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Prof. You-Lin Tain
Kaohsiung Chang Gung Memorial Hospital

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Research Keywords & Expertise

0 Chronic Kidney Disease
0 Hypertension
0 Nitric Oxide
0 Oxidative Stress
0 Melatonin

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Hypertension
Nitric Oxide
Oxidative Stress
arginine
Chronic Kidney Disease
Melatonin
resveratrol
DOHaD

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Short Biography

In 1992, You-Lin Tain graduated from China Medical University, Taiwan with an M.D. degree. He later received his residency training in pediatrics and fellow training in pediatric nephrology at Chang Gung Memorial Hospital (CGMH), Taiwan. From 1999 to 2002, Dr. Tain worked as an attending pediatrician at Kaohsiung CGMH, Taiwan. At the same time, he attained a master’s degree in biomedicine at the Chang Gung University, Taiwan. In 2003, he went to the U.S. with a pre-doctoral fellowship award from his hospital. In 2007, Dr. Tain graduated from the University of Florida, Graduate School of Medicine with a Ph.D. in Physiology. Later he returned to Taiwan and worked at the Kaohsiung CGMH. Presently, he is a Professor of Pediatrics at the Kaohsiung CGMH and Chang Gung University College of Medicine, a physician scientist, and the Director of the Department of Medical Research and Development, Kaohsiung CGMH, Taiwan. His research interests include nitric oxide, free radical medicine, chronic kidney disease, DOHaD, and hypertension.

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Journal article
Published: 30 August 2021 in Nutrients
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Maternal exposure to environmental pollutants affects fetal development, which can result in hypertension in adulthood. Gut microbiota-derived metabolite trimethylamine (TMA), trimethylamine-N-oxide (TMAO), and short chain fatty acids (SCFAs) have been associated with hypertension. We tested a hypothesis that maternal 3,3-Dimethyl-1-butanol (DMB, a TMA inhibitor) therapy prevents 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure-induced hypertension in adult offspring relevant to alterations of gut microbiota-derived metabolites, the mediation of aryl hydrocarbon receptor (AHR) signaling, and the renin-angiotensin system (RAS). Pregnant Sprague-Dawley rats were given weekly oral dose of TCDD 200 ng/kg for four doses (T), 1% DMB in drinking water (D), TCDD + DMB (TD), or vehicle (C) in pregnancy and lactation periods. Male progeny (n = 8/group) were sacrificed at the age of 12 weeks. Perinatal TCDD exposure caused hypertension in adult male offspring coinciding with reduced α-diversity, increased the Firmicutes to Bacteroidetes ratio, less abundant beneficial bacteria, impaired SCFA receptors’ expression, the activation of AHR signaling, and the aberrant activation of the RAS. Treatment with DMB during pregnancy and lactation rescued hypertension induced by perinatal TCDD exposure. This was accompanied by reshaping gut microbiota, mediating TMA-TMAO metabolic pathway, increasing acetic acid and its receptors, and restoring the AHR and RAS pathway. Our data provide new insights into the therapeutic potential of DMB, a microbiome-based metabolite treatment, for the prevention of hypertension of developmental origins.

ACS Style

Chien-Ning Hsu; Chih-Yao Hou; Chien-Te Lee; Guo-Ping Chang-Chien; Sufan Lin; You-Lin Tain. Maternal 3,3-Dimethyl-1-Butanol Therapy Protects Adult Male Rat Offspring against Hypertension Programmed by Perinatal TCDD Exposure. Nutrients 2021, 13, 3041 .

AMA Style

Chien-Ning Hsu, Chih-Yao Hou, Chien-Te Lee, Guo-Ping Chang-Chien, Sufan Lin, You-Lin Tain. Maternal 3,3-Dimethyl-1-Butanol Therapy Protects Adult Male Rat Offspring against Hypertension Programmed by Perinatal TCDD Exposure. Nutrients. 2021; 13 (9):3041.

Chicago/Turabian Style

Chien-Ning Hsu; Chih-Yao Hou; Chien-Te Lee; Guo-Ping Chang-Chien; Sufan Lin; You-Lin Tain. 2021. "Maternal 3,3-Dimethyl-1-Butanol Therapy Protects Adult Male Rat Offspring against Hypertension Programmed by Perinatal TCDD Exposure." Nutrients 13, no. 9: 3041.

Journal article
Published: 30 August 2021 in Antioxidants
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Exposure to environmental chemicals during pregnancy and lactation is a contributing factor in gut microbiota dysbiosis and linked to programming of hypertension. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), the most toxic dioxin, induces toxic effects by mediating aryl hydrocarbon receptor (AHR). Resveratrol, a potent antioxidant with prebiotic properties, can possess high affinity for AHR and protect against TCDD-activated AHR attack. We examined whether perinatal resveratrol therapy prevents offspring hypertension programmed by maternal TCDD exposure and whether its beneficial effects are related to reshaping gut microbiota and antagonizing AHR-mediated T helper 17 (TH17) cells responses using a maternal TCDD exposure rat model. Pregnant Sprague-Dawley rats were given a weekly oral dose of TCDD 200 ng/kg for four doses (T), 50 mg/L of resveratrol in drinking water (CR), TCDD + resveratrol (TR), or vehicle (C) in pregnancy and lactation periods. Male offspring (n = 7–8/group) were sacrificed at the age of 12 weeks. Perinatal TCDD exposure caused elevated blood pressure in adult male offspring, which resveratrol supplementation prevented. Additionally, the TCDD-induced programming of hypertension is coincided with the activation of AHR signaling, TH17-induced renal inflammation, and alterations of gut microbiota compositions. Conversely, TCDD-mediated induction of AHR signaling and TH17 responses were restored by maternal resveratrol supplementation. Furthermore, maternal resveratrol supplementation prevented the programming of hypertension and was related to increased genera Bacteroides, ASF356, and Lachnoclostridium. Taken together, these results suggest that the interplay between gut microbiota, AHR-mediated TH17 responses, and renal inflammation in the gut and kidneys may play an important role in the action of resveratrol against TCDD-induced programming of hypertension.

ACS Style

Chien-Ning Hsu; Chih-Hsing Hung; Chih-Yao Hou; Chi-I. Chang; You-Lin Tain. Perinatal Resveratrol Therapy to Dioxin-Exposed Dams Prevents the Programming of Hypertension in Adult Rat Offspring. Antioxidants 2021, 10, 1393 .

