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Dr. Li-Tung Huang
Kaohsiung Chang Gung Memorial Hospital, Chang Gung University, Taiwan

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Journal article
Published: 23 June 2021 in International Journal of Molecular Sciences
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With the improvement of the survival rate of acute lymphoblastic leukemia (ALL) in children, some children ALL survivors reveal inferior intellectual and cognition outcome. Methotrexate (MTX), while serving as an essential component in ALL treatment, has been reported to be related to various neurologic sequelae. Using combined intrathecal (IT) and intraperitoneal (IP) MTX model, we had demonstrated impaired spatial memory function in developing rats, which can be rescued by melatonin treatment. To elucidate the impact of MTX treatment on the epigenetic modifications of the myelination process, we examined the change of neurotrophin and myelination-related transcriptomes in the present study and found combined IT and IP MTX treatment resulted in altered epigenetic modification on the myelination process, mainly in the hippocampus. Further, melatonin can restore the MTX effect through alterations of the epigenetic pathways.

ACS Style

Yu-Chieh Chen; Jiunn-Ming Sheen; Su-Chen Wang; Mei-Hsin Hsu; Chih-Cheng Hsiao; Kow-Aung Chang; Li-Tung Huang. Methotrexate Neurotoxicity Is Related to Epigenetic Modification of the Myelination Process. International Journal of Molecular Sciences 2021, 22, 6718 .

AMA Style

Yu-Chieh Chen, Jiunn-Ming Sheen, Su-Chen Wang, Mei-Hsin Hsu, Chih-Cheng Hsiao, Kow-Aung Chang, Li-Tung Huang. Methotrexate Neurotoxicity Is Related to Epigenetic Modification of the Myelination Process. International Journal of Molecular Sciences. 2021; 22 (13):6718.

Chicago/Turabian Style

Yu-Chieh Chen; Jiunn-Ming Sheen; Su-Chen Wang; Mei-Hsin Hsu; Chih-Cheng Hsiao; Kow-Aung Chang; Li-Tung Huang. 2021. "Methotrexate Neurotoxicity Is Related to Epigenetic Modification of the Myelination Process." International Journal of Molecular Sciences 22, no. 13: 6718.

Editorial
Published: 30 October 2020 in International Journal of Environmental Research and Public Health
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Nutritional challenges prior to and during gestation, lactation, and early life are known to influence the lifelong health of the infant. In this editorial, I briefly discuss the 13 articles published in this Special Issue, “Maternal and Early-Life Nutrition and Health”. This Special Issue discusses topics including maternal nutrition behaviors, maternal overnutrition/obesity, maternal iron deficiency, breastfeeding, and others. This issue paves the way to better understand perinatal nutrition and how it can impact maternal and offspring health.

ACS Style

Li-Tung Huang. Maternal and Early-Life Nutrition and Health. International Journal of Environmental Research and Public Health 2020, 17, 7982 .

AMA Style

Li-Tung Huang. Maternal and Early-Life Nutrition and Health. International Journal of Environmental Research and Public Health. 2020; 17 (21):7982.

Chicago/Turabian Style

Li-Tung Huang. 2020. "Maternal and Early-Life Nutrition and Health." International Journal of Environmental Research and Public Health 17, no. 21: 7982.

Journal article
Published: 14 September 2020 in Molecules
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To facilitate broad applications and enhance bioactivity, resveratrol was esterified to resveratrol butyrate esters (RBE). Esterification with butyric acid was conducted by the Steglich esterification method at room temperature with N-ethyl-N′-(3-dimethylaminopropyl) carbodiimide (EDC) and 4-dimethyl aminopyridine (DMAP). Our experiments demonstrated the synthesis of RBE through EDC- and DMAP-facilitated esterification was successful and that the FTIR spectra of RBE revealed absorption (1751 cm−1) in the ester region. 13C-NMR spectrum of RBE showed a peak at 171 ppm corresponding to the ester group and peaks between 1700 and 1600 cm−1 in the FTIR spectra. RBE treatment (25 or 50 μM) decreased oleic acid-induced lipid accumulation in HepG2 cells. This effect was stronger than that of resveratrol and mediated through the downregulation of p-ACC and SREBP-2 expression. This is the first study demonstrating RBE could be synthesized by the Steglich method and that resulting RBE could inhibit lipid accumulation in HepG2 cells. These results suggest that RBE could potentially serve as functional food ingredients and supplements for health promotion.

ACS Style

You-Lin Tain; Li-Cheng Jheng; Sam K. C. Chang; Yu-Wei Chen; Li-Tung Huang; Jin-Xian Liao; Chih-Yao Hou. Synthesis and Characterization of Novel Resveratrol Butyrate Esters That Have the Ability to Prevent Fat Accumulation in a Liver Cell Culture Model. Molecules 2020, 25, 4199 .

AMA Style

You-Lin Tain, Li-Cheng Jheng, Sam K. C. Chang, Yu-Wei Chen, Li-Tung Huang, Jin-Xian Liao, Chih-Yao Hou. Synthesis and Characterization of Novel Resveratrol Butyrate Esters That Have the Ability to Prevent Fat Accumulation in a Liver Cell Culture Model. Molecules. 2020; 25 (18):4199.

Chicago/Turabian Style

You-Lin Tain; Li-Cheng Jheng; Sam K. C. Chang; Yu-Wei Chen; Li-Tung Huang; Jin-Xian Liao; Chih-Yao Hou. 2020. "Synthesis and Characterization of Novel Resveratrol Butyrate Esters That Have the Ability to Prevent Fat Accumulation in a Liver Cell Culture Model." Molecules 25, no. 18: 4199.

