scholarly journals The Interplay between Maternal and Post-Weaning High-Fat Diet and Gut Microbiota in the Developmental Programming of Hypertension

Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 1982 ◽  
Author(s):  
Chien-Ning Hsu ◽  
Chih-Yao Hou ◽  
Chien-Te Lee ◽  
Julie Y.H. Chan ◽  
You-Lin Tain
Keyword(s):  
Gut Microbiota ◽  
Short Chain Fatty Acids ◽  
Normal Diet ◽  
Nutrient Sensing ◽  
Male Offspring ◽  
Peroxisome Proliferator ◽  
Sprague Dawley ◽  
High Fat ◽  
Male Adult ◽  
Peroxisome Proliferator Activated Receptor

Excessive intake of saturated fat has been linked to hypertension. Gut microbiota and their metabolites, short-chain fatty acids (SCFAs), are known to be involved in the development of hypertension. We examined whether maternal and post-weaning high-fat (HF) diet-induced hypertension in adult male offspring is related to alterations of gut microbiota, mediation of SCFAs and their receptors, and downregulation of nutrient-sensing signals. Female Sprague–Dawley rats received either a normal diet (ND) or HF diet (D12331, Research Diets) during pregnancy and lactation. Male offspring were put on either the ND or HF diet from weaning to 16 weeks of age, and designated to four groups (maternal diet/post-weaning diet; n = 8/group): ND/ND, HF/ND, ND/HF, and HF/HF. Rats were sacrificed at 16 weeks of age. Combined HF/HF diets induced elevated blood pressure (BP) and increased body weight and kidney damage in male adult offspring. The rise in BP is related to a downregulated AMP-activated protein kinase (AMPK)–peroxisome proliferator-activated receptor co-activator 1α (PGC-1α) pathway. Additionally, HF/HF diets decreased fecal concentrations of propionate and butyrate and decreased G protein-coupled receptor 41 (GPR41), but increased olfactory receptor 78 (Oflr78) expression. Maternal HF diet has differential programming effects on the offspring’s microbiota at 3 and 16 weeks of age. Combined HF/HF diet induced BP elevation was associated with an increased Firmicutes to Bacteroidetes ratio, increased abundance of genus Akkermansia and phylum Verrucomicrobia, and reduced abundance in genus Lactobacillus. Maternal gut microbiota-targeted dietary interventions might be reprogramming strategies to protect against programmed hypertension in children and their mothers on consumption of a fat-rich diet.

scholarly journals Altered Gut Microbiota and Its Metabolites in Hypertension of Developmental Origins: Exploring Differences between Fructose and Antibiotics Exposure

2021 ◽  
Vol 22 (5) ◽  
pp. 2674
Author(s):  
Chien-Ning Hsu ◽  
Julie Y. H. Chan ◽  
Kay L. H. Wu ◽  
Hong-Ren Yu ◽  
Wei-Chia Lee ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Negative Impact ◽  
Short Chain Fatty Acids ◽  
Normal Diet ◽  
Male Offspring ◽  
Sprague Dawley ◽  
Minocycline Treatment ◽  
High Fructose ◽  
Induced Hypertension ◽  
Pregnancy And Lactation

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.

scholarly journals Maternal Melatonin Therapy Attenuates Methyl-Donor Diet-Induced Programmed Hypertension in Male Adult Rat Offspring

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1407 ◽  
Author(s):  
You-Lin Tain ◽  
Julie Chan ◽  
Chien-Te Lee ◽  
Chien-Ning Hsu
Keyword(s):  
Methylation Status ◽  
Normal Diet ◽  
Male Offspring ◽  
Adult Offspring ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Deficient Diet ◽  
Male Adult ◽  
Methyl Donor ◽  
Adult Rat