AMA Style

Chien-Ning Hsu, Chih-Hsing Hung, Chih-Yao Hou, Chi-I. Chang, You-Lin Tain. Perinatal Resveratrol Therapy to Dioxin-Exposed Dams Prevents the Programming of Hypertension in Adult Rat Offspring. Antioxidants. 2021; 10 (9):1393.

Chicago/Turabian Style

Chien-Ning Hsu; Chih-Hsing Hung; Chih-Yao Hou; Chi-I. Chang; You-Lin Tain. 2021. "Perinatal Resveratrol Therapy to Dioxin-Exposed Dams Prevents the Programming of Hypertension in Adult Rat Offspring." Antioxidants 10, no. 9: 1393.

Journal article
Published: 28 July 2021 in Antioxidants
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Melatonin, a signaling hormone with pleiotropic biofunctions, has shown health benefits. Trimethylamine-N-oxide (TMAO) and asymmetric dimethylarginine (ADMA) are uremic toxins involved in the development of hypertension. TMAO originates from trimethylamine (TMA), a gut microbial product. ADMA is an endogenous nitric oxide (NO) synthase inhibitor. We examined whether melatonin therapy could prevent hypertension and kidney disease by mediating gut microbiota-derived metabolites and the NO pathway using an adenine-induced chronic kidney disease (CKD) young rat model. Six-week-old young Sprague Dawley rats of both sexes were fed a regular diet (C group), a diet supplemented with 0.5% adenine (CKD group), or adenine plus 0.01% melatonin in their drinking water (CKD + M group) for three weeks (N = 8/group). Adenine-fed rats developed renal dysfunction, hypertension, renal hypertrophy and increased uremic toxin levels of TMAO and ADMA. Melatonin therapy prevented hypertension in both sexes and attenuated kidney injury in males. Melatonin reversed the changes to the plasma TMAO-to-TMA ratio induced by CKD in both sexes. Besides, the protective effects of melatonin were associated with restoration of gut microbiota alterations, including increased α-diversity, and enhancement of the abundance of the phylum Proteobacteria and the genus Roseburia in male rats. Melatonin therapy also partially prevented the increases in ADMA in male CKD rats. Melatonin sex-specifically protected young rats against hypertension and kidney injury induced by CKD. The results of this study contribute toward a greater understanding of the interaction between melatonin, gut microbiota-derived metabolites, and the NO pathway that is behind CKD, which will help to prevent CKD-related disorders in children.

ACS Style

Chien-Ning Hsu; Hung-Wei Yang; Chih-Yao Hou; Guo-Ping Chang-Chien; Sufan Lin; You-Lin Tain. Melatonin Prevents Chronic Kidney Disease-Induced Hypertension in Young Rat Treated with Adenine: Implications of Gut Microbiota-Derived Metabolites. Antioxidants 2021, 10, 1211 .

AMA Style

Chien-Ning Hsu, Hung-Wei Yang, Chih-Yao Hou, Guo-Ping Chang-Chien, Sufan Lin, You-Lin Tain. Melatonin Prevents Chronic Kidney Disease-Induced Hypertension in Young Rat Treated with Adenine: Implications of Gut Microbiota-Derived Metabolites. Antioxidants. 2021; 10 (8):1211.

Chicago/Turabian Style

Chien-Ning Hsu; Hung-Wei Yang; Chih-Yao Hou; Guo-Ping Chang-Chien; Sufan Lin; You-Lin Tain. 2021. "Melatonin Prevents Chronic Kidney Disease-Induced Hypertension in Young Rat Treated with Adenine: Implications of Gut Microbiota-Derived Metabolites." Antioxidants 10, no. 8: 1211.

Journal article
Published: 22 July 2021 in Children
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Cardiovascular disease (CVD) risk factors are present early in life in children with chronic kidney disease (CKD), consequently cardiovascular morbidity presents in early adulthood. However, risk factors of CVD have been rarely addressed in children with early stage of CKD. This study included 63 children and adolescents aged 8- to 18 years-old with CKD stage G1–G4. Cardiovascular assessments consisted of 24-h ambulatory blood pressure monitoring (ABPM), arterial stiffness index, and echocardiography. We also applied dual-energy x-ray absorptiometry (DXA) scanning to analyze percentage body fat (PBF), lean body mass index (LBMI), fat mass index (FMI), and the android to gynoid fat ratio (A/G ratio). Up to 63.5% of CKD children had abnormal changes in BP detected by ABPM. CKD children with abnormal ABPM were older, had higher numbers of CKD stage G2 to G4, hyperuricemia, obesity, and higher FMI z-score and A/G ratio compared to individuals with normal ABPM (all p< 0.05). Among these factors, only FMI z-score showed an independent association with abnormal ABPM using multivariate logistic regression analysis (p = 0.037). Our data highlight that body fat plays a key role for an abnormal ABPM in CKD children. The assessment of FMI may have clinical utility in discriminating CV risk in children and adolescents with early stages of CKD.

ACS Style

Chien-Ning Hsu; Pei-Chen Lu; You-Lin Tain. Fat Mass Index Associated with Blood Pressure Abnormalities in Children with Chronic Kidney Disease. Children 2021, 8, 621 .

AMA Style

Chien-Ning Hsu, Pei-Chen Lu, You-Lin Tain. Fat Mass Index Associated with Blood Pressure Abnormalities in Children with Chronic Kidney Disease. Children. 2021; 8 (8):621.

Chicago/Turabian Style

Chien-Ning Hsu; Pei-Chen Lu; You-Lin Tain. 2021. "Fat Mass Index Associated with Blood Pressure Abnormalities in Children with Chronic Kidney Disease." Children 8, no. 8: 621.

Review
Published: 21 July 2021 in International Journal of Molecular Sciences
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Nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H2S), three major gasotransmitters, are involved in pleiotropic biofunctions. Research on their roles in hypertension and kidney disease has greatly expanded recently. The developing kidney can be programmed by various adverse in utero conditions by so-called renal programming, giving rise to hypertension and kidney disease in adulthood. Accordingly, early gasotransmitter-based interventions may have therapeutic potential to revoke programming processes, subsequently preventing hypertension and kidney disease of developmental origins. In this review, we describe the current knowledge of NO, CO, and H2S implicated in pregnancy, including in physiological and pathophysiological processes, highlighting their key roles in hypertension and kidney disease. We summarize current evidence of gasotransmitter-based interventions for prevention of hypertension and kidney disease in animal models. Continued study is required to assess the interplay among the gasotransmitters NO, CO, and H2S and renal programming, as well as a greater focus on further clinical translation.

