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Effect of maternal high-fructose (HF) diet, probiotic Lactobacillus casei, and prebiotic inulin on systolic blood pressure in male offspring from 3 to 12 weeks of age. N = 7–8/group. * p < 0.05 versus control; # p < 0.05 versus HF.
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Excessive intake of fructose is associated with hypertension. Gut microbiota and their metabolites are thought to be associated with the development of hypertension. We examined whether maternal high-fructose (HF) diet-induced programmed hypertension via altering gut microbiota, regulating short-chain fatty acids (SCFAs) and their receptors, and me...
Similar publications
Hypertension can originate in early life caused by perinatal high-fat (HF) consumption. Gut microbiota and their metabolites short chain fatty acids (SCFAs), trimethylamine (TMA), and trimethylamine N-oxide (TMAO) are involved in the development of hypertension. Despite the beneficial effects of prebiotic/probiotic on human health, little is known...
Citations
... Interventions targeting the gut microbiota have been explored in various models related to oxidative-stress-associated MetS programming. These models encompass scenarios such as protein restriction [161], maternal high-fructose diet [162,163], high-fat diet [72,117,122,[164][165][166][167][168][169], maternal high-sucrose/fat diet [170], and maternal exposure to bisphenol A (BPA) [103,171,172]. ...
... Studies have indicated the beneficial effects of probiotics in MetS [175]. For instance, supplementation with Lactobacillus casei during gestation and lactation prevented hypertension in adult offspring born to dams fed a high-fructose diet [162]. Additionally, the perinatal supplementation of inulin, a well-known prebiotic, provided protection against hypertension programmed by a maternal high-fructose diet in adult progeny [162]. ...
... For instance, supplementation with Lactobacillus casei during gestation and lactation prevented hypertension in adult offspring born to dams fed a high-fructose diet [162]. Additionally, the perinatal supplementation of inulin, a well-known prebiotic, provided protection against hypertension programmed by a maternal high-fructose diet in adult progeny [162]. Inulin's beneficial action is associated with increased plasma propionate and the restoration of reduced GPR43 expression induced by a high-fructose diet. ...
Metabolic syndrome (MetS) denotes a constellation of risk factors associated with the development of cardiovascular disease, with its roots potentially traced back to early life. Given the pivotal role of oxidative stress and dysbiotic gut microbiota in MetS pathogenesis, comprehending their influence on MetS programming is crucial. Targeting these mechanisms during the early stages of life presents a promising avenue for preventing MetS later in life. This article begins by examining detrimental insults during early life that impact fetal programming, ultimately contributing to MetS in adulthood. Following that, we explore the role of oxidative stress and the dysregulation of gut microbiota in the initiation of MetS programming. The review also consolidates existing evidence on how gut-microbiota-targeted interventions can thwart oxidative-stress-associated MetS programming, encompassing approaches such as probiotics, prebiotics, postbiotics, and the modulation of bacterial metabolites. While animal studies demonstrate the favorable effects of gut-microbiota-targeted therapy in mitigating MetS programming, further clinical investigations are imperative to enhance our understanding of manipulating gut microbiota and oxidative stress for the prevention of MetS.
... Nutritional insults, such as high-fat diet and protein restriction, during pregnancy, lactation, and early childhood could trigger the development of cardiovascular and metabolic disorders later in offspring [131,132], including arterial hypertension associated with reduced baroreflex sensitivity and sympathetic hyperactivity [132][133][134]. Consuming a high-fat diet during pregnancy and lactation could alter the composition of maternal and offspring gut microbiota, causing gut barrier integrity impairment and arterial hypertension development programming [135]. ...
... Daily administration of L. casei (2 × 10 8 CFU) in female rats fed a high-fructose diet during pregnancy and lactation protected male offspring from arterial hypertension [135]. Similarly, daily administration of Lactiplantibacillus plantarum WJL30 (1 × 10 9 CFU/mL) in female rats fed a high-fat diet during pregnancy and lactation reduced blood pressure and improved endothelial function in male offspring [134]. ...