Although pregnant women are advised to consume methyl-donor food, some reports suggest an adverse outcome. We investigated whether maternal melatonin therapy can prevent hypertension induced by a high methyl-donor diet. Female Sprague-Dawley rats received either a normal diet, a methyl-deficient diet (L-MD), or a high methyl-donor diet (H-MD) during gestation and lactation. Male offspring were assigned to four groups (n = 7–8/group): control, L-MD, H-MD, and H-MD rats were given melatonin (100 mg/L) with their drinking water throughout the period of pregnancy and lactation (H-MD+M). At 12 weeks of age, male offspring exposed to a L-MD or a H-MD diet developed programmed hypertension. Maternal melatonin therapy attenuated high methyl-donor diet-induced programmed hypertension. A maternal L-MD diet and H-MD diet caused respectively 938 and 806 renal transcripts to be modified in adult offspring. The protective effects of melatonin against programmed hypertension relate to reduced oxidative stress, increased urinary NO2− level, and reduced renal expression of sodium transporters. A H-MD or L-MD diet may upset the balance of methylation status, leading to alterations of renal transcriptome and programmed hypertension. A better understanding of reprogramming effects of melatonin might aid in developing a therapeutic strategy for the prevention of hypertension in adult offspring exposed to an excessive maternal methyl-supplemented diet.

scholarly journals Beta-Glucan-Rich Extract fromPleurotus sajor-caju(Fr.) Singer Prevents Obesity and Oxidative Stress in C57BL/6J Mice Fed on a High-Fat Diet

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
G. Kanagasabapathy ◽  
S. N. A. Malek ◽  
A. A. Mahmood ◽  
K. H. Chua ◽  
S. Vikineswary ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Lipid Hydroperoxide ◽  
Protein Carbonyl ◽  
Normal Diet ◽  
Hormone Sensitive Lipase ◽  
Lipid Lowering ◽  
Peroxisome Proliferator ◽  
High Fat ◽  
Beta Glucan ◽  
Peroxisome Proliferator Activated Receptor

Mushrooms have been used in folk medicine for thousands of years. In this study, the effect ofβ-glucan-rich extract ofP. sajor-caju(GE) on lipid lowering and antioxidant potential was assessed in C57BL/6J mice fed on a high-fat diet. Obesity was induced in C57BL/6J mice by feeding a high-fat diet. The control groups in this study were ND (for normal diet) and HFD (for high-fat diet). The treated groups were ND240 (for normal diet) (240 mg/kg b.w) and HFD60, HFD120, and HFD240 (for high-fat diet), where the mice were administrated with three dosages of GE (60, 120, and 240 mg GE/kg b.w). Metformin (2 mg/kg b.w) served as positive control. GE-treated groups showed significantly reduced body weight, serum lipid, and liver enzymes levels. GE also attenuated protein carbonyl and lipid hydroperoxide levels by increasing the enzymic antioxidants (SOD, CAT, and GPx) activities in the mice. GE-treated groups induced the expression of hormone sensitive lipase (HSL) and adipose triglyceride lipase (ATGL) while downregulated the expression of peroxisome proliferator-activated receptor gamma (PPAR-γ), sterol regulatory binding protein-1c (SREBP-1c), and lipoprotein lipase (LPL). Hence, GE prevented weight gain in the mice by inducing lipolysis and may be valuable in the formulation of adjuvant therapy for obesity.

scholarly journals Effects of combined d-fagomine and omega-3 PUFAs on gut microbiota subpopulations and diabetes risk factors in rats fed a high-fat diet

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Mercè Hereu ◽  
Sara Ramos-Romero ◽  
Cristina Busquets ◽  
Lidia Atienza ◽  
Susana Amézqueta ◽  
...  
Keyword(s):  
Risk Factors ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Short Chain Fatty Acids ◽  
Standard Diet ◽  
Liver Inflammation ◽  
Omega 3 ◽  
Sprague Dawley ◽  
High Fat ◽  
Related Risk

