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Offspring of Mothers Fed a High Fat Diet Display Hepatic Cell Cycle Inhibition and Associated Changes in Gene Expression and DNA Methylation  [PDF]
Kevin J. Dudley, Deborah M. Sloboda, Kristin L. Connor, Jacques Beltrand, Mark H. Vickers
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0021662
Abstract: The association between an adverse early life environment and increased susceptibility to later-life metabolic disorders such as obesity, type 2 diabetes and cardiovascular disease is described by the developmental origins of health and disease hypothesis. Employing a rat model of maternal high fat (MHF) nutrition, we recently reported that offspring born to MHF mothers are small at birth and develop a postnatal phenotype that closely resembles that of the human metabolic syndrome. Livers of offspring born to MHF mothers also display a fatty phenotype reflecting hepatic steatosis and characteristics of non-alcoholic fatty liver disease. In the present study we hypothesised that a MHF diet leads to altered regulation of liver development in offspring; a derangement that may be detectable during early postnatal life. Livers were collected at postnatal days 2 (P2) and 27 (P27) from male offspring of control and MHF mothers (n = 8 per group). Cell cycle dynamics, measured by flow cytometry, revealed significant G0/G1 arrest in the livers of P2 offspring born to MHF mothers, associated with an increased expression of the hepatic cell cycle inhibitor Cdkn1a. In P2 livers, Cdkn1a was hypomethylated at specific CpG dinucleotides and first exon in offspring of MHF mothers and was shown to correlate with a demonstrable increase in mRNA expression levels. These modifications at P2 preceded observable reductions in liver weight and liver:brain weight ratio at P27, but there were no persistent changes in cell cycle dynamics or DNA methylation in MHF offspring at this time. Since Cdkn1a up-regulation has been associated with hepatocyte growth in pathologic states, our data may be suggestive of early hepatic dysfunction in neonates born to high fat fed mothers. It is likely that these offspring are predisposed to long-term hepatic dysfunction.
Keisuke Ishikura,Teruo Miyazaki,Song-Gyu Ra,Shoji Endo
Journal of Sports Science and Medicine , 2011,
Abstract: Taurine included abundantly in skeletal muscle, particularly in the slow-twitch fibers, enhances exercise performance. However, the exact mechanisms for this effect have been unclear. The present study investigated the influence of taurine supplementation on amino acids profile in skeletal muscles as one of mechanisms in the enhancement of exercise performance induced by taurine. In the rats that received taurine solution, amino acids concentrations were comprehensively quantified in two portions with different fiber compositions in the fast-twitch fiber dominant (FFD) gastrocnemius muscle after 2 weeks, and in the gastrocnemius and additional other FFD muscles, liver, and plasma with exhausted exercise after 3 weeks. In the FFD muscles after 2 weeks, a common phenomenon that decreased concentrations of threonine (-16%), serine (-15~-16%), and glycine (-6~-16%) were observed, and they are categorized in the pyruvate precursors for hepatic gluconeogenesis rather than biosynthesis, polar, and side-chain structures. The decreases in the three amino acids were significantly emphasized after an additional week of taurine supplementation in the FFD muscles (p values in three amino acids in these tissues were less than 0.001-0.05), but not in the liver and plasma, accompanied with significantly increase of running time to exhaustion (p <0.05). In contrast, the three amino acids (threonine and serine; p < 0.05, glycine; p < 0.01) and alanine (p < 0.01) in the liver were significantly decreased and increased, respectively, following the exhaustive exercise. In conclusion, the taurine-induced reductions of these amino acids in skeletal muscle might be one of the mechanisms which underpin the enhancement of exercise performance by taurine
Maternal Methyl Donors Supplementation during Lactation Prevents the Hyperhomocysteinemia Induced by a High-Fat-Sucrose Intake by Dams  [PDF]
Paul Cordero,Fermin I. Milagro,Javier Campion,J. Alfredo Martinez
International Journal of Molecular Sciences , 2013, DOI: 10.3390/ijms141224422
Abstract: Maternal perinatal nutrition may program offspring metabolic features. Epigenetic regulation is one of the candidate mechanisms that may be affected by maternal dietary methyl donors intake as potential controllers of plasma homocysteine levels. Thirty-two Wistar pregnant rats were randomly assigned into four dietary groups during lactation: control, control supplemented with methyl donors, high-fat-sucrose and high-fat-sucrose supplemented with methyl donors. Physiological outcomes in the offspring were measured, including hepatic mRNA expression and global DNA methylation after weaning. The newborns whose mothers were fed the obesogenic diet were heavier longer and with a higher adiposity and intrahepatic fat content. Interestingly, increased levels of plasma homocysteine induced by the maternal high-fat-sucrose dietary intake were prevented in both sexes by maternal methyl donors supplementation. Total hepatic DNA methylation decreased in females due to maternal methyl donors administration, while Dnmt3a hepatic mRNA levels decreased accompanying the high-fat-sucrose consumption. Furthermore, a negative association between Dnmt3a liver mRNA levels and plasma homocysteine concentrations was found. Maternal high-fat-sucrose diet during lactation could program offspring obesity features, while methyl donors supplementation prevented the onset of high hyperhomocysteinemia. Maternal dietary intake also affected hepatic DNA methylation metabolism, which could be linked with the regulation of the methionine-homocysteine cycle.