ACS Style

Chien-Ning Hsu; You-Lin Tain. Gasotransmitters for the Therapeutic Prevention of Hypertension and Kidney Disease. International Journal of Molecular Sciences 2021, 22, 7808 .

AMA Style

Chien-Ning Hsu, You-Lin Tain. Gasotransmitters for the Therapeutic Prevention of Hypertension and Kidney Disease. International Journal of Molecular Sciences. 2021; 22 (15):7808.

Chicago/Turabian Style

Chien-Ning Hsu; You-Lin Tain. 2021. "Gasotransmitters for the Therapeutic Prevention of Hypertension and Kidney Disease." International Journal of Molecular Sciences 22, no. 15: 7808.

Review
Published: 01 July 2021 in Nutrients
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Cardiovascular diseases (CVDs) can originate from early life. Accumulating evidence suggests that gut microbiota in early life is linked to CVDs in later life. Gut microbiota-targeted therapy has gained significant importance in recent decades for its health-promoting role in the prevention (rather than just treatment) of CVDs. Thus far, available gut microbiota-based treatment modalities used as reprogramming interventions include probiotics, prebiotics, and postbiotics. The purpose of this review is, first, to highlight current studies that link dysbiotic gut microbiota to the developmental origins of CVD. This is followed by a summary of the connections between the gut microbiota and CVD behind cardiovascular programming, such as short chain fatty acids (SCFAs) and their receptors, trimethylamine-N-oxide (TMAO), uremic toxins, and aryl hydrocarbon receptor (AhR), and the renin-angiotensin system (RAS). This review also presents an overview of how gut microbiota-targeted reprogramming interventions can prevent the developmental origins of CVD from animal studies. Overall, this review reveals that recent advances in gut microbiota-targeted therapy might provide the answers to reduce the global burden of CVDs. Still, additional studies will be needed to put research findings into practice.

ACS Style

Chien-Ning Hsu; Chih-Yao Hou; Wei-Hsuan Hsu; You-Lin Tain. Cardiovascular Diseases of Developmental Origins: Preventive Aspects of Gut Microbiota-Targeted Therapy. Nutrients 2021, 13, 2290 .

AMA Style

Chien-Ning Hsu, Chih-Yao Hou, Wei-Hsuan Hsu, You-Lin Tain. Cardiovascular Diseases of Developmental Origins: Preventive Aspects of Gut Microbiota-Targeted Therapy. Nutrients. 2021; 13 (7):2290.

Chicago/Turabian Style

Chien-Ning Hsu; Chih-Yao Hou; Wei-Hsuan Hsu; You-Lin Tain. 2021. "Cardiovascular Diseases of Developmental Origins: Preventive Aspects of Gut Microbiota-Targeted Therapy." Nutrients 13, no. 7: 2290.

Journal article
Published: 30 June 2021 in Molecules
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Resveratrol butyrate esters (RBE) are derivatives of resveratrol (RSV) and butyric acid and exhibit biological activity similar to that of RSV but with higher bioavailability. The aim of this study was designed as an animal experiment to explore the effects of RBE on the serum biochemistry, and fat deposits in the offspring rats exposed to bisphenol A (BPA), along with the growth and decline of gut microbiota. We constructed an animal model of perinatal Bisphenol A (BPA) exposure to observe the effects of RBE supplementation on obesity, blood lipids, and intestinal microbiota in female offspring rats. Perinatal exposure to BPA led to weight gain, lipid accumulation, high levels of blood lipids, and deterioration of intestinal microbiota in female offspring rats. RBE supplementation reduced the weight gain and lipid accumulation caused by BPA, optimised the levels of blood lipids, significantly reduced the Firmicutes/Bacteroidetes (F/B) ratio, and increased and decreased the abundance of S24-7 and Lactobacillus, respectively. The analysis of faecal short-chain fatty acid (SCFA) levels revealed that BPA exposure increased the faecal concentration of acetate, which could be reduced via RBE supplementation. However, the faecal concentrations of propionate and butyrate were not only significantly lower than that of acetate, but also did not significantly change in response to BPA exposure or RBE supplementation. Hence, RBE can suppress BPA-induced obesity in female offspring rats, and it demonstrates excellent modulatory activity on intestinal microbiota, with potential applications in perinatological research.

ACS Style

Ming-Kuei Shih; You-Lin Tain; Yu-Wei Chen; Wei-Hsuan Hsu; Yao-Tsung Yeh; Sam Chang; Jin-Xian Liao; Chih-Yao Hou. Resveratrol Butyrate Esters Inhibit Obesity Caused by Perinatal Exposure to Bisphenol A in Female Offspring Rats. Molecules 2021, 26, 4010 .

AMA Style

Ming-Kuei Shih, You-Lin Tain, Yu-Wei Chen, Wei-Hsuan Hsu, Yao-Tsung Yeh, Sam Chang, Jin-Xian Liao, Chih-Yao Hou. Resveratrol Butyrate Esters Inhibit Obesity Caused by Perinatal Exposure to Bisphenol A in Female Offspring Rats. Molecules. 2021; 26 (13):4010.

Chicago/Turabian Style

Ming-Kuei Shih; You-Lin Tain; Yu-Wei Chen; Wei-Hsuan Hsu; Yao-Tsung Yeh; Sam Chang; Jin-Xian Liao; Chih-Yao Hou. 2021. "Resveratrol Butyrate Esters Inhibit Obesity Caused by Perinatal Exposure to Bisphenol A in Female Offspring Rats." Molecules 26, no. 13: 4010.

