Maternal N-acetylcysteine therapy regulates hydrogen sulfide-generating pathway and prevents programmed hypertension in male offspring exposed to prenatal dexamethasone and postnatal high-fat diet

Nitric Oxide ◽  
2016 ◽  
Vol 53 ◽  
pp. 6-12 ◽  
Author(s):  
I-Hsin Tai ◽  
Jiunn-Ming Sheen ◽  
Yu-Ju Lin ◽  
Hong-Ren Yu ◽  
Mao-Meng Tiao ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
High Fat Diet ◽  
Male Offspring ◽  
High Fat

Hydrogen sulfide reduces serum triglyceride by activating liver autophagy via the AMPK-mTOR pathway

2015 ◽  
Vol 309 (11) ◽  
pp. E925-E935 ◽  
Author(s):  
Li Sun ◽  
Song Zhang ◽  
Chengyuan Yu ◽  
Zhenwei Pan ◽  
Yang Liu ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
High Fat Diet ◽  
Serum Triglyceride ◽  
Mtor Pathway ◽  
Autophagic Flux ◽  
High Fat ◽  
Sodium Hydrosulfide ◽  
Metabolism Inhibition ◽  
Qualitative Effect ◽  
First Time

Autophagy plays an important role in liver triglyceride (TG) metabolism. Inhibition of autophagy could reduce the clearance of TG in the liver. Hydrogen sulfide (H2S) is a potent stimulator of autophagic flux. Recent studies showed H2S is protective against hypertriglyceridemia (HTG) and noalcoholic fatty liver disease (NAFLD), while the mechanism remains to be explored. Here, we tested the hypothesis that H2S reduces serum TG level and ameliorates NAFLD by stimulating liver autophagic flux by the AMPK-mTOR pathway. The level of serum H2S in patients with HTG was lower than that of control subjects. Sodium hydrosulfide (NaHS, H2S donor) markedly reduced serum TG levels of male C57BL/6 mice fed a high-fat diet (HFD), which was abolished by coadministration of chloroquine (CQ), an inhibitor of autophagic flux. In HFD mice, administration of NaSH increased the LC3BII-to-LC3BI ratio and decreased the p62 protein level. Meanwhile, NaSH increased the phosphorylation of AMPK and thus reduced the phosphorylation of mTOR in a Western blot study. In cultured LO2 cells, high-fat treatment reduced the ratio of LC3BII to LC3BI and the phosphorylation of AMPK, which were reversed by the coadministration of NaSH. Knockdown of AMPK by siRNA in LO2 cells blocked the autophagic enhancing effects of NaSH. The same qualitative effect was observed in AMPKα2−/− mice. These results for the first time demonstrated that H2S could reduce serum TG level and ameliorate NAFLD by activating liver autophagy via the AMPK-mTOR pathway.

Taurine supplementation in high-fat diet fed male mice attenuates endocrine pancreatic dysfunction in their male offspring

Amino Acids ◽  
2019 ◽  
Vol 51 (4) ◽  
pp. 727-738 ◽  
Author(s):  
Israelle Netto Freitas ◽  
Thiago dos Reis Araujo ◽  
Jean Franciesco Vettorazzi ◽  
Emily Amorim Magalhães ◽  
Everardo Magalhães Carneiro ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Male Offspring ◽  
Male Mice ◽  
High Fat ◽  
Taurine Supplementation ◽  
Pancreatic Dysfunction

scholarly journals Effects of Maternal Resveratrol on Maternal High-Fat Diet/Obesity with or without Postnatal High-Fat Diet

2020 ◽  
Vol 21 (10) ◽  
pp. 3428 ◽  
Author(s):  
Mei-Hsin Hsu ◽  
Jiunn-Ming Sheen ◽  
I-Chun Lin ◽  
Hong-Ren Yu ◽  
Mao-Meng Tiao ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Cognitive Impairment ◽  
Adult Male ◽  
High Fat Diet ◽  
Dorsal Hippocampus ◽  
Fetal Brain ◽  
Male Offspring ◽  
High Fat ◽  
Peripheral Insulin Resistance

