Resveratrol prevents combined prenatal NG-nitro-L-arginine-methyl ester (L-NAME) treatment plus postnatal high-fat diet induced programmed hypertension in adult rat offspring: interplay between nutrient-sensing signals, oxidative stress and gut microbiota

Chen, Hung-En; Lin, Yu‐Ju; Lin, I-Chun; Yu, Hong‐Ren; Sheen, Jiunn‐Ming; Tsai, Ching‐Chou; Huang, Laura; Tain, You‐Lin

doi:10.1016/j.jnutbio.2019.04.002

Cited by 47 publications

(63 citation statements)

References 44 publications

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“…Care et al showed that maternal resveratrol supplementation during pregnancy and lactation ameliorated the development of hypertension in adult offspring [75]. Likewise, Chen et al reported that maternal resveratrol intake during pregnancy and lactation could alleviate programmed hypertension induced by combined maternal N G -nitro-L-arginine-methyl ester treatment and postnatal HFD [76]. In preeclampsia patients, both the time and dose of blood pressure control are significantly reduced in those who received resveratrol supplementation [77].…”

Section: Maternal Resveratrol Administration In the Context Of Maternmentioning

confidence: 99%

Maternal Obesity Programs Offspring Development and Resveratrol Potentially Reprograms the Effects of Maternal Obesity

Hsu

Chen

Sheen

et al. 2020

IJERPH

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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.

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Section: Maternal Resveratrol Administration In the Context Of Maternmentioning

confidence: 99%

Maternal Obesity Programs Offspring Development and Resveratrol Potentially Reprograms the Effects of Maternal Obesity

Hsu

Chen

Sheen

et al. 2020

IJERPH

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“…Our previous study reported that resveratrol, a known natural activator of AMPK, prevents hypertension programmed by HFD associated with increased protein levels of SIRT1 and AMPKα2 [25]. Additionally, we recently found that resveratrol therapy activated AMPK/SIRT1/PGC-1α pathway and protected offspring against hypertension and oxidative stress in another hypertension model of programming [31].…”

Section: Discussionmentioning

confidence: 95%

“…Early-life environmental insults can program AMPK and other nutrient-sensing signals to regulate PPARs and their target genes, hence provoking programmed hypertension [29]. Since that systemic BP was higher in AMPKα2 knockout mice than in wildtype mice [30], and that our previous studies showed AMPKα2 protein is related to programmed hypertension [25,31], we mainly focused on determining AMPKα2 protein level in the current study. Our previous study reported that resveratrol, a known natural activator of AMPK, prevents hypertension programmed by HFD associated with increased protein levels of SIRT1 and AMPKα2 [25].…”

Section: Discussionmentioning

confidence: 99%

Whether AICAR in Pregnancy or Lactation Prevents Hypertension Programmed by High Saturated Fat Diet: A Pilot Study

2020

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High consumption of saturated fats links to the development of hypertension. AMP-activated protein kinase (AMPK), a nutrient-sensing signal, is involved in the pathogenesis of hypertension. We examined whether early intervention with a direct AMPK activator 5-aminoimidazole-4-carboxamide riboside (AICAR) during pregnancy or lactation can protect adult male offspring against hypertension programmed by high saturated fat consumption via regulation of nutrient sensing signals, nitric oxide (NO) pathway, and oxidative stress. Pregnant Sprague-Dawley rats received regular chow or high saturated fat diet (HFD) throughout pregnancy and lactation. AICAR treatment was introduced by intraperitoneal injection at 50 mg/kg twice a day for 3 weeks throughout the pregnancy period (AICAR/P) or lactation period (AICAR/L). Male offspring (n = 7-8/group) were assigned to five groups: control, HFD, AICAR/P, HFD + AICAR/L, and HFD + AICAR/P. Male offspring were killed at 16 weeks of age. HFD caused hypertension and obesity in male adult offspring, which could be prevented by AICAR therapy used either during pregnancy or lactation. As a result, we demonstrated that HFD downregulated AMPK/SIRT1/PGC-1α pathway in offspring kidneys. In contrast, AICAR therapy in pregnancy and, to a greater extent, in lactation activated AMPK signaling pathway. The beneficial effects of AICAR therapy in pregnancy is related to restoration of NO pathway. While AICAR uses in pregnancy and lactation both diminished oxidative stress induced by HFD. Our results highlighted that pharmacological AMPK activation might be a promising strategy to prevent hypertension programmed by excessive consumption of high-fat food.A high-fat diet is commonly used in animal models to induce obesity-related diseases, such as hypertension [5]. Maternal high-fat intake has been reported to induce an increase [6,7] or no change [7,8] on offspring's BPs, mainly depending on the age, sex, and diverse fatty acids compositions [9]. Accumulative evidence indicates that diets containing high saturated fatty acids cause obesity/metabolic risk phenotypes, while high-fat diets based on poly-unsaturated fatty acids relates to beneficial effects [10]. Our previous study showed maternal and post-weaning high saturated fat (coconut oil-based) diets induced elevation of BP and kidney damage in male offspring at 24 weeks of age [7].Dysregulated nutrient-sensing signals and impaired asymmetric dimethylarginine (ADMA, an endogenous inhibitor of nitric oxide synthase)-nitric oxide (NO) pathway are the proposed mechanisms underlying renal programming and programmed hypertension [11,12]. Fetal metabolism and development in response to maternal nutritional insults is mainly modulated by nutrient-sensing signaling pathways. In the kidney, several nutrient-sensing signals exist, including silent information regulator transcript (SIRT), cyclic adenosine monophosphate (AMP)-activated protein kinase (AMPK), peroxisome proliferator-activated receptors (PPARs), and PPARγ coactivator-1α (PGC-1α) [13]. Among th...