Journal article
Published: 11 June 2021 in International Journal of Environmental Research and Public Health
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Introduction: Phthalates are substances that are added to plastic products to increase their plasticity. These substances are released easily into the environment and can act as endocrine disruptors. Epidemiological studies in children have showed inconsistent findings regarding the relationship between prenatal or postnatal exposure to phthalates and the risk of allergic disease. Our hypothesis is that prenatal exposure to phthalates may contribute to the development of allergies in children. Material and methods: The objective of this study was to determine the associations between urinary phthalate metabolite concentrations in pregnant women, maternal atopic diathesis, maternal lifestyle, and cord blood IgE. Pregnant mothers and paired newborns (n = 101) were enrolled from an antenatal clinic. The epidemiologic data and the clinical information were collected using standard questionnaires and medical records. The maternal blood and urine samples were collected at 24–28 weeks gestation, and cord blood IgE, IL-12p70, IL-4, and IL-10 levels were determined from the newborns at birth. The link between phthalates and maternal IgE was also assessed. To investigate the effects of phthalates on neonatal immunity, cord blood mononuclear cells (MNCs) were used for cytokine induction in another in vitro experiment. Results: We found that maternal urine monoethyl phthalate (MEP) (a metabolite of di-ethyl phthalate (DEP)) concentrations are positively correlated with the cord blood IgE of the corresponding newborns. The cord blood IL-12p70 levels of mothers with higher maternal urine MEP groups (high DEP exposure) were lower than mothers with low DEP exposure. In vitro experiments demonstrated that DEP could enhance IL-4 production of cord blood MNCs rather than adult MNCs. Conclusion: Prenatal DEP exposure is related to neonatal IgE level and alternation of cytokines relevant to Th1/Th2 polarization. This suggests the existence of a link between prenatal exposure to specific plasticizers and the future development of allergies.

ACS Style

Chang-Ku Tsai; Hsin-Hsin Cheng; Te-Yao Hsu; Jiu-Yao Wang; Chih-Hsing Hung; Ching-Chang Tsai; Yun-Ju Lai; Yu-Ju Lin; Hsin-Chun Huang; Julie Chan; You-Lin Tain; Chih-Cheng Chen; Ti-An Tsai; Hong-Ren Yu. Prenatal Exposure to Di-Ethyl Phthalate (DEP) Is Related to Increasing Neonatal IgE Levels and the Altering of the Immune Polarization of Helper-T Cells. International Journal of Environmental Research and Public Health 2021, 18, 6364 .

AMA Style

Chang-Ku Tsai, Hsin-Hsin Cheng, Te-Yao Hsu, Jiu-Yao Wang, Chih-Hsing Hung, Ching-Chang Tsai, Yun-Ju Lai, Yu-Ju Lin, Hsin-Chun Huang, Julie Chan, You-Lin Tain, Chih-Cheng Chen, Ti-An Tsai, Hong-Ren Yu. Prenatal Exposure to Di-Ethyl Phthalate (DEP) Is Related to Increasing Neonatal IgE Levels and the Altering of the Immune Polarization of Helper-T Cells. International Journal of Environmental Research and Public Health. 2021; 18 (12):6364.

Chicago/Turabian Style

Chang-Ku Tsai; Hsin-Hsin Cheng; Te-Yao Hsu; Jiu-Yao Wang; Chih-Hsing Hung; Ching-Chang Tsai; Yun-Ju Lai; Yu-Ju Lin; Hsin-Chun Huang; Julie Chan; You-Lin Tain; Chih-Cheng Chen; Ti-An Tsai; Hong-Ren Yu. 2021. "Prenatal Exposure to Di-Ethyl Phthalate (DEP) Is Related to Increasing Neonatal IgE Levels and the Altering of the Immune Polarization of Helper-T Cells." International Journal of Environmental Research and Public Health 18, no. 12: 6364.

Review
Published: 31 May 2021 in Biomedicines
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Increasing evidence suggests that fetal programming through environmental exposure during a critical window of early life leads to long-term detrimental outcomes, by so-called developmental origins of health and disease (DOHaD). Hypertension can originate in early life. Animal models are essential for providing convincing evidence of a causal relationship between diverse early-life insults and the developmental programming of hypertension in later life. These insults include nutritional imbalances, maternal illnesses, exposure to environmental chemicals, and medication use. In addition to reviewing the various insults that contribute to hypertension of developmental origins, this review focuses on the benefits of animal models in addressing the underlying mechanisms by which early-life interventions can reprogram disease processes and prevent the development of hypertension. Our understanding of hypertension of developmental origins has been enhanced by each of these animal models, narrowing the knowledge gap between animal models and future clinical translation.

ACS Style

Chien-Ning Hsu; You-Lin Tain. Animal Models for DOHaD Research: Focus on Hypertension of Developmental Origins. Biomedicines 2021, 9, 623 .

AMA Style

Chien-Ning Hsu, You-Lin Tain. Animal Models for DOHaD Research: Focus on Hypertension of Developmental Origins. Biomedicines. 2021; 9 (6):623.

Chicago/Turabian Style

Chien-Ning Hsu; You-Lin Tain. 2021. "Animal Models for DOHaD Research: Focus on Hypertension of Developmental Origins." Biomedicines 9, no. 6: 623.

Journal article
Published: 17 May 2021 in International Journal of Molecular Sciences
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Resveratrol can affect the physiology or biochemistry of offspring in the maternal–fetal animal model. However, it exhibits low bioavailability in humans and animals. Fifteen-week SD pregnant female rats were orally administered bisphenol A (BPA) and/or resveratrol butyrate ester (RBE), and the male offspring rats (n = 4–8 per group) were evaluated. The results show that RBE treatment (BPA + R30) compared with the BPA group can reduce the damage caused by BPA (p< 0.05). RBE enhanced the expression of selected genes and induced extramedullary hematopoiesis and mononuclear cell infiltration. RBE increased the abundance of S24-7 and Adlercreutzia in the intestines of the male offspring rats, as well as the concentrations of short-chain fatty acids (SCFAs) in the feces. RBE also increased the antioxidant capacity of the liver by inducing Nrf2, promoting the expression of HO-1, SOD, and CAT. It also increased the concentration of intestinal SCFAs, enhancing the barrier formed by intestinal cells, thereby preventing BPA-induced metabolic disruption in the male offspring rats, and reduced liver inflammation. This study identified a potential mechanism underlying the protective effects of RBE against the liver damage caused by BPA exposure during the peri-pregnancy period, and the influence of the gut microbiota on the gut–liver axis in the offspring.

ACS Style

Jin-Xian Liao; Yu-Wei Chen; Ming-Kuei Shih; You-Lin Tain; Yao-Tsung Yeh; Min-Hsi Chiu; Sam Chang; Chih-Yao Hou. Resveratrol Butyrate Esters Inhibit BPA-Induced Liver Damage in Male Offspring Rats by Modulating Antioxidant Capacity and Gut Microbiota. International Journal of Molecular Sciences 2021, 22, 5273 .