Abstract Food contains bioactive compounds that may prevent changes in gut microbiota associated with Westernized diets. The aim of this study is to explore the possible additive effects of d-fagomine and ω-3 PUFAs (EPA/DHA 1:1) on gut microbiota and related risk factors during early stages in the development of fat-induced pre-diabetes. Male Sprague Dawley (SD) rats were fed a standard diet, or a high-fat (HF) diet supplemented with d-fagomine, EPA/DHA 1:1, a combination of both, or neither, for 24 weeks. The variables measured were fasting glucose and glucose tolerance, plasma insulin, liver inflammation, fecal/cecal gut bacterial subgroups and short-chain fatty acids (SCFAs). The animals supplemented with d-fagomine alone and in combination with ω-3 PUFAs accumulated less fat than those in the non-supplemented HF group and those given only ω-3 PUFAs. The combined supplements attenuated the high-fat-induced incipient insulin resistance (IR), and liver inflammation, while increasing the cecal content, the Bacteroidetes:Firmicutes ratio and the populations of Bifidobacteriales. The functional effects of the combination of d-fagomine and EPA/DHA 1:1 against gut dysbiosis and the very early metabolic alterations induced by a high-fat diet are mainly those of d-fagomine complemented by the anti-inflammatory action of ω-3 PUFAs.

scholarly journals Stigmasterol Restores the Balance of Treg/Th17 Cells by Activating the Butyrate-PPARγ Axis in Colitis

2021 ◽  
Vol 12 ◽  
Author(s):  
Shuting Wen ◽  
Long He ◽  
Zhuotai Zhong ◽  
Runyuan Zhao ◽  
Senhui Weng ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Th17 Cells ◽  
Experimental Colitis ◽  
Short Chain Fatty Acids ◽  
Peroxisome Proliferator ◽  
Inflammatory Disorder ◽  
T Helper 17 ◽  
Peroxisome Proliferator Activated Receptor ◽  
Chronic Inflammatory Disorder ◽  
Immune Imbalance

Inflammatory bowel disease (IBD) is a chronic inflammatory disorder with gut microbiota disequilibrium and regulatory T (Treg)/T helper 17 (Th17) immune imbalance. Stigmasterol, a plant-derived sterol, has shown anti-inflammatory effects. Our study aimed to identify the effects of stigmasterol on experimental colitis and the related mechanisms. Stigmasterol treatment restored the Treg/Th17 balance and altered the gut microbiota in a dextran sodium sulfate (DSS)-induced colitis model. Transplantation of the faecal microbiota of stigmasterol-treated mice significantly alleviated inflammation. Additionally, stigmasterol treatment enhanced the production of gut microbiota-derived short-chain fatty acids (SCFAs), particularly butyrate. Next, human naïve CD4+ T cells sorted from IBD patients were cultured under Treg- or Th17-polarizing conditions; butyrate supplementation increased the differentiation of Tregs and decreased Th17 cell differentiation. Mechanistically, butyrate activated peroxisome proliferator-activated receptor gamma (PPARγ) and reprogrammed energy metabolism, thereby promoting Treg differentiation and inhibiting Th17 differentiation. Our results demonstrate that butyrate-mediated PPARγ activation restores the balance of Treg/Th17 cells, and this may be a possible mechanism, by which stigmasterol attenuates IBD.

scholarly journals Co-Administration of Conjugated Linoleic Acid and Rosiglitazone Increases Atherogenic Co-Efficient and Alters Isoprenaline-Induced Vasodilatation in Rats Fed High Fat Diet

2018 ◽  
pp. 729-740
Author(s):  
B. K. CHAI ◽  
Y. S. LAU ◽  
B. J. LOONG ◽  
M. M. RAIS ◽  
K. N. TING ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Linoleic Acid ◽  
Conjugated Linoleic Acid ◽  
High Fat Diet ◽  
Normal Diet ◽  
High Density Lipoproteins ◽  
Oral Glucose ◽  
Peroxisome Proliferator ◽  
Sprague Dawley ◽  
High Fat