Journal article
Published: 20 August 2020 in International Journal of Environmental Research and Public Health
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Iron is an essential micronutrient for the brain development of the fetus. Altered intestinal microbiota might affect behavior and cognition through the so-called microbiota-gut-brain axis. We used a Sprague-Dawley rat model of a maternal low-iron diet to explore the changes in cognition, dorsal hippocampal brain-derived neurotrophic factor (BDNF) and related pathways, gut microbiota, and related metabolites in adult male offspring. We established maternal iron-deficient rats by feeding them a low-iron diet (2.9 mg/kg), while the control rats were fed a standard diet (52.3 mg/kg). We used a Morris water maze test to assess spatial learning and long-term memory. Western blot (WB) assays and a quantitative reverse-transcription polymerase chain reaction (qRT-PCR) were used to detect the BDNF concentration and related signaling pathways. We collected fecal samples for microbiota profiling and measured the concentrations of plasma short-chain fatty acids. The adult male offspring of maternal rats fed low-iron diets before pregnancy, during pregnancy and throughout the lactation period had (1) spatial deficits, (2) a decreased BDNF mRNA expression and protein concentrations, accompanied by a decreased TrkB protein abundance, (3) a decreased plasma acetate concentration, and (4) an enrichment of the Bacteroidaceae genus Bacteroides and Lachnospiraceae genus Marvinbryantia. Maternal iron deficiency leads to an offspring spatial deficit and is associated with alternations in gastrointestinal microbiota and metabolites.

ACS Style

Hsin-Yi Hsieh; Yu-Chieh Chen; Mei-Hsin Hsu; Hong-Ren Yu; Chung-Hao Su; You-Lin Tain; Li-Tung Huang; Jiunn-Ming Sheen. Maternal Iron Deficiency Programs Offspring Cognition and Its Relationship with Gastrointestinal Microbiota and Metabolites. International Journal of Environmental Research and Public Health 2020, 17, 6070 .

AMA Style

Hsin-Yi Hsieh, Yu-Chieh Chen, Mei-Hsin Hsu, Hong-Ren Yu, Chung-Hao Su, You-Lin Tain, Li-Tung Huang, Jiunn-Ming Sheen. Maternal Iron Deficiency Programs Offspring Cognition and Its Relationship with Gastrointestinal Microbiota and Metabolites. International Journal of Environmental Research and Public Health. 2020; 17 (17):6070.

Chicago/Turabian Style

Hsin-Yi Hsieh; Yu-Chieh Chen; Mei-Hsin Hsu; Hong-Ren Yu; Chung-Hao Su; You-Lin Tain; Li-Tung Huang; Jiunn-Ming Sheen. 2020. "Maternal Iron Deficiency Programs Offspring Cognition and Its Relationship with Gastrointestinal Microbiota and Metabolites." International Journal of Environmental Research and Public Health 17, no. 17: 6070.

Journal article
Published: 25 July 2020 in Lipids in Health and Disease
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Background Maternal obesity is an emerging problem in the modern world. Growing evidence suggests that intrauterine high-fat (HF) exposure may predispose progeny to subsequent metabolic challenges. Progeny born to mothers who ate an HF diet also tends to eat an HF diet when growing and aggravate metabolic issues. Thus, the generational transmission of obesity is cyclical. Developing a strategy to prevent the occurrence of metabolic syndrome related to prenatal and/or postnatal HF diet is important. In this study, the reprogramming effects of maternal resveratrol treatment for the progeny with maternal HF/postnatal HF diets were investigated. Methods Sprague-Dawley dams were fed either a control or a high-fat/high sucrose diet (HFHS) from mating to lactation. After weaning, the progeny was fed chow or an HF diet. Four experimental groups were yielded: CC (maternal/postnatal control diet), HC (maternal HF/postnatal control diet), CH (maternal control/postnatal HFHS diet), and HH (maternal/postnatal HFHS diet). A fifth group (HRH) received a maternal HFHS diet plus maternal resveratrol treatment and a postnatal chow diet to study the effects of maternal resveratrol therapy. Results Maternal resveratrol treatment lessened the weight and adiposity of progeny that were programmed by combined prenatal and postnatal HFHS diets. Maternal resveratrol therapy ameliorated the decreased abundance of the sirtuin 1 (SIRT1) enzyme in retroperitoneal tissue and the altered leptin/soluble leptin receptor ratio of progeny. Maternal resveratrol therapy also decreased lipogenesis and increased lipolysis for progeny. Conclusions Maternal resveratrol intervention can prevent adiposity programmed by maternal and postnatal HFHS diets by inducing lipid metabolic modulation. This study offers a novel reprogramming role for the effect of maternal resveratrol supplements against obesity.

ACS Style

Ta-Yu Liu; Hong-Ren Yu; Ching-Chou Tsai; Li-Tung Huang; Chih-Cheng Chen; Jium-Ming Sheen; Mao-Meng Tiao; You-Lin Tain; I-Chun Lin; Yun-Ju Lai; Yu-Ju Lin; Te-Yao Hsu. Resveratrol intake during pregnancy and lactation re-programs adiposity and ameliorates leptin resistance in male progeny induced by maternal high-fat/high sucrose plus postnatal high-fat/high sucrose diets via fat metabolism regulation. Lipids in Health and Disease 2020, 19, 1 -13.

AMA Style

Ta-Yu Liu, Hong-Ren Yu, Ching-Chou Tsai, Li-Tung Huang, Chih-Cheng Chen, Jium-Ming Sheen, Mao-Meng Tiao, You-Lin Tain, I-Chun Lin, Yun-Ju Lai, Yu-Ju Lin, Te-Yao Hsu. Resveratrol intake during pregnancy and lactation re-programs adiposity and ameliorates leptin resistance in male progeny induced by maternal high-fat/high sucrose plus postnatal high-fat/high sucrose diets via fat metabolism regulation. Lipids in Health and Disease. 2020; 19 (1):1-13.

Chicago/Turabian Style

Ta-Yu Liu; Hong-Ren Yu; Ching-Chou Tsai; Li-Tung Huang; Chih-Cheng Chen; Jium-Ming Sheen; Mao-Meng Tiao; You-Lin Tain; I-Chun Lin; Yun-Ju Lai; Yu-Ju Lin; Te-Yao Hsu. 2020. "Resveratrol intake during pregnancy and lactation re-programs adiposity and ameliorates leptin resistance in male progeny induced by maternal high-fat/high sucrose plus postnatal high-fat/high sucrose diets via fat metabolism regulation." Lipids in Health and Disease 19, no. 1: 1-13.

