IR injury without impairing FA oxidation. These findings indicate that T3 depression during ECMO is maladaptive, and that restoring levels improves metabolic flux and enhances contractile function during weaning.
| S-EPMC5570456 | biostudies-other
Project description:Effect of post-weaning glutamine and/or milk supplementation on pig growth and intestinal development
| PRJEB76745 | ENA
Project description:Seaweeds, including the green Ulva lactuca, can potentially reduce competition between feed, food, and fuel. They can also contribute to the improved development of weaned piglets. However, their indigestible polysaccharides of the cell wall pose a challenge. This can be addressed through carbohydrase supplementation, such as the recombinant ulvan lyase. The objective of our study was to assess the muscle metabolism of weaned piglets fed with 7% U. lactuca and 0.01% ulvan lyase supplementation, using an integrated transcriptomics (RNA-seq) and proteomics (LC-MS) approach.
2024-04-03 | GSE252125 | GEO
Project description:Background: Consumption of high fat diets has negative impacts on health and well-being, some of which may be epigenetically regulated. Selenium and folate are two compounds which influence epigenetic mechanisms. We investigated the hypothesis that post-weaning supplementation with adequate levels of selenium and folate in mouse offspring fed a high fat, low selenium and folate diet during gestation and lactation will lead to epigenetic changes of potential importance for long-term health. Female offspring of mothers fed the experimental diet were either maintained on this diet (HF-low-low), or weaned onto a high-fat diet with sufficient levels of selenium and folate (HF-low-suf), for 8 weeks. Gene and protein expression, DNA methylation, and histone modifications were measured in colon and liver of female offspring. Results: Adequate levels of selenium and folate post-weaning affected gene expression in colon and liver of offspring, including decreasing Slc2a4 gene expression. Protein expression was only altered in the liver. There was no effect of adequate levels of selenium and folate on global histone modifications in the liver. Global liver DNA methylation was decreased in mice switched to adequate levels of selenium and folate, but there was no effect on methylation of specific CpG sites within the Slc2a4 gene in liver. Conclusions: Post-weaning supplementation with adequate levels of selenium and folate in female offspring of mice fed high-fat diets during gestation and lactation can alter global DNA methylation in liver. This may be one mechanism by which the negative effects of a poor diet during early life can be ameliorated. Further research is required to establish what role epigenetic changes play in mediating observed changes in gene and protein expression, and the relevance of these changes to health.
2013-06-01 | GSE43038 | GEO
Project description:The weaning process has been identified as being associated with stress, weight loss and stereotypies. To limit these problems, some breeders wean the foals gradually. This article presents the effects of a progressive weaning on various physiological parameters (cortisol, C reactive protein, length of telomeres) and on the blood transcriptome, among the foals and the mares. Results indicate that a progressive weaning has beneficial short-term effects in foals, and that in the longer term the foals weaned abruptly have compensated this gap. In mothers, the beneficial effects of the progressive weaning are less important.
2018-06-01 | GSE97907 | GEO
Project description:The weaning process has been identified as being associated with stress, weight loss and stereotypies. To limit these problems, some breeders wean the foals gradually. This article presents the effects of a progressive weaning on various physiological parameters (cortisol, C reactive protein, length of telomeres) and on the blood transcriptome, among the foals and the mares. Results indicate that a progressive weaning has beneficial short-term effects in foals, and that in the longer term the foals weaned abruptly have compensated this gap. In mothers, the beneficial effects of the progressive weaning are less important.
2018-06-01 | GSE97906 | GEO
Project description:Zinc deficiency during pregnancy and postnatal life can adversely affect the health and predispose to an increased risk of developing human diseases at adulthood. The present study was designed to evaluate whether dietary zinc deficiency or supplementation during the pregnancy, lactation and juvenile stages interferes with the development of mammary tumors induced by 7,12-dimethylbenzanthracene (DMBA) in female Sprague-Dawley (SD) rats. Pregnant females SD were allocated into three groups: dams received diets containing adequate (35 mg/Kg chow), deficient (3 mg/Kg chow) or supplemented (180 mg/Kg chow) zinc levels during gestational day 10 (GD 10) until the litters weaning. Female offspring were allocated into three groups and received the same diets as their dams until postnatal day (PND) 51. At PND 51, females SD (n=16 each group) received a single dose of DMBA (50 mg/kg, ig) for initiation of mammary carcinogenesis, adequate zinc diets and were euthanized at PND 180. Tumors samples were collected and processed for histological evaluation and microarray analysis. Dietary zinc deficiency induced a significant reduction in female offspring body weight evolution at parturition, weaning and pubertal phases. At late in life, the early in life dietary zinc deficiency or supplementation did not alter the latency, incidence, multiplicity and volume or histological types of mammary tumors in relation to the adequate zinc group, and changed the expression of a small amount of genes. The present findings indicate that early-in life dietary zinc deficiency or supplementation did not significantly modify the susceptibility to development of mammary tumors induced by DMBA.
2017-04-08 | GSE86270 | GEO
Project description:Background: Low protein intake is associated with various negative health outcomes at any life stage. When diets do not contain sufficient protein, phosphorus availability is compromised because proteins are the major sources of phosphorus. However, whether mineral phosphorus supplementation mitigates this problem is unknown, to our knowledge. Objective: Our goal was to determine the impact of dietary phosphorus supplementation on food intake, weight gain, energy efficiency, body composition, blood metabolites, and liver histology in rats fed a low-protein diet for 9 wk. Methods: Forty-nine 6-wk-old male Sprague-Dawley rats were randomly allocated to 5 groups and consumed 5 isocaloric diets ad libitum that varied only in protein (egg white) and phosphorus concentrations for 9 wk. The control group received a 20% protein diet with 0.3% P (NP-0.3P). The 4 other groups were fed a low-protein (10%) diet with a phosphorus concentration of 0.015%, 0.056%, 0.1%, or 0.3% (LP-0.3P). The rats' weight, body and liver composition, and plasma biomarkers were then assessed. Results: The addition of phosphorus to the low-protein diet significantly increased food intake, weight gain, and energy efficiency, which were similar among the groups that received 0.3% P (LP-0.3P and NP-0.3P) regardless of dietary protein content. In addition, phosphorus supplementation of low-protein diets reduced plasma urea nitrogen and increased total body protein content (defatted). Changes in food intake and efficiency, body weight and composition, and plasma urea concentration were highly pronounced at a dietary phosphorus content <0.1%, which may represent a critical threshold. Conclusions: The addition of phosphorus to low-protein diets improved growth measures in rats, mainly as a result of enhanced energy efficiency. A dietary phosphorus concentration of 0.3% mitigated detrimental effects of low-protein diets on growth parameters.
| S-EPMC5998359 | biostudies-literature