AMA Style

Jin-Xian Liao, Yu-Wei Chen, Ming-Kuei Shih, You-Lin Tain, Yao-Tsung Yeh, Min-Hsi Chiu, Sam Chang, Chih-Yao Hou. Resveratrol Butyrate Esters Inhibit BPA-Induced Liver Damage in Male Offspring Rats by Modulating Antioxidant Capacity and Gut Microbiota. International Journal of Molecular Sciences. 2021; 22 (10):5273.

Chicago/Turabian Style

Jin-Xian Liao; Yu-Wei Chen; Ming-Kuei Shih; You-Lin Tain; Yao-Tsung Yeh; Min-Hsi Chiu; Sam Chang; Chih-Yao Hou. 2021. "Resveratrol Butyrate Esters Inhibit BPA-Induced Liver Damage in Male Offspring Rats by Modulating Antioxidant Capacity and Gut Microbiota." International Journal of Molecular Sciences 22, no. 10: 5273.

Review
Published: 19 April 2021 in International Journal of Molecular Sciences
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The increase in the incidence of cardiovascular diseases (CVDs) and kidney disease has stimulated research for strategies that could prevent, rather than just treat, both interconnected disorders. Resveratrol, a polyphenolic compound with pleiotropic biofunctions, has shown health benefits. Emerging epidemiological data supports that early life environmental insults are regarded as increased risks of developing CVDs and kidney disease in adulthood. Conversely, both disorders could be reversed or postponed by shifting interventions from adulthood to earlier stage by so-called reprogramming. The purpose of this review is first to highlight current epidemiological studies linking cardiovascular and renal programming to resulting CVD and kidney disease of developmental origins. This will be followed by a summary of how resveratrol could exert a positive influence on CVDs and kidney disease. This review also presents an overview of the evidence documenting resveratrol as a reprogramming agent to protect against CVD and kidney disease of developmental origins from animal studies and to outline the advances in understanding the underlying molecular mechanisms. Overall, this review reveals the need for future research to further clarify the reprogramming effects of resveratrol before clinical translation.

ACS Style

Chien-Ning Hsu; Chih-Yao Hou; You-Lin Tain. Preventive Aspects of Early Resveratrol Supplementation in Cardiovascular and Kidney Disease of Developmental Origins. International Journal of Molecular Sciences 2021, 22, 4210 .

AMA Style

Chien-Ning Hsu, Chih-Yao Hou, You-Lin Tain. Preventive Aspects of Early Resveratrol Supplementation in Cardiovascular and Kidney Disease of Developmental Origins. International Journal of Molecular Sciences. 2021; 22 (8):4210.

Chicago/Turabian Style

Chien-Ning Hsu; Chih-Yao Hou; You-Lin Tain. 2021. "Preventive Aspects of Early Resveratrol Supplementation in Cardiovascular and Kidney Disease of Developmental Origins." International Journal of Molecular Sciences 22, no. 8: 4210.

Journal article
Published: 30 March 2021 in The Journal of Nutritional Biochemistry
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Resveratrol, a phytochemical, has shown antioxidant properties and potential benefits in hypertension. Asymmetric dimethylarginine (ADMA)-related nitric oxide deficiency and gut microbiota-derived metabolite trimethylamine-N-oxide (TMAO) have been linked to hypertension. We aimed to test whether maternal resveratrol therapy would protect adult offspring against hypertension programmed by prenatal exposure to ADMA and TMAO. Pregnant Sprague-Dawley rats received ADMA 10 mg/kg/day (A), TMAO 0.65 mg/hr (T), ADMA+TMAO (AT), or vesicle (CV). One group of ADMA+TMAO-exposed rats received 50 mg/L of resveratrol in drinking water during pregnancy and lactation periods (ATR). Male offspring (n = 8/group) were assigned to five groups: CV, A, T, AT, and ATR. Rats were killed at 12 weeks of age. ADMA exposure caused the elevation of blood pressure in 12-week-old male offspring, which was exacerbated by TMAO exposure. Treatment with resveratrol rescued hypertension programmed by combined ADMA and TMAO exposure. This was accompanied by alterations in the compositions of gut microbiota and increased fecal butyrate levels. Both the abundance of the butyrate-producing genera Lachnospiraceae and Ruminococcaceae were augmented by resveratrol. Meanwhile, resveratrol therapy significantly increased the abundance of the Cyanobiaceae and Erysipelotrichaceae families. Moreover, the protective effects of resveratrol were related to the mediation of the renin-angiotensin system . Our data provide new insights into the protective mechanisms of resveratrol against hypertension programmed by ADMA and TMAO, including regulation of gut microbiota and their metabolites, the renin-angiotensin system, and nitric oxide pathway. Resveratrol might be a potential reprogramming strategy to protect against the hypertension of developmental origins.

ACS Style

Chien-Ning Hsu; Chih-Yao Hou; Guo-Ping Chang-Chien; Sufan Lin; Julie Y.H. Chan; Chien-Te Lee; You-Lin Tain. Maternal resveratrol therapy protected adult rat offspring against hypertension programmed by combined exposures to asymmetric dimethylarginine and trimethylamine-N-oxide. The Journal of Nutritional Biochemistry 2021, 93, 108630 .

AMA Style

Chien-Ning Hsu, Chih-Yao Hou, Guo-Ping Chang-Chien, Sufan Lin, Julie Y.H. Chan, Chien-Te Lee, You-Lin Tain. Maternal resveratrol therapy protected adult rat offspring against hypertension programmed by combined exposures to asymmetric dimethylarginine and trimethylamine-N-oxide. The Journal of Nutritional Biochemistry. 2021; 93 ():108630.

Chicago/Turabian Style

Chien-Ning Hsu; Chih-Yao Hou; Guo-Ping Chang-Chien; Sufan Lin; Julie Y.H. Chan; Chien-Te Lee; You-Lin Tain. 2021. "Maternal resveratrol therapy protected adult rat offspring against hypertension programmed by combined exposures to asymmetric dimethylarginine and trimethylamine-N-oxide." The Journal of Nutritional Biochemistry 93, no. : 108630.