Journal article
Published: 26 June 2020 in International Journal of Molecular Sciences
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Hypertension and chronic kidney disease (CKD) can originate during early-life. Tryptophan metabolites generated by different pathways have both detrimental and beneficial effects. In CKD, uremic toxins from the tryptophan-generating metabolites are endogenous ligands of the aryl hydrocarbon receptor (AHR). The interplay between AHR, nitric oxide (NO), the renin–angiotensin system (RAS), and gut microbiota is involved in the development of hypertension. We examined whether tryptophan supplementation in pregnancy can prevent hypertension and kidney disease programmed by maternal CKD in adult offspring via the aforementioned mechanisms. Sprague–Dawley (SD) female rats received regular chow or chow supplemented with 0.5% adenine for 3 weeks to induce CKD before pregnancy. Pregnant controls or CKD rats received vehicle or tryptophan 200 mg/kg per day via oral gavage during pregnancy. Male offspring were divided into four groups (n = 8/group): control, CKD, tryptophan supplementation (Trp), and CKD plus tryptophan supplementation (CKDTrp). All rats were sacrificed at the age of 12 weeks. We found maternal CKD induced hypertension in adult offspring, which tryptophan supplementation prevented. Maternal CKD-induced hypertension is related to impaired NO bioavailability and non-classical RAS axis. Maternal CKD and tryptophan supplementation differentially shaped distinct gut microbiota profile in adult offspring. The protective effect of tryptophan supplementation against maternal CKD-induced programmed hypertension is relevant to alterations to several tryptophan-metabolizing microbes and AHR signaling pathway. Our findings support interplay among tryptophan-metabolizing microbiome, AHR, NO, and the RAS in hypertension of developmental origins. Furthermore, tryptophan supplementation in pregnancy could be a potential approach to prevent hypertension programmed by maternal CKD.

ACS Style

Chien-Ning Hsu; I-Chun Lin; Hong-Ren Yu; Li-Tung Huang; Mao-Meng Tiao; You-Lin Tain. Maternal Tryptophan Supplementation Protects Adult Rat Offspring against Hypertension Programmed by Maternal Chronic Kidney Disease: Implication of Tryptophan-Metabolizing Microbiome and Aryl Hydrocarbon Receptor. International Journal of Molecular Sciences 2020, 21, 4552 .

AMA Style

Chien-Ning Hsu, I-Chun Lin, Hong-Ren Yu, Li-Tung Huang, Mao-Meng Tiao, You-Lin Tain. Maternal Tryptophan Supplementation Protects Adult Rat Offspring against Hypertension Programmed by Maternal Chronic Kidney Disease: Implication of Tryptophan-Metabolizing Microbiome and Aryl Hydrocarbon Receptor. International Journal of Molecular Sciences. 2020; 21 (12):4552.

Chicago/Turabian Style

Chien-Ning Hsu; I-Chun Lin; Hong-Ren Yu; Li-Tung Huang; Mao-Meng Tiao; You-Lin Tain. 2020. "Maternal Tryptophan Supplementation Protects Adult Rat Offspring against Hypertension Programmed by Maternal Chronic Kidney Disease: Implication of Tryptophan-Metabolizing Microbiome and Aryl Hydrocarbon Receptor." International Journal of Molecular Sciences 21, no. 12: 4552.

Journal article
Published: 12 May 2020 in International Journal of Molecular Sciences
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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.

ACS Style

Mei-Hsin Hsu; Jiunn-Ming Sheen; I-Chun Lin; Hong-Ren Yu; Mao-Meng Tiao; You-Lin Tain; Li-Tung Huang. Effects of Maternal Resveratrol on Maternal High-Fat Diet/Obesity with or without Postnatal High-Fat Diet. International Journal of Molecular Sciences 2020, 21, 3428 .

AMA Style

Mei-Hsin Hsu, Jiunn-Ming Sheen, I-Chun Lin, Hong-Ren Yu, Mao-Meng Tiao, You-Lin Tain, Li-Tung Huang. Effects of Maternal Resveratrol on Maternal High-Fat Diet/Obesity with or without Postnatal High-Fat Diet. International Journal of Molecular Sciences. 2020; 21 (10):3428.

Chicago/Turabian Style

Mei-Hsin Hsu; Jiunn-Ming Sheen; I-Chun Lin; Hong-Ren Yu; Mao-Meng Tiao; You-Lin Tain; Li-Tung Huang. 2020. "Effects of Maternal Resveratrol on Maternal High-Fat Diet/Obesity with or without Postnatal High-Fat Diet." International Journal of Molecular Sciences 21, no. 10: 3428.

Journal article
Published: 17 April 2020 in International Journal of Environmental Research and Public Health
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Obesity during pregnancy increases the risk of cardiovascular problems, diabetes, asthma, and cognitive impairments, affecting the offspring. It is important to reduce the negative effects of obesity and high-fat (HF) diet during pregnancy. We employed a rat model of maternal HF diet to evaluate the possible de-programming effects of resveratrol in rodent male offspring with maternal HF diet/obesity. Male rat offspring were randomized into four groups: maternal control diet/postnatal control diet, maternal HF diet/postnatal control diet, maternal control diet plus maternal resveratrol treatment/postnatal control diet, and maternal HF diet plus maternal resveratrol treatment/postnatal control diet. Maternal HF diet during pregnancy plus lactation resulted in retroperitoneal adiposity in the male offspring. Maternal resveratrol treatment re-programmed maternal HF exposure-induced visceral adiposity. Offspring that received prenatal HF diet showed higher leptin/soluble leptin receptor (sOB-R) ratio than offspring that received prenatal control diet. Maternal resveratrol treatment ameliorated maternal HF exposure-induced increase in leptin/sOB-R ratio and altered the expression of genes for crucial fatty acid synthesis enzymes in the offspring. Thus, maternal resveratrol administration reduces retroperitoneal adiposity in rat offspring exposed to prenatal HF diet/obesity and could be used to ameliorate negative effects of maternal HF diet in the offspring.

ACS Style

Ti-An Tsai; Chang-Ku Tsai; Li-Tung Huang; Jiunn-Ming Sheen; Mao-Meng Tiao; You-Lin Tain; Chih-Cheng Chen; I-Chun Lin; Yun-Ju Lai; Ching-Chou Tsai; Yu-Ju Lin; Hong-Ren Yu. Maternal Resveratrol Treatment Re-Programs and Maternal High-Fat Diet-Induced Retroperitoneal Adiposity in Male Offspring. International Journal of Environmental Research and Public Health 2020, 17, 2780 .