Fruits and their processing by-products are sources of potentially probiotic strains. Limosilactobacillus (L.) fermentum strains isolated from fruit processing by-products have shown probiotic-related properties. This review presents and discusses the results of the available studies that evaluated the probiotic properties of L. fermentum in promoting host health benefits, their application by the food industry, and the development of biotherapeutics. The results showed that administration of L. fermentum for 4 to 8 weeks promoted host health benefits in rats, including the modulation of gut microbiota, improvement of metabolic parameters, and antihypertensive, antioxidant, and anti-inflammatory effects. The results also showed the relevance of L. fermentum strains for application in the food industry and for the formulation of novel biotherapeutics, especially nutraceuticals. This review provides evidence that L. fermentum strains isolated from fruit processing by-products have great potential for promoting host health and indicate the need for a translational approach to confirm their effects in humans using randomized, double-blind, placebo-controlled trials.
... These contradictory sex-specific findings are likely due to many experimental design factors that influence the outcomes of rodent model studies assessing the transgenerational impact of maternal obesity, 32 including the source and amount of dietary fiber. The limited amount of work that has been conducted with maternal dietary fiber intervention during pregnancy in rodents has been conducted with a variety of fiber sources including galacto-oligosaccharides, 33 fructooligiosacccharides, 29 inulin, 30,34 and oligofructose and inulin. 28 Dietary fibers are known to elicit differential metabolic responses based on their physiochemical properties (i.e., viscosity, fermentability, soluble to insoluble ratio, etc.), 35,36 thus conflicting findings between studies may be expected. ...
We investigated the influence of maternal yellow-pea fiber supplementation in obese pregnancies on offspring metabolic health in adulthood. Sixty newly-weaned female Sprague-Dawley rats were randomized to either a low-calorie control diet (CON) or high calorie obesogenic diet (HC) for 6-weeks. Obese animals were then fed either the HC diet alone or the HC diet supplemented with yellow-pea fiber (HC + FBR) for an additional 4-weeks prior to breeding and throughout gestation and lactation. On postnatal day (PND) 21, 1 male and 1 female offspring from each dam were weaned onto the CON diet until adulthood (PND 120) for metabolic phenotyping. Adult male, but not female, HC offspring demonstrated increased body weight and feed intake vs CON offspring, however no protection was offered by maternal FBR supplementation. HC male and female adult offspring demonstrated increased serum glucose and insulin resistance (HOMA-IR) compared with CON offspring. Maternal FBR supplementation improved glycemic control in male, but not female offspring. Compared with CON offspring, male offspring from HC dams demonstrated marked dyslipidemia (higher serum cholesterol, increased number of TG-rich lipoproteins, and smaller LDL particles) which was largely normalized in offspring from HC + FBR mothers. Male offspring born to obese mothers (HC) had higher hepatic TG, which tended to be lowered (p = 0.07) by maternal FBR supplementation.
Supplementation of a maternal high calorie diet with yellow-pea fiber in prepregnancy and throughout gestation and lactation protects male offspring from metabolic dysfunction in the absence of any change in body weight status in adulthood.
... Although a meta-analysis of 702 individuals showed that probiotic fermented milk had a hypotensive effect on adults with prehypertension or hypertension (Dong et al., 2013), the role of probiotics in reprogramming the way hypertension develops was not widely known. Hsu et al. (Hsu et al., 2018) presented evidence in their study that early probiotic treatment with Lactobacillus casei can inhibit programmed hypertension in adult offspring generated by maternal HF. Akin to probiotic therapy, studies have also shown that maternal prebiotic inulin treatment can prevent developmental hypertension caused by maternal HF intake. ...
... In addition, probiotics or prebiotics significantly increased the abundance of Akkermansiamuciniphila, a beneficial intestinal propionate-producing microorganism (Cani and de Vos, 2017). At the same time, probiotic or probiotic therapy can protect programmed hypertension caused by maternal HF diet associated with decreased abundance of Bacteroides acidis (Hsu et al., 2018). Data from a study suggest that altering gut microbiota through maternal prebiotic or probiotic treatment might assist in resolving hypertension caused by early overnutrition due to the HF diet (Hsu et al., 2019b). ...