Natural taurine promotes apoptosis of human hepatic stellate cells in proteomics analysis  [cached]
Xin Deng, Jian Liang, Zhi-Xiu Lin, Fa-Sheng Wu, Ya-Ping Zhang, Zhi-Wei Zhang
World Journal of Gastroenterology , 2010,
Abstract: AIM: To study the differential expression of proteins between natural taurine treated hepatic stellate cells and controls, and investigate the underlying regulatory mechanism of natural taurine in inhibiting hepatic fibrosis.METHODS: A proteomic strategy combining two-dimensional gel electrophoresis and ultra-performance liquid chromatography-electrospray ionization-tandem mass spectrometry (UPLC-ESI-MS/MS) was used to study the differential expression of proteins and Western blotting was used to validate the results. Gene ontology (GO) method was utilized to analyze the functional enrichment of differentially expressed proteins. Flow cytometry was performed to compare the apoptosis rate between taurine-treated and untreated hepatic stellate cells (HSCs).RESULTS: Nineteen differentially expressed proteins (11 up-regulated and 8 down-regulated) were identified by 2D/MS, and the expression profiles of GLO1 and ANXA1 were validated by Western blotting. GO analysis found that these differentially expressed proteins were enriched within biological processes such as “cellular apoptosis”, “oxidation reaction” and “metabolic process” in clusters. Flow cytometric analysis showed that taurine-treated HSCs had a significantly increased apoptosis rate when compared with the control group.CONCLUSION: Natural taurine can promote HSC apoptosis so as to inhibit hepatic fibrosis.
Effects of taurine supplementation on response of the cardiac injury biomarkers to Bruce diagnostic protocol in patients with heart failure  [cached]
Valiollah Dabidi Roshan,Mahshid Kadkhodai Khalafi,Sirrus Choobineh
Koomesh , 2011,
Abstract: Introduction: Taurine has an important role in regulating the cardiac electric activity and anti-arrhythmias effects and it may improve heart failure. This study was designed to investigate the effect of taurine supplementation on response of the cardiac injury biomarkers to Bruce diagnostic protocol and exhaustive time in patients with heart failure. Materials and Methods: Sixteen patients between 50 to 65 years with heart failure, who were classified in II and III classes, were randomly divided into the taurine and placebo groups. The taurine received 1.5g taurine supplement 3 times a day in 500 milligram capsules and the placebo group consume starch capsules for two weeks. Plasma taurine, cardiac troponin I and CPK-MB concentrations were measured before and after taurine supplementation and also in each stage before and after performing the Bruce protocol (totally, 4 stages). Plasma taurine, cardiac troponin I and CPK-MB concentrations were detected by using HPLC, ELISA and immunological methods, respectively. Results: Results showed that Bruce protocol led to significant increase in cardiac troponin I and CPK-MB concentrations and significant decrease in plasma taurine. Furthermore, taurine supplemen--------tation results in the resting level decrease of cardiac troponin I and CPK-MB. Also, taurine supplementation led to increase exhaustive time in comparison with placebo group and before supplementation stage, but it couldn't completely create preventive effect on cardiac troponin I and CPK-MB concentration after the Bruce protocol. Conclusion: Taurine supplementation in patients with heart failure who are taking standard medical treatment can increase their exercise capacity. Furthermore, our study supports this idea that the use of taurine supplementation can be recommended to people who suffer from cardiac events as a preventive strategy.