AMA Style

Ti-An Tsai, Chang-Ku Tsai, Li-Tung Huang, Jiunn-Ming Sheen, Mao-Meng Tiao, You-Lin Tain, Chih-Cheng Chen, I-Chun Lin, Yun-Ju Lai, Ching-Chou Tsai, Yu-Ju Lin, Hong-Ren Yu. Maternal Resveratrol Treatment Re-Programs and Maternal High-Fat Diet-Induced Retroperitoneal Adiposity in Male Offspring. International Journal of Environmental Research and Public Health. 2020; 17 (8):2780.

Chicago/Turabian Style

Ti-An Tsai; Chang-Ku Tsai; Li-Tung Huang; Jiunn-Ming Sheen; Mao-Meng Tiao; You-Lin Tain; Chih-Cheng Chen; I-Chun Lin; Yun-Ju Lai; Ching-Chou Tsai; Yu-Ju Lin; Hong-Ren Yu. 2020. "Maternal Resveratrol Treatment Re-Programs and Maternal High-Fat Diet-Induced Retroperitoneal Adiposity in Male Offspring." International Journal of Environmental Research and Public Health 17, no. 8: 2780.

Review
Published: 02 March 2020 in International Journal of Environmental Research and Public Health
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Maternal obesity during pregnancy is a now a public health burden that may be the culprit underlying the ever-increasing rates of adult obesity worldwide. Understanding the association between maternal obesity and adult offspring’s obesity would inform policy and practice regarding offspring health through available resources and interventions. This review first summarizes the programming effects of maternal obesity and discusses the possible underlying mechanisms. We then summarize the current evidence suggesting that maternal consumption of resveratrol is helpful in maternal obesity and alleviates its consequences. In conclusion, maternal obesity can program offspring development in an adverse way. Maternal resveratrol could be considered as a potential regimen in reprogramming adverse outcomes in the context of maternal obesity.

ACS Style

Mei-Hsin Hsu; Yu-Chieh Chen; Jiunn-Ming Sheen; Li-Tung Huang. Maternal Obesity Programs Offspring Development and Resveratrol Potentially Reprograms the Effects of Maternal Obesity. International Journal of Environmental Research and Public Health 2020, 17, 1610 .

AMA Style

Mei-Hsin Hsu, Yu-Chieh Chen, Jiunn-Ming Sheen, Li-Tung Huang. Maternal Obesity Programs Offspring Development and Resveratrol Potentially Reprograms the Effects of Maternal Obesity. International Journal of Environmental Research and Public Health. 2020; 17 (5):1610.

Chicago/Turabian Style

Mei-Hsin Hsu; Yu-Chieh Chen; Jiunn-Ming Sheen; Li-Tung Huang. 2020. "Maternal Obesity Programs Offspring Development and Resveratrol Potentially Reprograms the Effects of Maternal Obesity." International Journal of Environmental Research and Public Health 17, no. 5: 1610.

Article
Published: 05 February 2020 in NeuroReport
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This study aimed to examine the combined effects of prenatal glucocorticoid exposure and a postnatal high-fat diet (HFD) on offspring brain development and metabolic disturbance. Besides, the effects of an enriched environment were assessed. Pregnant Sprague–Dawley rats were administered vehicle or dexamethasone between gestation days 14 and 21. Male offspring was then weaned onto either a standard chow or HFD. An enriched environment was implemented between postnatal days 22 and 180 in a subset of rats with prenatal dexamethasone and a postnatal HFD. Adult male offspring with prenatal exposure to dexamethasone and a postnatal HFD showed obesity, increased systolic blood pressure, peripheral and central insulin resistance, and spatial learning and memory impairment detected by Morris water maze. An enriched environment displayed beneficial effects in reducing body weight, decreasing systolic blood pressure, reducing insulin resistance, ameliorating brain molecular alterations, and alleviating spatial deficit in rats with prenatal dexamethasone and a postnatal HFD. In conclusion, adult male offspring with prenatal dexamethasone exposure and a postnatal HFD showed obesity, increased systolic blood pressure, peripheral and central insulin resistance, and spatial learning and memory impairment. In addition, an enriched environment had beneficial effects in this context.

ACS Style

Mei-Hsin Hsu; Jiunn-Ming Sheen; Yu-Chieh Chen; Hong-Ren Yu; You-Lin Tain; Li-Tung Huang. Rats with prenatal dexamethasone exposure and postnatal high-fat diet exhibited insulin resistance, and spatial learning and memory impairment: effects of enriched environment. NeuroReport 2020, 31, 265 -273.

AMA Style

Mei-Hsin Hsu, Jiunn-Ming Sheen, Yu-Chieh Chen, Hong-Ren Yu, You-Lin Tain, Li-Tung Huang. Rats with prenatal dexamethasone exposure and postnatal high-fat diet exhibited insulin resistance, and spatial learning and memory impairment: effects of enriched environment. NeuroReport. 2020; 31 (3):265-273.

Chicago/Turabian Style

Mei-Hsin Hsu; Jiunn-Ming Sheen; Yu-Chieh Chen; Hong-Ren Yu; You-Lin Tain; Li-Tung Huang. 2020. "Rats with prenatal dexamethasone exposure and postnatal high-fat diet exhibited insulin resistance, and spatial learning and memory impairment: effects of enriched environment." NeuroReport 31, no. 3: 265-273.

Journal article
Published: 01 February 2020 in Life Sciences
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With the improvement of the survival rates in children acute lymphoblastic leukemia (ALL), some children ALL survivors show impaired cognitive function. Methotrexate (MTX), an essential component in ALL treatment, has been reported to be related to neurologic sequelae and to increased oxidative stress through its interactions with enzymes in the folate pathway. Asymmetric dimethylarginine (ADMA) is the main endogenous inhibitor of nitric oxide synthase, and increased ADMA may result from increased oxidants. Melatonin is an antioxidant; however, its role in MTX neuropathy is not well studied. We developed a rat model mimicking child ALL treatment to explore peripheral and central homocysteine and ADMA regulation after MTX and found potential treatment choice. Preweaning male Sprague-Dawley rats were used in this study. Experiment 1 evaluated spatial performance in rats with intrathecal (IT) MTX, intraperitoneal (IP) MTX, or combined IT and IP MTX, protocols mimicking ALL treatment in children. Experiment 2 focused on rats with combined IT and IP MTX, evaluating spatial performance and plasma and dorsal hippocampal homocysteine and ADMA levels, their regulation, and the protective effect of melatonin. Combined IT and IP MTX treatment caused in spatial deficits in developing rats, and melatonin restored the spatial performance. Alterations in peripheral and central homocysteine and ADMA concentrations and their regulation were found and could be alleviated by melatonin treatment. Combined IP and IT MTX treatment caused spatial deficits in developing rats. Melatonin could restore spatial performance through alleviating the effects on the imbalance of oxidative stress.