Preeclampsia is a specific disease during pregnancy and is a significant factor in the increased mortality in perinatal women. Gut microbiota, an intricate and abundant microbial community in the digestive tract, is crucial for host metabolism, immunity, and nutrient absorption. The onset and progression of preeclampsia are closely correlated with the changes in maternal gut microbiota. Research purpose was to compile the existing bits of present scientific data and to close the gap in the knowledge of changes in gut microbiota in preeclampsia and their association with preeclampsia. We searched studies from two electronic databases (PubMed and Web of Science) included from 2014 to 2023. This review is divided into three parts. In the first part, the author elaborates longitudinal differences of maternal gut microbiota during different gestation periods. In the second part, we discuss that gut microbiota can lead to the occurrence of preeclampsia by systemic immune response, influencing the release of active peptides, short-chain fatty acids, trimethylamine-N-oxide (TMAO) and other metabolites, vascular factors and Microorganism-immune axis. In the third part, we proposed that a high-fiber diet combined with drugs and microecological regulators may be therapeutic in enhancing or preventing the emergence and evolution of preeclampsia, which needs further exploration. Although the pathogenesis of preeclampsia is still nebulous and there is no clear and valid clinical treatment, our study provides new ideas for the pathogenesis, prevention and treatment of preeclampsia.
... Notably, the protective effect of probiotics on hypertension has been studied. Hsu et al. found that Lactobacillus casei could protect against hypertension, which was related to reduced plasma acetate levels and decreased renal Olfr78 expression (13). Other studies indicated that probiotics could improve endothelial dysfunction via releasing converting enzyme inhibitory peptides and impairing lipopolysaccharide signaling, ultimately reducing BP (14,15). ...
High-fructose intake is one of the high-risk factors for hypertension. Several probiotics have been reported to reduce high blood pressure (BP) via modulating gut microbiota, but the mechanism of the antihypertensive effect of probiotics is insufficiently understood. Herein, we investigated the antihypertensive effect of Bifidobacterium lactis M8 and Lactobacillus rhamnosus M9 based on the integrative analysis of gut metagenome and serum metabolome in high-fructose-treated mice. After 16-week intervention, M8 and M9 significantly reduced the median blood pressure by 16.92% and 15.39% in SBP, and 18.56% and 20.62% in DBP, respectively. Metagenomic analysis revealed that the increased Lawsonia and Pyrolobus, and reduced Alistipes and Alloprevotella levels were tightly correlated with lowered BP. Functionally, the decreased pathways of “base excision repair” (BER) and “D-glutamine and D-glutamate metabolism” were associated with BP reduction. Metabolomics data analysis further revealed that the probiotic interventions regulated vascular smooth muscle contraction, serotonergic synapse, cholinergic synapse, and lipid and vitamin metabolism in BP control. Additionally, association analyses indicated a strong negative correlation between Alistipes and “steroid hormone biosynthesis,” suggesting that Alistipes could affect blood pressure by changing steroid hormone levels. In conclusion, our findings indicate that the probiotic efficacies in alleviating hypertension are linked to specific gut microbes and metabolic pathways, which provide a potential mechanistic understanding of probiotics modulated blood pressure, paving the way for future assessment of the therapeutic potential of probiotics in hypertension management.
IMPORTANCE
Elevated blood pressure affects 40% of the adult population, which accounts for high cardiovascular disease risk and further high mortality yearly. The global understanding of the gut microbiome for hypertension may provide important insights into the prevention. Bifidobacterium lactis M8 and Lactobacillus rhamnosus M9 originated from human breast milk, were able to decrease blood pressure, and modified metabolites in a high fructose-induced elevated blood pressure mouse model. Moreover, we found there was a close relationship between unexplored gut microbes and elevated blood pressure. Also, subsequently, the cross-link was explored among gut microbes, metabolites, and some metabolic pathways in gut microbial environment through introducing novel prediction methodology and bioinformatic analysis. It allowed us to hypothesize that probiotics can prevent elevated blood pressure via gut microbiota and related metabolism.Thus, utilization of dietary strategies (such as probiotics) to maintain the blood pressure level is of crucial importance.
... Another disorder, hypertension, is caused by fructoserich diet which is thought to be associated with the metabolic disturbance caused by gut microbiota. This condition can be improved by the consumption of inulin along with probiotic Lactobacillus casei [39]. A variety of mushrooms such as P. ostreatus, P. florida, and P. sajor-caju are the rich source of inulin. ...