The cis(c)-9, trans(t)-11 (c9,t11) and t10,c12 isomers of conjugated linoleic acid (CLA) have been reported as agonists of peroxisome proliferator-activated receptor (PPAR) and beneficial in lipidemia and glycemia. However, it is unclear whether CLA isomers enhance or antagonize effects of conventional drugs targeting PPAR. Male Sprague-Dawley rats were fed high fat diet (HFD) for 8 weeks and treated without or with CLA, rosiglitazone or both for 4 weeks. Oral glucose tolerance and surrogate markers of insulin resistance were not significantly different for all treatments compared to untreated normal diet (ND) or HFD group, except lipoprotein levels. The combination of CLA and rosiglitazone had suppressed levels of low and high density lipoproteins (46 % and 25 %, respectively), compared to HFD-alone. Conversely, the atherogenic co-efficient of the animals received HFD or HFD+rosiglitazone+CLA was 2-folds higher than ND, HFD+rosiglitazone or HFD+CLA. Isolated aortic rings from the combined CLA and rosiglitazone treated animals were less sensitive to isoprenaline-induced relaxation among endothelium-denuded aortas with a decreased efficacy and potency (Rmax=53±4.7 %; pEC50=6±0.2) compared to endothelium-intact aortas (Rmax=100±9.9 %; pEC50=7±0.2). Our findings illustrate that the combination of CLA and rosiglitazone precede the atherogenic state with impaired endothelium-independent vasodilatation before the onset of HFD-induced insulin resistance.

scholarly journals The Effect of Short-chain Fatty Acid Supplementation on Acute Colonic Inflammation in Rats Fed With Western Diet: Role of the Peroxisome Proliferator-activated Receptor-gamma

2021 ◽  
Author(s):  
Mustafa Sevim ◽  
Çiğdem Çantalı-Öztürk ◽  
Ali Mergen ◽  
Eda Ceren Güllü ◽  
Elif Yaren Ayvaz ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Lipid Profile ◽  
Short Chain Fatty Acids ◽  
Normal Diet ◽  
Short Chain ◽  
Albino Rats ◽  
Peroxisome Proliferator ◽  
Protective Effects ◽  
Colonic Inflammation ◽  
Peroxisome Proliferator Activated Receptor

Abstract Increased incidence of inflammatory bowel disease (IBD) is associated with the consumption of westernized diet (WD). In male Wistar albino rats induced with colitis by oral intake of dextran-sulfate sodium (DSS) for 10 days, we investigated how colitis-induced oxidative damage is affected by WD consumption started 3 weeks before DSS intake. Secondly, the putative protective effects of short-chain fatty acids (SCFAs) were evaluated in both WD-fed and normal diet (ND)-fed rats. WD consumption prior to colitis induction alleviated oxidative damage and suppressed inflammatory response of the colon via the modulation of peroxisome proliferator-activated receptor (PPAR)-γ activity, suggesting a preconditioning impact of the WD. Moreover, addition of SCFA to WD abolished the elevations in lipid profile, while SCFA added to either ND or WD during the 10-day development of colonic inflammation depressed the pro-inflammatory TNF-α and IL-6 expressions and upregulated IL-10, but the reduction in oxidative damage due to WD was not further changed. The results demonstrated that acute colonic inflammation is alleviated when it is preceded by the consumption of WD, and SCFAs improved WD-induced disruption in lipid profile, implicating that SCFAs would be advantageous in IBD patients comorbid with metabolic syndrome.

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

Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 448 ◽  
Author(s):  
Wan-Long Tsai ◽  
Chien-Ning Hsu ◽  
You-Lin Tain
Keyword(s):  
Oxidative Stress ◽  
Saturated Fat ◽  
Nutrient Sensing ◽  
Male Offspring ◽  
Lactation Period ◽  
Sprague Dawley ◽  
Male Adult ◽  
Ampk Signaling ◽  
Pregnancy And Lactation ◽  
In Pregnancy

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.

scholarly journals Effect ofLactobacillus plantarumStrain K21 on High-Fat Diet-Fed Obese Mice

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Chien-Chen Wu ◽  
Wei-Lien Weng ◽  
Wen-Lin Lai ◽  
Hui-Ping Tsai ◽  
Wei-Hsien Liu ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Body Weight Gain ◽  
Normal Diet ◽  
Peroxisome Proliferator ◽  
Bacterial Strains ◽  
High Fat ◽  
Peroxisome Proliferator Activated Receptor ◽  
Hepatic Expression ◽  
Beneficial Effects