ACS Style

Yu-Chieh Chen; Jiunn-Ming Sheen; Mei-Hsin Hsu; Chih-Cheng Hsiao; Su-Chen Wang; Li-Tung Huang. Melatonin rescued methotrexate-induced spatial deficit and hyperhomocysteinemia and increased asymmetric dimethylarginine in plasma and dorsal hippocampus in developing rats. Life Sciences 2020, 242, 116931 .

AMA Style

Yu-Chieh Chen, Jiunn-Ming Sheen, Mei-Hsin Hsu, Chih-Cheng Hsiao, Su-Chen Wang, Li-Tung Huang. Melatonin rescued methotrexate-induced spatial deficit and hyperhomocysteinemia and increased asymmetric dimethylarginine in plasma and dorsal hippocampus in developing rats. Life Sciences. 2020; 242 ():116931.

Chicago/Turabian Style

Yu-Chieh Chen; Jiunn-Ming Sheen; Mei-Hsin Hsu; Chih-Cheng Hsiao; Su-Chen Wang; Li-Tung Huang. 2020. "Melatonin rescued methotrexate-induced spatial deficit and hyperhomocysteinemia and increased asymmetric dimethylarginine in plasma and dorsal hippocampus in developing rats." Life Sciences 242, no. : 116931.

Review
Published: 13 November 2019 in International Journal of Molecular Sciences
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Cardiovascular and neurological diseases can originate in early life. Melatonin, a biologically active substance, acts as a pleiotropic hormone essential for pregnancy and fetal development. Maternal melatonin can easily pass the placenta and provide photoperiodic signals to the fetus. Though melatonin uses in pregnant or lactating women have not yet been recommended, there is a growing body of evidence from animal studies in support of melatonin as a reprogramming strategy to prevent the developmental programming of cardiovascular and neurological diseases. Here, we review several key themes in melatonin use in pregnancy and lactation within offspring health and disease. We have particularly focused on the following areas: the pathophysiological roles of melatonin in pregnancy, lactation, and fetal development; clinical uses of melatonin in fetal and neonatal diseases; experimental evidence supporting melatonin as a reprogramming therapy to prevent cardiovascular and neurological diseases; and reprogramming mechanisms of melatonin within developmental programming. The targeting of melatonin uses in pregnancy and lactation will be valuable in the prevention of various adult chronic diseases in later life, and especially cardiovascular and neurological diseases.

ACS Style

Chien-Ning Hsu; Li-Tung Huang; You-Lin Tain. Perinatal Use of Melatonin for Offspring Health: Focus on Cardiovascular and Neurological Diseases. International Journal of Molecular Sciences 2019, 20, 5681 .

AMA Style

Chien-Ning Hsu, Li-Tung Huang, You-Lin Tain. Perinatal Use of Melatonin for Offspring Health: Focus on Cardiovascular and Neurological Diseases. International Journal of Molecular Sciences. 2019; 20 (22):5681.

Chicago/Turabian Style

Chien-Ning Hsu; Li-Tung Huang; You-Lin Tain. 2019. "Perinatal Use of Melatonin for Offspring Health: Focus on Cardiovascular and Neurological Diseases." International Journal of Molecular Sciences 20, no. 22: 5681.

Journal article
Published: 14 August 2019 in International Journal of Molecular Sciences
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Hypertension can originate from early-life exposure to oxidative stress. As reported, dimethyl fumarate (DMF) activates nuclear factor erythroid-derived 2-related factor 2 (Nrf2) and protects against oxidative stress damage. We examined whether maternal DMF therapy protects adult offspring against hypertension programmed by prenatal dexamethasone (DEX) and postnatal high-fat (HF) diet exposure. We examined male Sprague Dawley rat offspring at 4 months of age from five groups (n = 11-13/group): control, DEX (0.1mg/kg i.p. from gestational day 16 to 22), HF (D12331 diet from weaning to 16 weeks of age), DEX+HF, and DEX+HF+DMF (50mg/kg/day via gastric gavage for 3 weeks during pregnancy). Maternal DMF therapy prevented male offspring against hypertension programmed by combined DEX and HF exposures. The protective effects of maternal DMF include reduced oxidative stress, decreased plasma asymmetric dimethylarginine (ADMA) levels, downregulated the renin-angiotensin system (i.e. Ren, Agt, Ace, and Agtr1a), increased renal protein levels of certain nutrient-sensing signals, and promoted autophagy. In conclusion, maternal Nrf2 activation by DMF protects male adult offspring against hypertension programmed by combined DEX and HF exposures. Our results cast a new light on the therapeutic potential of targeting Nrf2 signaling pathway as reprogramming strategies to prevent programmed hypertension in children exposed to antenatal corticosteroids and postnatally excessive consumption of fat.

ACS Style

Chien-Ning Hsu; Yu-Ju Lin; Hong-Ren Yu; I-Chun Lin; Jiunn-Ming Sheen; Li-Tung Huang; You-Lin Tain. Protection of Male Rat Offspring against Hypertension Programmed by Prenatal Dexamethasone Administration and Postnatal High-Fat Diet with the Nrf2 Activator Dimethyl Fumarate during Pregnancy. International Journal of Molecular Sciences 2019, 20, 3957 .

AMA Style

Chien-Ning Hsu, Yu-Ju Lin, Hong-Ren Yu, I-Chun Lin, Jiunn-Ming Sheen, Li-Tung Huang, You-Lin Tain. Protection of Male Rat Offspring against Hypertension Programmed by Prenatal Dexamethasone Administration and Postnatal High-Fat Diet with the Nrf2 Activator Dimethyl Fumarate during Pregnancy. International Journal of Molecular Sciences. 2019; 20 (16):3957.

Chicago/Turabian Style

Chien-Ning Hsu; Yu-Ju Lin; Hong-Ren Yu; I-Chun Lin; Jiunn-Ming Sheen; Li-Tung Huang; You-Lin Tain. 2019. "Protection of Male Rat Offspring against Hypertension Programmed by Prenatal Dexamethasone Administration and Postnatal High-Fat Diet with the Nrf2 Activator Dimethyl Fumarate during Pregnancy." International Journal of Molecular Sciences 20, no. 16: 3957.