Journal article
Published: 10 March 2021 in Antioxidants
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To expand the applications and enhance the stability and bioactivity of resveratrol (RE), and to simultaneously include the potential health benefits of short chain fatty acids (SCFA) esters of RE were prepared by Steglich reactions with acetic, propionic, and butyric acids, respectively. RE and the esterified RE-SCFA products (including RAE, RPE, and RBE) were analyzed using nuclear magnetic resonance (NMR), Fourier-transform infrared (FTIR) spectroscopy, thermogravimetric analysis (TGA), differential thermal analysis (DTA), and liquid chromatography–mass spectrometry (LC–MS). The FTIR and 13C NMR spectra of the esterified products included ester-characteristic peaks at 1751 cm−1 and 171 ppm, respectively. Moreover, the peaks in the range of 1700 to 1600 cm−1 in the FTIR spectra of the esterified products indicated that the esterification of RE-SCFA was successful. The TGA results revealed that the RE-SCFA esters decomposed at lower temperatures than RE. The peaks in the LC–MS profiles of the esterified products indicated the formation of mono- and diesters, and the calculated monoester synthesis rates ranged between 45.81 and 49.64%. The RE esters inhibited the Cu2+-induced low-density lipoprotein oxidation reaction, exhibited antioxidant activity in bulk oil, and effectively inhibited the hydroxyl radical-induced DNA scission. Moreover, the RE-SCFA esters had better hydrogen peroxide scavenging activity than RE. Our results are the first in the literature to successfully including short chain fatty acids in the esters of resveratrol, and the products could be used as a functional food ingredient in processed foods or can be used as dietary supplements to promote health.

ACS Style

You-Lin Tain; Sam Chang; Jin-Xian Liao; Yu-Wei Chen; Hung-Tse Huang; Yu-Lun Li; Chih-Yao Hou. Synthesis of Short-Chain-Fatty-Acid Resveratrol Esters and Their Antioxidant Properties. Antioxidants 2021, 10, 420 .

AMA Style

You-Lin Tain, Sam Chang, Jin-Xian Liao, Yu-Wei Chen, Hung-Tse Huang, Yu-Lun Li, Chih-Yao Hou. Synthesis of Short-Chain-Fatty-Acid Resveratrol Esters and Their Antioxidant Properties. Antioxidants. 2021; 10 (3):420.

Chicago/Turabian Style

You-Lin Tain; Sam Chang; Jin-Xian Liao; Yu-Wei Chen; Hung-Tse Huang; Yu-Lun Li; Chih-Yao Hou. 2021. "Synthesis of Short-Chain-Fatty-Acid Resveratrol Esters and Their Antioxidant Properties." Antioxidants 10, no. 3: 420.

Journal article
Published: 06 March 2021 in International Journal of Molecular Sciences
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Gut microbiota-derived metabolites, in particular short chain fatty acids (SCFAs) and their receptors, are linked to hypertension. Fructose and antibiotics are commonly used worldwide, and they have a negative impact on the gut microbiota. Our previous study revealed that maternal high-fructose (HF) diet-induced hypertension in adult offspring is relevant to altered gut microbiome and its metabolites. We, therefore, intended to examine whether minocycline administration during pregnancy and lactation may further affect blood pressure (BP) programmed by maternal HF intake via mediating gut microbiota and SCFAs. Pregnant Sprague-Dawley rats received a normal diet or diet containing 60% fructose throughout pregnancy and lactation periods. Additionally, pregnant dams received minocycline (50 mg/kg/day) via oral gavage or a vehicle during pregnancy and lactation periods. Four groups of male offspring were studied (n = 8 per group): normal diet (ND), high-fructose diet (HF), normal diet + minocycline (NDM), and HF + minocycline (HFM). Male offspring were killed at 12 weeks of age. We observed that the HF diet and minocycline administration, both individually and together, causes the elevation of BP in adult male offspring, while there is no synergistic effect between them. Four groups displayed distinct enterotypes. Minocycline treatment leads to an increase in the F/B ratio, but decreased abundance of genera Lactobacillus, Ruminococcus, and Odoribacter. Additionally, minocycline treatment decreases plasma acetic acid and butyric acid levels. Hypertension programmed by maternal HF diet plus minocycline exposure is related to the increased expression of several SCFA receptors. Moreover, minocycline- and HF-induced hypertension, individually or together, is associated with the aberrant activation of the renin–angiotensin system (RAS). Conclusively, our results provide a new insight into the support of gut microbiota and its metabolite SCAFs in the developmental programming of hypertension and cast new light on the role of RAS in this process, which will help prevent hypertension programmed by maternal high-fructose and antibiotic exposure.

ACS Style

Chien-Ning Hsu; Julie Chan; Kay Wu; Hong-Ren Yu; Wei-Chia Lee; Chih-Yao Hou; You-Lin Tain. Altered Gut Microbiota and Its Metabolites in Hypertension of Developmental Origins: Exploring Differences between Fructose and Antibiotics Exposure. International Journal of Molecular Sciences 2021, 22, 2674 .

AMA Style

Chien-Ning Hsu, Julie Chan, Kay Wu, Hong-Ren Yu, Wei-Chia Lee, Chih-Yao Hou, You-Lin Tain. Altered Gut Microbiota and Its Metabolites in Hypertension of Developmental Origins: Exploring Differences between Fructose and Antibiotics Exposure. International Journal of Molecular Sciences. 2021; 22 (5):2674.

Chicago/Turabian Style

Chien-Ning Hsu; Julie Chan; Kay Wu; Hong-Ren Yu; Wei-Chia Lee; Chih-Yao Hou; You-Lin Tain. 2021. "Altered Gut Microbiota and Its Metabolites in Hypertension of Developmental Origins: Exploring Differences between Fructose and Antibiotics Exposure." International Journal of Molecular Sciences 22, no. 5: 2674.

Review
Published: 25 February 2021 in International Journal of Molecular Sciences
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The renin-angiotensin-aldosterone system (RAAS) is implicated in hypertension and kidney disease. The developing kidney can be programmed by various early-life insults by so-called renal programming, resulting in hypertension and kidney disease in adulthood. This theory is known as developmental origins of health and disease (DOHaD). Conversely, early RAAS-based interventions could reverse program processes to prevent a disease from occurring by so-called reprogramming. In the current review, we mainly summarize (1) the current knowledge on the RAAS implicated in renal programming; (2) current evidence supporting the connections between the aberrant RAAS and other mechanisms behind renal programming, such as oxidative stress, nitric oxide deficiency, epigenetic regulation, and gut microbiota dysbiosis; and (3) an overview of how RAAS-based reprogramming interventions may prevent hypertension and kidney disease of developmental origins. To accelerate the transition of RAAS-based interventions for prevention of hypertension and kidney disease, an extended comprehension of the RAAS implicated in renal programming is needed, as well as a greater focus on further clinical translation.