A reproductive history of mothers with spina bifida offspring-a new look at old issues
Thomas L Farley
Fluids and Barriers of the CNS , 2006, DOI: 10.1186/1743-8454-3-10
Abstract: Data from 271 mothers was collected by interview 18.3 mean years after the affected child's birth. Data analysis was by χ-square, Fisher exact test and t test with a p value less than 0.05 considered significant.Females made up 56.5% of affected offspring (probands) and 53.1% of unaffected offspring. The spina bifida and anencephaly recurrence rate was 4.0%. The twinning rate was 8.6/1000 live births. 24.4% of mothers had a history of spontaneous abortion and the rate varied by pregnancy order from 87 to 185/1000 live births. Duration of pregnancies subsequent to probands was shorter for female than male probands. Mean birth weight of probands with high lesions exceeded those with low lesions. A spontaneous abortion preceded female probands more often than males as compared to live births. Affected males with high lesions conceived by white mothers were at greater risk to be spontaneously aborted. Previous inter-gestational interval for mothers with no history of spontaneous abortion was longer for probands than unaffected offspring but not for mothers with a history of spontaneous abortion.Overall, and for every major subgroup of these mothers, more affected and unaffected female than male offspring were born. Differences by gender and lesion level among probands and between probands and unaffected offspring were consistent with an etiology of unknown genetic factors, hormonal and/or immune system factors.Spina bifida is a disorder of the cerebrospinal fluid system resulting from a failure of neural tube closure in the fetus and associated with accompanying deformities leading to hydrocephalus. Over the past twenty-five years, a number of studies [1] have demonstrated that environmental and genetic factors play an important part in neural tube defect (NTD) etiology. Dietary folic acid fortification [2] and supplementation [3], in particular, have shown success as preventative measures. However, despite such progress, much is still unknown about the complex, multi-f
PROLACTIN-Deficiency in Adult Offspring of Diabetic Mothers  [PDF]
Leona Aerts,Rieta Van Bree,F. André Van Assche
Experimental Diabetes Research , 2000, DOI: 10.1155/edr.2000.31
Abstract: Maternal diabetes induces fetal alterations, resulting in lasting consequences for the glucose tolerance of the offspring over several generations. In our experimental rat model, circulating prolactin, oestradiol, progesterone and corticosterone levels, known to influence insulin secretion and action, are determined in plasma of female adult offspring of mildly and severely diabetic mothers. Prolactin and progesterone levels are equally low in both groups as compared to controls, stressing the involvement of the CNS in the transgeneration effect; oestradiol and corticosterone levels are normal. No correlation is found between these hormonal alterations and the known differences in glucose tolerance.
Effects of Nutritional Supplementation during Pregnancy on Early Adult Disease Risk: Follow Up of Offspring of Participants in a Randomised Controlled Trial Investigating Effects of Supplementation on Infant Birth Weight  [PDF]
John Macleod, Lie Tang, F. D. Richard Hobbs, Brian Wharton, Roger Holder, Shakir Hussain, Linda Nichols, Paul Stewart, Penny Clark, Steve Luzio, Jeff Holly, George Davey Smith
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0083371
Abstract: Background Observational evidence suggests that improving fetal growth may improve adult health. Experimental evidence from nutritional supplementation trials undertaken amongst pregnant women in the less developed world does not show strong or consistent effects on adult disease risk and no trials from the more developed world have previously been reported. Objective To test the hypothesis that nutritional supplementation during pregnancy influences offspring disease risk in adulthood Design Clinical assessment of a range of established diseases risk markers in young adult offspring of 283 South Asian mothers who participated in two trials of nutritional supplementation during pregnancy (protein/energy/vitamins; energy/vitamins or vitamins only) at Sorrento Maternity Hospital in Birmingham UK either unselected or selected on the basis of nutritional status. Results 236 (83%) offspring were traced and 118 (50%) of these were assessed in clinic. Protein/energy/vitamins supplementation amongst undernourished mothers was associated with increased infant birthweight. Nutritional supplementation showed no strong association with any one of a comprehensive range of markers of adult disease risk and no consistent pattern of association with risk across markers in offspring of either unselected or undernourished mothers. Conclusions We found no evidence that nutritional supplements given to pregnant women are an important influence on adult disease risk however our study lacked power to estimate small effects. Our findings do not provide support for a policy of nutritional supplementation for pregnant women as an effective means to improve adult health in more developed societies.