Research article
Published: 20 April 2019 in Molecular Nutrition & Food Research
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Objective Prenatal high fat (HF) and postnatal HF diet are both associated with obesity and metabolic disturbances in adults. Leptin resistance induced by obesity limits its biological effects. The anti‐obesity mechanism of resveratrol in visceral adiposity was investigated here. Methods During mating and lactation, Sprague‐Dawley dams were fed either control or a HF diet. Subsequently, the offspring were fed chow or a HF diet. A fifth group that received maternal/postnatal HF diet and resveratrol after weaning (HHR) was used to study the effects of resveratrol treatment. Results Resveratrol treatment alleviated adiposity programmed by maternal and postnatal HF diet by decreasing feed intake or inducing metabolic changes. Resveratrol treatment was also found to ameliorate the decrease in SIRT1 abundance observed in retroperitoneal adipose tissue, programmed by maternal and postnatal HF diet. Moreover, resveratrol therapy decreased plasma leptin level and increased leptin receptor expression in retroperitoneal adipose tissue through DNA methylation modification. Conclusions These results suggest that resveratrol can alleviate peripheral leptin resistance programmed by the combined effect of prenatal and postnatal HF diet through epigenetic regulation of genes coding leptin and its receptor. It provides insights into a novel mechanism explaining the beneficial effects of resveratrol in obesity management. This article is protected by copyright. All rights reserved

ACS Style

Hong‐Ren Yu; Jiunn‐Ming Sheen; Mao‐Meng Tiao; You‐Lin Tain; Chih‐Cheng Chen; I‐Chun Lin; Yun‐Ju Lai; Ching‐Chou Tsai; Yu‐Ju Lin; Ching‐Chang Tsai; Kow‐Aung Chang; Li‐Tung Huang. Resveratrol Treatment Ameliorates Leptin Resistance and Adiposity Programed by the Combined Effect of Maternal and Post‐Weaning High‐Fat Diet. Molecular Nutrition & Food Research 2019, e1801385 .

AMA Style

Hong‐Ren Yu, Jiunn‐Ming Sheen, Mao‐Meng Tiao, You‐Lin Tain, Chih‐Cheng Chen, I‐Chun Lin, Yun‐Ju Lai, Ching‐Chou Tsai, Yu‐Ju Lin, Ching‐Chang Tsai, Kow‐Aung Chang, Li‐Tung Huang. Resveratrol Treatment Ameliorates Leptin Resistance and Adiposity Programed by the Combined Effect of Maternal and Post‐Weaning High‐Fat Diet. Molecular Nutrition & Food Research. 2019; ():e1801385.

Chicago/Turabian Style

Hong‐Ren Yu; Jiunn‐Ming Sheen; Mao‐Meng Tiao; You‐Lin Tain; Chih‐Cheng Chen; I‐Chun Lin; Yun‐Ju Lai; Ching‐Chou Tsai; Yu‐Ju Lin; Ching‐Chang Tsai; Kow‐Aung Chang; Li‐Tung Huang. 2019. "Resveratrol Treatment Ameliorates Leptin Resistance and Adiposity Programed by the Combined Effect of Maternal and Post‐Weaning High‐Fat Diet." Molecular Nutrition & Food Research , no. : e1801385.

Journal article
Published: 12 March 2019 in Placenta
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Maternal nutrition is an extremely important health issue. We evaluated the impact of maternal high fat diet (HFD) on pregnancy outcomes, elucidated how the rat placenta and fetus respond to diet manipulation based on fetal sex, and identified candidate genes and pathways. Rats were fed a normal or HFD diet for 10 weeks before conception and during gestation. The placenta was collected on gestational day 21 and sexed. Placental histology was analyzed and placental candidate genes and pathways were identified using whole-genome RNA next-generation sequencing. Pup weights in both sexes from HFD dams were reduced. The weight of the placenta from the HFD group was also decreased in both sexes, but changes in placental layer distributions were only significant for female fetuses. Maternal HFD altered the placental transcriptome in a sex-specific manner. Activation of the placental renin-angiotensin system (RAS) by maternal HFD was associated with fetal growth restriction in both fetal sexes. The placenta reacts to maternal HFD by altering the placental layer distribution and gene expression in a sex-specific manner. The male placenta in late gestation is thought to exhibit greater plasticity relative to the female placenta; however, fetuses of both sexes exhibited similar growth restriction. Our data reveal an association between the placental RAS and HFD-induced fetal growth restriction.

ACS Style

Yu-Ju Lin; Li-Tung Huang; Ching-Chou Tsai; Jiunn-Ming Sheen; Mao-Meng Tiao; Hong-Ren Yu; I-Chun Lin; You-Lin Tain. Maternal high-fat diet sex-specifically alters placental morphology and transcriptome in rats: Assessment by next-generation sequencing. Placenta 2019, 78, 44 -53.

AMA Style

Yu-Ju Lin, Li-Tung Huang, Ching-Chou Tsai, Jiunn-Ming Sheen, Mao-Meng Tiao, Hong-Ren Yu, I-Chun Lin, You-Lin Tain. Maternal high-fat diet sex-specifically alters placental morphology and transcriptome in rats: Assessment by next-generation sequencing. Placenta. 2019; 78 ():44-53.

Chicago/Turabian Style

Yu-Ju Lin; Li-Tung Huang; Ching-Chou Tsai; Jiunn-Ming Sheen; Mao-Meng Tiao; Hong-Ren Yu; I-Chun Lin; You-Lin Tain. 2019. "Maternal high-fat diet sex-specifically alters placental morphology and transcriptome in rats: Assessment by next-generation sequencing." Placenta 78, no. : 44-53.

Review
Published: 28 January 2019 in International Journal of Molecular Sciences
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Resveratrol, also known as 3,5,4′-trihydroxystilbene, is a natural polyphenol that occurs as a phytoalexin. It is produced by plant sources such as grapes, apples, blueberries, plums, peanuts, and other oilseeds. This compound has a variety of effects on human health and diseases. This review summarizes the mounting evidence that resveratrol is helpful in treating metabolic syndrome and related disorders. Resveratrol can be provided either early as a reprogramming agent or later as part of treatment. A few of the main mechanisms underlying the beneficial effects of resveratrol on metabolic syndrome are outlined. This review also discusses the potential of resveratrol derivatives as a complementary or alternative medicine. In conclusion, resveratrol could be a useful regimen for the prevention and treatment of metabolic syndrome and its related conditions.