To examine the effects of maternal resveratrol in rats borne to dams with gestational high-fat diet (HFD)/obesity with or without postnatal high-fat diet. We first tested the effects of maternal resveratrol intake on placenta and male fetus brain in rats borne to dams with gestational HFD/obesity. Then, we assessed the possible priming effect of a subsequent insult, male offspring were weaned onto either a rat chow or a HFD. Spatial learning and memory were assessed by Morris water maze test. Blood pressure and peripheral insulin resistance were examined. Maternal HFD/obesity decreased adiponectin, phosphorylation alpha serine/threonine-protein kinase (pAKT), sirtuin 1 (SIRT1), and brain-derived neurotrophic factor (BDNF) in rat placenta, male fetal brain, and adult male offspring dorsal hippocampus. Maternal resveratrol treatment restored adiponectin, pAKT, and BDNF in fetal brain. It also reduced body weight, peripheral insulin resistance, increased blood pressure, and alleviated cognitive impairment in adult male offspring with combined maternal HFD and postnatal HFD. Maternal resveratrol treatment restored hippocampal pAKT and BDNF in rats with combined maternal HFD and postnatal HFD in adult male offspring dorsal hippocampus. Maternal resveratrol intake protects the fetal brain in the context of maternal HFD/obesity. It effectively reduced the synergistic effects of maternal HFD/obesity and postnatal HFD on metabolic disturbances and cognitive impairment in adult male offspring. Our data suggest that maternal resveratrol intake may serve as an effective therapeutic strategy in the context of maternal HFD/obesity.

Exercise restores bioavailability of hydrogen sulfide and promotes autophagy influx in livers of mice fed with high-fat diet

2017 ◽  
Vol 95 (6) ◽  
pp. 667-674 ◽  
Author(s):  
Bing Wang ◽  
Jing Zeng ◽  
Qi Gu
Keyword(s):  
Hydrogen Sulfide ◽  
Exercise Training ◽  
High Fat Diet ◽  
Mass Gain ◽  
Moderate Intensity ◽  
High Fat ◽  
Moderate Intensity Exercise ◽  
Nonalcoholic Fatty Liver ◽  
Mercaptopyruvate Sulfurtransferase ◽  
Underlying Mechanisms

In the gold standard treatment for nonalcoholic fatty liver disease (NAFLD), exercise training has been shown to effectively improve nonalcoholic steatohepatitis (NASH). However, limited data are available about the underlying mechanisms involved. This work was undertaken to investigate the mechanisms underlying the beneficial effect of exercise training on high-fat diet (HFD)-induced NAFLD in mice. Male mice were fed with HFD and given moderate-intensity exercise for 24 weeks. Exercise training lowered mass gain, attenuated systemic insulin resistance and glucose intolerance, and mitigated hepatic steatosis and fibrosis in mice fed with HFD. Exercise training improved mitochondrial function and enhanced mitochondrial β-oxidation in livers of HFD-fed mice. Exercise training enhanced hydrogen sulfide (H2S) levels in plasma and livers, and mRNA expression of cystathionine β-synthase (CBS), cystathionine γ-lyase (CES), and 3-mercaptopyruvate sulfurtransferase (3-MST) in livers of HFD-fed mice. Exercise training had no significant effect on the ratio of LC3-II/LC3-I, but decreased p62 protein expression in livers of HFD-fed mice. Additionally, exercise training reduced formation of malondialdehyde, enhanced ratio of GSH/GSSG, and down-regulated expression of TNF-α and IL-6 in livers of HFD-fed mice. Exercise training restored bioavailability of H2S and promoted autophagy influx in livers, which might contribute to its benefit on HFD-induced NAFLD.

scholarly journals Maternal high-fat diet programs white and brown adipose tissue lipidome and transcriptome in offspring in a sex- and tissue-dependent manner in mice

2022 ◽  
Author(s):  
Christina Savva ◽  
Luisa A. Helguero ◽  
Marcela González-Granillo ◽  
Tânia Melo ◽  
Daniela Couto ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Metabolic Profile ◽  
Maternal Diet ◽  
Overweight And Obesity ◽  
Male Offspring ◽  
Metabolic Adaptation ◽  
Dependent Manner ◽  
High Fat ◽  
The Metabolic Syndrome ◽  
Metabolic Complication