Asymmetric Dimethylarginine Is Associated with Developmental Programming of Adult Kidney Disease and Hypertension in Offspring of Streptozotocin-Treated Mothers  [PDF]
You-Lin Tain, Wen-Chin Lee, Chien-Ning Hsu, Wei-Chia Lee, Li-Tung Huang, Chien-Te Lee, Ching-Yuang Lin
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0055420
Abstract: Diabetes mellitus complicates pregnancies, leading to diseases in adult life in the offspring. Asymmetric dimethylarginine (ADMA) is increased in diabetes mellitus, kidney disease, and hypertension. We tested whether maternal diabetes causes increased ADMA in rats, resulting in kidney disease and hypertension in the adult offspring, and whether these can be prevented by maternal citrulline supplementation. Newborn female and pregnant Sprague-Dawley rats were injected with streptozotocin (STZ), which made up the nSTZ and STZ models, respectively. For the STZ model, 4 groups of male offspring were killed at age 3 months: the control, STZ, and Cit and STZ+Cit (control and STZ rats treated with 0.25% l-citrulline solution, respectively) groups. The nSTZ rats had lower nephron numbers. The renal level of ADMA was higher in the nSTZ rats than in controls. The STZ group developed kidney injury, renal hypertrophy, and elevated blood pressure at the age of 12 weeks. These conditions were found to be associated with increased ADMA levels, decreased nitric oxide (NO) production, and decreased dimethylarginine dimethylaminohydrolase (DDAH) activity in the kidney. In addition, ADMA caused a nephron deficit in cultured rat metanephroi. Maternal citrulline supplementation prevented hypertension and kidney injury, increased the renal DDAH-2 protein level, and restored the levels of ADMA and NO in the STZ+Cit group. Reduced nephron number and increased ADMA contribute to adult kidney disease and hypertension in offspring of mothers with STZ-induced diabetes. Manipulation of the ADMA-NO pathway by citrulline supplementation may be a potential approach to prevent these conditions.
Evaluation of the effect of taurine on cisplatin-induced hepatic injury and oxidative stress in male rats
Maryam Norozi Sarkarabad,Samad Zare
Physiology and Pharmacology , 2011,
Abstract: Introduction: The principal dose-limiting factor in the use of cisplatin as an antineoplastic drug is its hepatic toxicity. This study was designed to investigate the protective role of taurine against cisplatin-induced hepatic injury. Methods: Male albino rats (180-220 g) were divided in to 4 groups (n=8) as follows: (1) saline-treated group (2): cisplatin-treated group (10 mg/kg ip) (3): group that received taurine (200 mg/kg ip) for 1hr before cisplatin (10 mg/kg ip) administration (4): taurine treated group (200 mg/kg ip). After 7 days, the animals were sacrificed and blood samples collected from the heart as well as liver tissues were kept at -70 °C till further analyses. Results: analyses showed that cisplatin significantly increased ALT and AST serum levels (P<0.05) while pretreatment with taurine resulted in the reduction of these markers. Catalase activity in cisplatin-treated rats was significantly decreased (P<0.05) and taurine administration could recover this reduction. MDA content of the liver tissue was significantly increased in cisplatin-exposed animals, while taurine treatment reduced the amount of MDA in liver tissue. Conclusion: Our data suggest that taurine prevents from cisplatin-induced hepatic injury and this effect may be due to its antioxidant properties.
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