Mushrooms are considered as sustainable foods as they require less effort and can be cultivated on different agro-industrial wastes. Besides, these possess many nutraceuticals for providing health benefits along with supplementing nutrition. The mushrooms are also used as prebiotics for their ability to support beneficial microbes in the gut and inhibit the growth of pathogens. Furthermore, these remain undigested in the upper gut and reach the intestine to replenish the gut microbiota. The mushrooms boost health by inhibiting the binding of pathogenic bacteria, by promoting the growth of specific gut microbiota, producing short chain fatty acids, and regulating lipid metabolism and cancer. Research has been initiated in the commercial formulation of various products such as yogurt and symbiotic capsules. This paper sheds light on health-promoting effect, disease controlling, and regulating effect of mushroom prebiotics. This paper also presented a glimpse of commercialization of mushroom prebiotics. In the future, proper standardization of mushroom-based prebiotic formulations will be available to boost human health.
... Moreover, emerging evidence suggests that alterations in maternal GM can influence the composition of the fetal microbiota, and the maternal gut environment may have longterm effects on the health of offspring through mechanisms such as developmental programming (Alexander, 2006;Torres et al., 2020). Studies in animal models have demonstrated that prenatal modulation of maternal microbiota through the administration of probiotics or prebiotics can confer protection against cardiovascular diseases, including hypertension, in the offspring (Hsu et al., 2018). Additionally, maternal GM has been shown to shape the immune system of offspring, as pups born to pregnant mice with transiently modified GM during pregnancy exhibit enhanced ability to modulate inflammatory responses to GM (Gomez De Agüero et al., 2016;Koch et al., 2016). ...
Background
Preeclampsia (PE) is a common pregnancy-related disorder characterized by disrupted maternal-fetal immune tolerance, involving diffuse inflammatory responses and vascular endothelial damage. Alterations in the gut microbiota (GM) during pregnancy can affect intestinal barrier function and immune balance.
Aims and purpose
This comprehensive review aims to investigate the potential role of short-chain fatty acids (SCFAs), essential metabolites produced by the GM, in the development of PE. The purpose is to examine their impact on colonic peripheral regulatory T (Treg) cells, the pathogenic potential of antigen-specific helper T (Th) cells, and the inflammatory pathways associated with immune homeostasis.
Key insights
An increasing body of evidence suggests that dysbiosis in the GM can lead to alterations in SCFA levels, which may significantly contribute to the development of PE. SCFAs enhance the number and function of colonic Treg cells, mitigate the pathogenic potential of GM-specific Th cells, and inhibit inflammatory progression, thereby maintaining immune homeostasis. These insights highlight the potential significance of GM dysregulation and SCFAs produced by GM in the pathogenesis of PE. While the exact causes of PE remain elusive, and definitive clinical treatments are lacking, the GM and SCFAs present promising avenues for future clinical applications related to PE, offering a novel approach for prophylaxis and therapy.
... These gut microbiota-targeted therapies cover probiotics, prebiotics, postbiotics, fecal microbiota transplantation, bacterial metabolite modulation, etc. [27]. So far, probiotics, prebiotics, and TMAO modulation have shown benefits against maternal HF diet-primed offspring hypertension [14,28]. As far as we are aware, this is the first time to show that postbiotic supplementation with butyrate or propionate during gestation and lactation has the ability to protect against offspring hypertension in this model. ...
Maternal nutrition has a key role in the developmental programming of adult disease. Excessive maternal fructose intake contributes to offspring hypertension. Newly discovered evidence supports the idea that early-life gut microbiota are connected to hypertension later in life. Short-chain fatty acids (SCFAs), butyrate, and propionate are microbiota-derived metabolites, also known as postbiotics. The present study aimed to determine whether maternal butyrate or propionate supplementation can protect offspring from hypertension using a maternal high-fructose (HF) diet rat model. Female Sprague Dawley rats were allocated during pregnancy and lactation to (1) regular chow (ND); (2) 60% high-fructose diet (HF); (3) HF diet plus butyrate (HFB, 400 mg/kg/day); and (4) HF diet plus propionate (HFP, 200 mmol/L). Male offspring were sacrificed at 12 weeks of age. The maternal HF diet impaired the offspring’s BP, which was prevented by perinatal butyrate or propionate supplementation. Both butyrate and propionate treatments similarly increased plasma concentrations of propionic acid, isobutyric acid, and valeric acid in adult offspring. Butyrate supplementation had a more profound impact on trimethylamine N-oxide metabolism and nitric oxide parameters. Whilst propionate treatment mainly influenced gut microbiota composition, it directly altered the abundance of genera Anaerovorax, Lactobacillus, Macellibacteroides, and Rothia. Our results shed new light on targeting gut microbiota through the use of postbiotics to prevent maternal HF intake-primed hypertension, a finding worthy of clinical translation.