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“…These findings confer a novel role for the dysfunctional AMPK/SIRT1 signaling in fetal programming of oxidative stress in RVLM from maternal HFD insult. Dysregulated AMPK-PGC-1α signal has recently been reported to be engaged in adult hypertension programmed by prenatal NO deficiency plus postnatal high-fat diet exposure [56]. In addition to biogenesis impairment, mitochondrial ROS generated from curtail in bioenergetics [19,21,30,31] and activation of cyclophilin D (a regulatory subunit of the mitochondrial permeability transition pore) [57] also contribute to hypertension development.…”

Section: Discussionmentioning

confidence: 99%

Anomalous AMPK-regulated angiotensin AT1R expression and SIRT1-mediated mitochondrial biogenesis at RVLM in hypertension programming of offspring to maternal high fructose exposure

Chao

Tsai

et al. 2020

J Biomed Sci

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Background: Tissue oxidative stress, sympathetic activation and nutrient sensing signals are closely related to adult hypertension of fetal origin, although their interactions in hypertension programming remain unclear. Based on a maternal high-fructose diet (HFD) model of programmed hypertension, we tested the hypothesis that dysfunction of AMP-activated protein kinase (AMPK)-regulated angiotensin type 1 receptor (AT 1 R) expression and sirtuin1 (SIRT1)-dependent mitochondrial biogenesis contribute to tissue oxidative stress and sympathoexcitation in programmed hypertension of young offspring. Methods: Pregnant female rats were randomly assigned to receive normal diet (ND) or HFD (60% fructose) chow during pregnancy and lactation. Both ND and HFD offspring returned to ND chow after weaning, and blood pressure (BP) was monitored from age 6 to 12 weeks. At age of 8 weeks, ND and HFD offspring received oral administration of simvastatin or metformin; or brain microinfusion of losartan. BP was monitored under conscious condition by the tail-cuff method. Nutrient sensing molecules, AT 1 R, subunits of NADPH oxidase, mitochondrial biogenesis markers in rostral ventrolateral medulla (RVLM) were measured by Western blot analyses. RVLM oxidative stress was measured by fluorescent probe dihydroethidium and lipid peroxidation by malondialdehyde assay. Mitochondrial DNA copy number was determined by quantitative real-time polymerase chain reaction.

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Resveratrol prevents combined prenatal NG-nitro-L-arginine-methyl ester (L-NAME) treatment plus postnatal high-fat diet induced programmed hypertension in adult rat offspring: interplay between nutrient-sensing signals, oxidative stress and gut microbiota

Cited by 47 publications

References 44 publications

Maternal Obesity Programs Offspring Development and Resveratrol Potentially Reprograms the Effects of Maternal Obesity

Maternal Obesity Programs Offspring Development and Resveratrol Potentially Reprograms the Effects of Maternal Obesity

Whether AICAR in Pregnancy or Lactation Prevents Hypertension Programmed by High Saturated Fat Diet: A Pilot Study

Anomalous AMPK-regulated angiotensin AT1R expression and SIRT1-mediated mitochondrial biogenesis at RVLM in hypertension programming of offspring to maternal high fructose exposure

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