ACS Style

Chien-Ning Hsu; You-Lin Tain. Targeting the Renin–Angiotensin–Aldosterone System to Prevent Hypertension and Kidney Disease of Developmental Origins. International Journal of Molecular Sciences 2021, 22, 2298 .

AMA Style

Chien-Ning Hsu, You-Lin Tain. Targeting the Renin–Angiotensin–Aldosterone System to Prevent Hypertension and Kidney Disease of Developmental Origins. International Journal of Molecular Sciences. 2021; 22 (5):2298.

Chicago/Turabian Style

Chien-Ning Hsu; You-Lin Tain. 2021. "Targeting the Renin–Angiotensin–Aldosterone System to Prevent Hypertension and Kidney Disease of Developmental Origins." International Journal of Molecular Sciences 22, no. 5: 2298.

Review
Published: 05 February 2021 in Antioxidants
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The cardiovascular system can be programmed by a diversity of early-life insults, leading to cardiovascular disease (CVD) in adulthood. This notion is now termed developmental origins of health and disease (DOHaD). Emerging evidence indicates hydrogen sulfide (H2S), a crucial regulator of cardiovascular homeostasis, plays a pathogenetic role in CVD of developmental origins. Conversely, early H2S-based interventions have proved beneficial in preventing adult-onset CVD in animal studies via reversing programming processes by so-called reprogramming. The focus of this review will first summarize the current knowledge on H2S implicated in cardiovascular programming. This will be followed by supporting evidence for the links between H2S signaling and underlying mechanisms of cardiovascular programming, such as oxidative stress, nitric oxide deficiency, dysregulated nutrient-sensing signals, activation of the renin–angiotensin system, and gut microbiota dysbiosis. It will also provide an overview from animal models regarding how H2S-based reprogramming interventions, such as precursors of H2S and H2S donors, may prevent CVD of developmental origins. A better understanding of cardiovascular programming and recent advances in H2S-based interventions might provide the answers to bring down the global burden of CVD.

ACS Style

Chien-Ning Hsu; You-Lin Tain. Preventing Developmental Origins of Cardiovascular Disease: Hydrogen Sulfide as a Potential Target? Antioxidants 2021, 10, 247 .

AMA Style

Chien-Ning Hsu, You-Lin Tain. Preventing Developmental Origins of Cardiovascular Disease: Hydrogen Sulfide as a Potential Target? Antioxidants. 2021; 10 (2):247.

Chicago/Turabian Style

Chien-Ning Hsu; You-Lin Tain. 2021. "Preventing Developmental Origins of Cardiovascular Disease: Hydrogen Sulfide as a Potential Target?" Antioxidants 10, no. 2: 247.

Research article
Published: 05 February 2021 in Molecular Nutrition & Food Research
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Scope Perinatal high‐fat (HF) diet induces hypertension in adult offspring. Garlic, a naturally dietary source of Hydrogen sulfide (H2S) donor, has been shown benefits in hypertension. We examined whether maternal garlic oil supplementation can prevent hypertension induced by HF diet and elucidated its protective effects. Methods and Results Pregnant rats received either a normal diet or HF diet. Rat dams were given garlic oil or vehicle daily by oral gavage at 100 mg/kg/day during pregnancy and lactation. Male offspring were sacrificed at 16 weeks of age. Garlic oil supplementation during pregnancy and lactation protected against hypertension induced by HF diet in adult male offspring. The beneficial effects of garlic oil were associated with increased renal mRNA expression and activity of H2S‐generating enzymes, increased NO bioavailability, increased plasma short chain fatty acid levels, and alterations of gut microbiota composition. Garlic oil supplementation increased abundance of genus Lactobacillus, but decreased genera Turicibacter and Staphylococcus. Conclusion Our data revealed associations between H2S‐generating pathway in the gut and kidneys, NO system, gut microbiota, and microbiota‐derived metabolites in hypertension induced by HF intake and provided insight to garlic oil as a hypertension reprogramming strategy for further translational research. This article is protected by copyright. All rights reserved

ACS Style

Chien‐Ning Hsu; Chih‐Yao Hou; Guo‐Ping Chang‐Chien; Sufan Lin; You‐Lin Tain. Maternal Garlic Oil Supplementation Prevents High‐Fat Diet‐Induced Hypertension in Adult Rat Offspring: Implications of H2S‐Generating Pathway in the Gut and Kidneys. Molecular Nutrition & Food Research 2021, 65, 2001116 .

AMA Style

Chien‐Ning Hsu, Chih‐Yao Hou, Guo‐Ping Chang‐Chien, Sufan Lin, You‐Lin Tain. Maternal Garlic Oil Supplementation Prevents High‐Fat Diet‐Induced Hypertension in Adult Rat Offspring: Implications of H2S‐Generating Pathway in the Gut and Kidneys. Molecular Nutrition & Food Research. 2021; 65 (11):2001116.

Chicago/Turabian Style

Chien‐Ning Hsu; Chih‐Yao Hou; Guo‐Ping Chang‐Chien; Sufan Lin; You‐Lin Tain. 2021. "Maternal Garlic Oil Supplementation Prevents High‐Fat Diet‐Induced Hypertension in Adult Rat Offspring: Implications of H2S‐Generating Pathway in the Gut and Kidneys." Molecular Nutrition & Food Research 65, no. 11: 2001116.

Review
Published: 30 December 2020 in Antioxidants
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The “developmental origins of health and disease” theory indicates that many adult-onset diseases can originate in the earliest stages of life. The developing kidney has emerged as being particularly vulnerable to adverse in utero conditions leading to morphological and functional changes, namely renal programming. Emerging evidence indicates oxidative stress, an imbalance between reactive oxygen/nitrogen species (ROS/RNS) and antioxidant systems, plays a pathogenetic role in the developmental programming of kidney disease. Conversely, perinatal use of antioxidants has been implemented to reverse programming processes and prevent adult-onset diseases. We have termed this reprogramming. The focus of this review is twofold: (1) To summarize the current knowledge on oxidative stress implicated in renal programming and kidney disease of developmental origins; and (2) to provide an overview of reprogramming effects of perinatal antioxidant therapy on renal programming and how this may prevent adult-onset kidney disease. Although early-life oxidative stress is implicated in mediating renal programming and adverse offspring renal outcomes, and animal models provide promising results to allow perinatal antioxidants applied as potential reprogramming interventions, it is still awaiting clinical translation. This presents exciting new challenges and areas for future research.