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Chih-Yao Hou; You-Lin Tain; Hong-Ren Yu; Li-Tung Huang. The Effects of Resveratrol in the Treatment of Metabolic Syndrome. International Journal of Molecular Sciences 2019, 20, 535 .

AMA Style

Chih-Yao Hou, You-Lin Tain, Hong-Ren Yu, Li-Tung Huang. The Effects of Resveratrol in the Treatment of Metabolic Syndrome. International Journal of Molecular Sciences. 2019; 20 (3):535.

Chicago/Turabian Style

Chih-Yao Hou; You-Lin Tain; Hong-Ren Yu; Li-Tung Huang. 2019. "The Effects of Resveratrol in the Treatment of Metabolic Syndrome." International Journal of Molecular Sciences 20, no. 3: 535.

Journal article
Published: 12 November 2018 in International Journal of Molecular Sciences
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We examined the mechanisms of chronic liver steatosis after prenatal dexamethasone exposure and whether melatonin rescues adult offspring with liver steatosis. Melatonin rescued prenatal dexamethasone-exposed livers with steatosis in young rats. Sprague-Dawley rats pregnant at gestational day 14–21 were administered with intraperitoneal dexamethasone (DEX) or prenatal dexamethasone and melatonin between gestational day 14 and postnatal day ~120 (DEX+MEL). Chronic programming effects in the liver were assessed at day ~120. Liver steatosis increased in the DEX compared with that in the vehicle group and decreased in the DEX+MEL group (p < 0.05), with no changes in cellular apoptosis. Expression of leptin and its receptor decreased in the DEX (p < 0.05) and increased in the DEX+MEL group (p < 0.05), as revealed by RT-PCR and Western blotting. Tumor necrosis factor alpha (TNF-α) and interleukin (IL)-6 expression increased in the DEX group compared with that in the vehicle group and decreased in the DEX+MEL group (p < 0.05). Liver DNA methyltransferase activity and leptin methylation increased in the DEX group (p < 0.05) and decreased in the DEX+MEL group (p < 0.05), with no changes in HDAC activity. Thus, prenatal dexamethasone induces liver steatosis at ~120 days via altered leptin expression and liver inflammation without leptin resistance. Melatonin reverses leptin methylation and expression and decreases inflammation and chronic liver steatosis not via apoptosis or histone deacetylation (HDAC).

ACS Style

Ching-Chou Tsai; Yu-Ju Lin; Hong-Ren Yu; Jiunn-Ming Sheen; I-Chun Lin; Yun-Ju Lai; You-Lin Tain; Li-Tung Huang; Mao-Meng Tiao. Regulation of Leptin Methylation Not via Apoptosis by Melatonin in the Rescue of Chronic Programming Liver Steatosis. International Journal of Molecular Sciences 2018, 19, 3565 .

AMA Style

Ching-Chou Tsai, Yu-Ju Lin, Hong-Ren Yu, Jiunn-Ming Sheen, I-Chun Lin, Yun-Ju Lai, You-Lin Tain, Li-Tung Huang, Mao-Meng Tiao. Regulation of Leptin Methylation Not via Apoptosis by Melatonin in the Rescue of Chronic Programming Liver Steatosis. International Journal of Molecular Sciences. 2018; 19 (11):3565.

Chicago/Turabian Style

Ching-Chou Tsai; Yu-Ju Lin; Hong-Ren Yu; Jiunn-Ming Sheen; I-Chun Lin; Yun-Ju Lai; You-Lin Tain; Li-Tung Huang; Mao-Meng Tiao. 2018. "Regulation of Leptin Methylation Not via Apoptosis by Melatonin in the Rescue of Chronic Programming Liver Steatosis." International Journal of Molecular Sciences 19, no. 11: 3565.

Journal article
Published: 06 June 2018 in Experimental and Therapeutic Medicine
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Prenatal exposure to glucocorticoids is associated with negative health consequences for the offspring that persist into adulthood, including liver steatosis. Melatonin has previously been demonstrated to suppress liver steatosis and oxidative stress in humans with non-alcoholic fatty liver disease and in animal models of obesity. The present study aimed to determine whether melatonin protects against liver steatosis induced by prenatal dexamethasone exposure followed by postnatal high-fat diet. Pregnant Sprague-Dawley rats at gestational days 14–21 were administered dexamethasone (0.1 mg/kg/day) or saline via intraperitoneal injection. The offspring were then divided into five groups, as follows: Vehicle, postnatal high-fat diet (VHF), prenatal dexamethasone exposure (DEX), prenatal dexamethasone exposure + postnatal high-fat diet (DHF), and prenatal dexamethasone exposure + postnatal high-fat diet + melatonin (DHFM) group. Following vehicle or dexamethasone exposure of the maternal rats, the offspring rats in the VHF, DHF and DHFM groups received a high-fat diet (58% fat) between weaning and 6 months of age. In the DHFM group, melatonin was administered to the mothers from gestational days 14–21 until weaning. The offspring continued to receive melatonin until they were sacrificed at 6 months old. Oil Red O staining demonstrated stronger intensity in the DHF group compared with that in the other four groups. Western blot analysis also revealed higher levels of cleaved caspase-3, tumor necrosis factor-α (TNF-α), suppressor of cytokine signaling 3 (SOCS3) and malondialdehyde (MDA), as well as reduced expression of manganese superoxide dismutase (MnSOD) and phosphoinositide 3-kinase (PI3K) in the DHF group compared with the vehicle and DHFM groups. In addition, melatonin reduced the Oil Red O staining intensity and the levels of cleaved caspase-3, TNF-α, SOCS3 and MDA, while it increased the MnSOD and PI3K levels, in the DHFM group compared with the DHF group. In conclusion, postnatal high-fat diet aggravated the prenatal dexamethasone-induced liver steatosis in adult rat offspring via inflammation, oxidative stress and cellular apoptosis, which may be ameliorated by prenatal melatonin therapy.