... On the other hand, over-nutrition arising from excessive intake of specific nutrients can lead to hypertension programming [58]. Feeding pregnant rats a diet high in sucrose or fructose induced hypertension in their offspring [41][42][43][44][45][46]. A maternal high-fructose diet not only caused hypertension, but also obesity, insulin resistance, and fatty liver [59]. ...
... In a maternal high fructose diet model, the elevation of offspring's BP was accompanying by decreased renal GPR41 and GPR43 expression [45]. Another study demonstrated that perinatal 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure-primed hypertension in adult offspring coincided with downregulation of renal GPR43 expression [99]. ...
... Little reliable data presently exists about the reprogramming effects of specific micronutrients on hypertension programming. Nutritional supplementation interventions starting during gestation as a reprogramming intervention to avert developmental programming of hypertension in rodent models are listed in Table 3 [27,28,35,45,55,[116][117][118][119][120][121][122][123][124][125][126][127][128][129][130]. Among them, amino acids are the most commonly used nutrients for prevention of programmed hypertension. ...
Hypertension can have its origin in early life. During pregnancy, many metabolic alterations occur in the mother that have a crucial role in fetal development. In response to maternal insults, fetal programming may occur after metabolic disturbance, resulting in programmed hypertension later in life. Maternal dietary nutrients act as metabolic substrates for various metabolic processes via nutrient-sensing signals. Different nutrient-sensing pathways that detect levels of sugars, amino acids, lipids and energy are integrated during pregnancy, while disturbed nutrient-sensing signals have a role in the developmental programming of hypertension. Metabolism-modulated metabolites and nutrient-sensing signals are promising targets for new drug discovery due to their pathogenic link to hypertension programming. Hence, in this review, we pay particular attention to the maternal nutritional insults and metabolic wastes affecting fetal programming. We then discuss the role of nutrient-sensing signals linking the disturbed metabolism to hypertension programming. This review also summarizes current evidence to give directions for future studies regarding how to prevent hypertension via reprogramming strategies, such as nutritional intervention, targeting nutrient-sensing signals, and reduction of metabolic wastes. Better prevention for hypertension may be possible with the help of novel early-life interventions that target altered metabolism.
... Various environmental insults have been examined in animal models, including maternal nutritional imbalance [69][70][71][72][73][74][75][76][77][78][79][80][81][82][83][84][85], pregnancy complications [86][87][88][89][90][91][92][93][94], maternal illness [95][96][97][98][99][100][101][102][103][104][105][106], and toxin/chemical exposure [107][108][109][110][111][112][113][114][115][116][117][118]. Maternal nutritional imbalance can induce nutritional programming. ...
... Mother rats receiving a high-fat diet saw an elevation in BP, body weight, blood lipids, and insulin level in their offspring [74][75][76][77]. Likewise, hypertension, abnormal regulation of lipid metabolism, and insulin signaling can be programmed by a maternal high-fructose diet [80][81][82]. ...
Metabolic syndrome (MetS) is a worldwide public health issue characterized by a set of risk factors for cardiovascular disease. MetS can originate in early life by developmental programming. Increasing evidence suggests that oxidative stress, which is characterized as an imbalance between reactive oxygen species (ROS), nitric oxide (NO), and antioxidant systems, plays a decisive role in MetS programming. Results from human and animal studies indicate that maternal-derived insults induce MetS later in life, accompanied by oxidative stress programming of various organ systems. On the contrary, perinatal use of antioxidants can offset oxidative stress and thereby prevent MetS traits in adult offspring. This review provides an overview of current knowledge about the core mechanisms behind MetS programming, with particular focus on the occurrence of oxidative-stress-related pathogenesis as well as the use of potential oxidative-stress-targeted interventions as a reprogramming strategy to avert MetS of developmental origins. Future clinical studies should provide important proof of concept for the effectiveness of these reprogramming interventions to prevent a MetS epidemic.