ACS Style

Chien-Ning Hsu; You-Lin Tain. Developmental Origins of Kidney Disease: Why Oxidative Stress Matters? Antioxidants 2020, 10, 33 .

AMA Style

Chien-Ning Hsu, You-Lin Tain. Developmental Origins of Kidney Disease: Why Oxidative Stress Matters? Antioxidants. 2020; 10 (1):33.

Chicago/Turabian Style

Chien-Ning Hsu; You-Lin Tain. 2020. "Developmental Origins of Kidney Disease: Why Oxidative Stress Matters?" Antioxidants 10, no. 1: 33.

Journal article
Published: 04 December 2020 in Biomedicines
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The gut microbiota plays a critical role in kidney disease and hypertension; however, whether maternal chronic kidney disease (CKD)-induced offspring hypertension is associated with alterations of the microbiota and microbial metabolites remains elusive. Using rat as an animal model, we conducted a maternal adenine-induced CKD model to examine whether adult male offspring develop hypertension and kidney disease. As resveratrol has antioxidant and prebiotic properties, we also aimed to elucidate whether its use in pregnancy and lactation can benefit hypertension programmed by maternal CKD via mediation of the gut microbiota and oxidative stress. Female Sprague–Dawley rats received regular chow (C) or chow supplemented with 0.5% adenine (CKD) from 3 weeks before pregnancy until lactation. One group of the adenine-induced CKD pregnant rats received resveratrol (R; 50 mg/L) in drinking water during gestation and lactation. Male offspring were divided into three groups: C, CKD, and CKD+R. The microbial metabolites analyzed were short chain fatty acids (SCFAs) in feces and trimethylamine (TMA)/trimethylamine N-oxide (TMAO) in plasma. We found perinatal resveratrol therapy protected against maternal CKD-induced hypertension in adult male offspring. The overall microbial compositions and diversity of bacterial community in the three groups were different. Resveratrol therapy increased α-diversity, decreased the Firmicutes to Bacteroidetes ratio, and increased the abundance of the genera Lactobacillus and Bifidobacterium. Perinatal resveratrol therapy increased plasma TMA levels but decreased the plasma TMAO-to-TMA ratio. Although resveratrol had negligible effect on fecal concentrations of SCFAs, it increased G-protein coupled receptor-41 (GPR41) protein levels in the offspring’s kidneys. Additionally, resveratrol therapy increased plasma levels of L-arginine and the L-arginine-to-ADMA ratio (AAR), and decreased oxidative stress. Overall, the protective effects of resveratrol against programmed hypertension are related to gut microbiome remodeling, including an increased abundance of beneficial microbes, mediation of the TMA–TMAO pathway, and alterations of SCFA receptors. Our results highlighted that targeting the microbiome and their metabolites might be potential therapeutic strategies to prevent maternal CKD-induced adverse pregnancy and offspring outcomes.

ACS Style

Chien-Ning Hsu; Chih-Yao Hou; Guo-Ping Chang-Chien; Sufan Lin; Hung-Wei Yang; You-Lin Tain. Perinatal Resveratrol Therapy Prevents Hypertension Programmed by Maternal Chronic Kidney Disease in Adult Male Offspring: Implications of the Gut Microbiome and Their Metabolites. Biomedicines 2020, 8, 567 .

AMA Style

Chien-Ning Hsu, Chih-Yao Hou, Guo-Ping Chang-Chien, Sufan Lin, Hung-Wei Yang, You-Lin Tain. Perinatal Resveratrol Therapy Prevents Hypertension Programmed by Maternal Chronic Kidney Disease in Adult Male Offspring: Implications of the Gut Microbiome and Their Metabolites. Biomedicines. 2020; 8 (12):567.

Chicago/Turabian Style

Chien-Ning Hsu; Chih-Yao Hou; Guo-Ping Chang-Chien; Sufan Lin; Hung-Wei Yang; You-Lin Tain. 2020. "Perinatal Resveratrol Therapy Prevents Hypertension Programmed by Maternal Chronic Kidney Disease in Adult Male Offspring: Implications of the Gut Microbiome and Their Metabolites." Biomedicines 8, no. 12: 567.

Review
Published: 18 November 2020 in International Journal of Molecular Sciences
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The concept that hypertension and chronic kidney disease (CKD) originate in early life has emerged recently. During pregnancy, tryptophan is crucial for maternal protein synthesis and fetal development. On one hand, impaired tryptophan metabolic pathway in pregnancy impacts fetal programming, resulting in the developmental programming of hypertension and kidney disease in adult offspring. On the other hand, tryptophan-related interventions might serve as reprogramming strategies to prevent a disease from occurring. In the present review, we aim to summarize (1) the three major tryptophan metabolic pathways, (2) the impact of tryptophan metabolism in pregnancy, (3) the interplay occurring between tryptophan metabolites and gut microbiota on the production of uremic toxins, (4) the role of tryptophan-derived metabolites-induced hypertension and CKD of developmental origin, (5) the therapeutic options in pregnancy that could aid in reprogramming adverse effects to protect offspring against hypertension and CKD, and (6) possible mechanisms linking tryptophan metabolism to developmental programming of hypertension and kidney disease.

ACS Style

Chien-Ning Hsu; You-Lin Tain. Developmental Programming and Reprogramming of Hypertension and Kidney Disease: Impact of Tryptophan Metabolism. International Journal of Molecular Sciences 2020, 21, 8705 .

AMA Style

Chien-Ning Hsu, You-Lin Tain. Developmental Programming and Reprogramming of Hypertension and Kidney Disease: Impact of Tryptophan Metabolism. International Journal of Molecular Sciences. 2020; 21 (22):8705.

Chicago/Turabian Style

Chien-Ning Hsu; You-Lin Tain. 2020. "Developmental Programming and Reprogramming of Hypertension and Kidney Disease: Impact of Tryptophan Metabolism." International Journal of Molecular Sciences 21, no. 22: 8705.