ACS Style

Ching‑Chou Tsai; Yu‑Ju Lin; Hong‑Ren Yu; Jiunn‑Ming Sheen; You-Lin Tain; Li‑Tung Huang; Mao‑Meng Tiao. Melatonin alleviates liver steatosis induced by prenatal dexamethasone exposure and postnatal high‑fat diet. Experimental and Therapeutic Medicine 2018, 16, 917 -924.

AMA Style

Ching‑Chou Tsai, Yu‑Ju Lin, Hong‑Ren Yu, Jiunn‑Ming Sheen, You-Lin Tain, Li‑Tung Huang, Mao‑Meng Tiao. Melatonin alleviates liver steatosis induced by prenatal dexamethasone exposure and postnatal high‑fat diet. Experimental and Therapeutic Medicine. 2018; 16 (2):917-924.

Chicago/Turabian Style

Ching‑Chou Tsai; Yu‑Ju Lin; Hong‑Ren Yu; Jiunn‑Ming Sheen; You-Lin Tain; Li‑Tung Huang; Mao‑Meng Tiao. 2018. "Melatonin alleviates liver steatosis induced by prenatal dexamethasone exposure and postnatal high‑fat diet." Experimental and Therapeutic Medicine 16, no. 2: 917-924.

Article
Published: 02 May 2018 in NeuroReport
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Bile duct ligation (BDL) in young rats can cause impaired liver function and cognition deficits. Nitric oxide is implicated in hepatic encephalopathy and is also involved in cognition. In this study, we examined the role of brain asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor, in young BDL rats with spatial deficits. Young male Sprague-Dawley rats aged 17 days were assigned to four groups: laparotomy (SHAM), laparotomy plus 5 mg melatonin delivered through a pellet (SHAMM) for 4 weeks, BDL for 4 weeks, and BDL plus 5 mg melatonin delivered through a pellet (BDLM) for 4 weeks. Their spatial memory was assessed using a Morris water-maze task. Plasma and brains were collected for biochemical and ADMA analyses. We found that the BDL group had significantly elevated levels of ADMA in the plasma, the prefrontal cortex, and the dorsal hippocampus, and worse spatial performance than that of the control groups. Melatonin administration prevented an increase in the ADMA levels in the plasma, prefrontal cortex, and dorsal hippocampus, and prevented spatial deficits in BDL rats. In addition, melatonin maintained brain-derived neurotrophic factor in the dorsal hippocampus at a level comparable with controls. We concluded that melatonin is effective in preventing spatial deficits and decreasing ADMA levels in the plasma, prefrontal cortex, and dorsal hippocampus in young BDL rats. Brain ADMA levels might play a role in BDL-induced spatial deficits. This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0/

ACS Style

Mei-Hsin Hsu; Yu-Chieh Chen; Jiunn-Ming Sheen; Shih-Wen Li; Li-Tung Huang. Melatonin prevented spatial deficits and increases in brain asymmetric dimethylarginine in young bile duct ligation rats. NeuroReport 2018, 29, 541 -546.

AMA Style

Mei-Hsin Hsu, Yu-Chieh Chen, Jiunn-Ming Sheen, Shih-Wen Li, Li-Tung Huang. Melatonin prevented spatial deficits and increases in brain asymmetric dimethylarginine in young bile duct ligation rats. NeuroReport. 2018; 29 (7):541-546.

Chicago/Turabian Style

Mei-Hsin Hsu; Yu-Chieh Chen; Jiunn-Ming Sheen; Shih-Wen Li; Li-Tung Huang. 2018. "Melatonin prevented spatial deficits and increases in brain asymmetric dimethylarginine in young bile duct ligation rats." NeuroReport 29, no. 7: 541-546.

Journal article
Published: 04 April 2018 in Scientific Reports
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This study aimed to study the impact of a combination of maternal and post-weaning high-fat diets and whether resveratrol was beneficial. Sprague-Dawley dams were fed either chow or a high-fat diet, before mating, during pregnancy, and into lactation. At weaning, their offspring were randomly fed chow or a high-fat diet. Four experimental groups were generated: CC (maternal/postnatal chow diet), HC (maternal high-fat/postnatal chow diet), CH (maternal chow/postnatal high-fat diet), and HH (maternal/postnatal high-fat diet). A fifth group consisted of HH plus resveratrol. The 4 month-old offspring of HH group had higher body weight, higher levels of plasma triglycerides, leptin, angiotensin I and angiotensin II and abnormal intraperitoneal glucose tolerance test results, which fulfilled the features of metabolic syndrome. The dysregulation of the renin-angiotensin system was seen in multiple organs. Sirtuin 1 expression/abundance was reduced by a maternal/postnatal high-fat diet, in all the organs examined. Resveratrol ameliorated most of the features of metabolic syndrome and molecular alterations. The administration of a high-fat diet in both periods showed interactive metabolic effects in the plasma and many organs. Our results suggest that a maternal high-fat diet sensitizes offspring to the adverse effects of subsequent high-fat intake on multiple organs.

ACS Style

Jiunn-Ming Sheen; Hong-Ren Yu; You-Lin Tain; Wan-Long Tsai; Mao-Meng Tiao; I-Chun Lin; Ching-Chou Tsai; Yu-Ju Lin; Li-Tung Huang. Combined maternal and postnatal high-fat diet leads to metabolic syndrome and is effectively reversed by resveratrol: a multiple-organ study. Scientific Reports 2018, 8, 1 -12.

AMA Style

Jiunn-Ming Sheen, Hong-Ren Yu, You-Lin Tain, Wan-Long Tsai, Mao-Meng Tiao, I-Chun Lin, Ching-Chou Tsai, Yu-Ju Lin, Li-Tung Huang. Combined maternal and postnatal high-fat diet leads to metabolic syndrome and is effectively reversed by resveratrol: a multiple-organ study. Scientific Reports. 2018; 8 (1):1-12.

Chicago/Turabian Style

Jiunn-Ming Sheen; Hong-Ren Yu; You-Lin Tain; Wan-Long Tsai; Mao-Meng Tiao; I-Chun Lin; Ching-Chou Tsai; Yu-Ju Lin; Li-Tung Huang. 2018. "Combined maternal and postnatal high-fat diet leads to metabolic syndrome and is effectively reversed by resveratrol: a multiple-organ study." Scientific Reports 8, no. 1: 1-12.