Abstract Objective The prevalence of overweight and obesity among children has drastically increased during the last decades and maternal obesity has been demonstrated as one of the ultimate factors. Nutrition-stimulated transgenerational regulation of key metabolic genes is fundamental to the developmental origins of the metabolic syndrome. Fetal nutrition may differently influence female and male offspring. Methods Mice dam were fed either a control diet or a high-fat diet (HFD) for 6-week prior mating and continued their respective diet during gestation and lactation. At weaning, female and male offspring were fed the HFD until sacrifice. White (WAT) and brown (BAT) adipose tissues were investigated in vivo by nuclear magnetic resonance at two different timepoints in life (midterm and endterm) and tissues were collected at endterm for lipidomic analysis and RNA sequencing. We explored the sex-dependent metabolic adaptation and gene programming changes by maternal HFD in visceral AT (VAT), subcutaneous AT (SAT) and BAT of offspring. Results We show that the triglyceride profile varies between adipose depots, sexes and maternal diet. In female offspring, maternal HFD remodels the triglycerides profile in SAT and BAT, and increases thermogenesis and cell differentiation in BAT, which may prevent metabolic complication later in life. Male offspring exhibit whitening of BAT and hyperplasia in VAT when born from high-fat mothers, with impaired metabolic profile. Maternal HFD differentially programs gene expression in WAT and BAT of female and male offspring. Conclusion Maternal HFD modulates metabolic profile in offspring in a sex-dependent manner. A sex- and maternal diet-dependent gene programming exists in VAT, SAT, and BAT which may be key player in the sexual dimorphism in the metabolic adaptation later in life.

scholarly journals Cancer Stem Cell Enrichment and Metabolic Substrate Adaptability are Driven by Hydrogen Sulfide Suppression in Glioblastoma

2020 ◽  
Author(s):  
Daniel J. Silver ◽  
Gustavo A. Roversi ◽  
Nazmin Bithi ◽  
Chase K. A. Neumann ◽  
Katie M. Troike ◽  
...  
Keyword(s):  
Stem Cell ◽  
Hydrogen Sulfide ◽  
Cancer Stem Cell ◽  
High Fat Diet ◽  
Control Diet ◽  
Chemotherapy Resistance ◽  
Cellular Metabolism ◽  
Protein S ◽  
High Fat ◽  
The Impact

AbstractGlioblastoma (GBM) remains among the deadliest of human malignancies. The emergence of the cancer stem cell (CSC) phenotype represents a major challenge to disease management and durable treatment response. The extrinsic, environmental, and lifestyle factors that result in CSC enrichment are not well understood. The CSC state endows cells with a fluid metabolic profile, enabling the utilization of multiple nutrient sources. Therefore, to test the impact of diet on CSC enrichment, we evaluated disease progression in tumor-bearing mice fed an obesity-inducing high-fat diet (HFD) versus an energy-balanced, low-fat control diet. HFD consumption resulted in hyper-aggressive disease that was accompanied by CSC enrichment and shortened survival. HFD consumption also drove intracerebral accumulation of saturated fats, which in turn inhibited the production and signaling of the gasotransmitter hydrogen sulfide (H2S). H2S is an endogenously produced bio-active metabolite derived from sulfur amino acid catabolism. It functions principally through protein S-sulfhydration and regulates a variety of programs including mitochondrial bioenergetics and cellular metabolism. Inhibition of H2S synthesis resulted in increased proliferation and chemotherapy resistance, whereas treatment with H2S donors led to cytotoxicity and death of cultured GBM cells. Compared to non-cancerous controls, patient GBM specimens were reduced in overall protein S-sulfhydration, which was primarily lost from proteins regulating cellular metabolism. These findings support the hypothesis that diet-regulated H2S signaling serves to suppress GBM by restricting metabolic adaptability, while its loss triggers CSC enrichment and disease acceleration. Interventions augmenting H2S bioavailability concurrent with GBM standard of care may improve outcomes for GBM patients.One Sentence SummaryConsumption of a high-fat diet (HFD) accelerates glioblastoma (GBM) by inhibiting the production and signaling of the tumor-suppressive metabolite hydrogen sulfide (H2S).

scholarly journals Maternal high fat diet induces Dickkopf‐1(Dkk1) mRNA in male offspring liver

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Dan Zhou ◽  
Xiyuan Zhang ◽  
Yukun Zhang ◽  
Yuan‐Xiang Pan
Keyword(s):  
High Fat Diet ◽  
Male Offspring ◽  
High Fat ◽  
Dickkopf 1
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