Recent studies have demonstrated beneficial effects of specific probiotics on alleviating obesity-related disorders. Here we aimed to identify probiotics with potential antiobesity activity among 88 lactic acid bacterial strains viain vitroscreening assays, and aLactobacillus plantarumstrain K21 was found to harbor abilities required for hydrolyzing bile salt, reducing cholesterol, and inhibiting the accumulation of lipid in 3T3-L1 preadipocytes. Furthermore, effects of K21 on diet-induced obese (DIO) mice were examined. Male C57Bl/6J mice received a normal diet, high-fat diet (HFD), or HFD with K21 administration (109 CFU in 0.2 mL PBS/day) for eight weeks. Supplementation of K21, but not placebo, appeared to alleviate body weight gain and epididymal fat mass accumulation, reduce plasma leptin levels, decrease cholesterol and triglyceride levels, and mitigate liver damage in DIO mice. Moreover, the hepatic expression of peroxisome proliferator-activated receptor-γ(PPAR-γ) related to adipogenesis was significantly downregulated in DIO mice by K21 intervention. We also found that K21 supplementation strengthens intestinal permeability and modulates the amount ofLactobacillusspp.,Bifidobacteriumspp., andClostridium perfringensin the cecal contents of DIO mice. In conclusion, our results suggest that dietary intake of K21 protects against the onset of HFD-induced obesity through multiple mechanisms of action.

scholarly journals Hypertension Programmed by Perinatal High-Fat Diet: Effect of Maternal Gut Microbiota-Targeted Therapy

Nutrients ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 2908 ◽  
Author(s):  
Chien-Ning Hsu ◽  
Chih-Yao Hou ◽  
Julie Y.H. Chan ◽  
Chien-Te Lee ◽  
You-Lin Tain
Keyword(s):  
Gut Microbiota ◽  
Lactobacillus Casei ◽  
Renin Angiotensin System ◽  
Short Chain Fatty Acids ◽  
Lactobacillus Species ◽  
Sprague Dawley ◽  
High Fat ◽  
Beneficial Effects ◽  
Therapeutic Uses ◽  
Pregnancy And Lactation

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 whether maternal use of prebiotics/probiotics could protect offspring against the development of hypertension in adulthood. We investigated whether perinatal HF diet-induced programmed hypertension in adult offspring can be prevented by therapeutic uses of prebiotic inulin or probiotic Lactobacillus casei during gestation and lactation. Pregnant Sprague–Dawley rats received regular chow or HF diet (D12331, Research Diets), with 5% w/w long chain inulin (PRE), or 2 × 108 CFU/day Lactobacillus casei via oral gavage (PRO) during pregnancy and lactation. Male offspring (n = 8/group) were assigned to four groups: control, HF, PRE, and PRO. Rats were sacrificed at 16 weeks of age. Maternal prebiotic or probiotic therapy prevents elevated blood pressure (BP) programmed by perinatal HF consumption. Both prebiotic and probiotic therapies decreased the Firmicutes to Bacteroidetes ratio and renal mRNA expression of Ace, but increased abundance of genus Lactobacillus and Akkermansia. Additionally, prebiotic treatment prevents HF-induced elevation of BP is associated with reduced fecal propionate and acetate levels, while probiotic therapy restored several Lactobacillus species. Maternal probiotic or prebiotic therapy caused a reduction in plasma TMAO level and TMAO-to-TMA ratio. The beneficial effects of prebiotic or probiotic therapy on elevated BP programmed by perinatal HF diet are relevant to alterations of microbial populations, modulation of microbial-derived metabolites, and mediation of the renin-angiotensin system. Our results cast a new light on the use of maternal prebiotic/probiotic therapy to prevent hypertension programmed by perinatal HF consumption. The possibility of applying gut microbiota-targeted therapies as a reprogramming strategy for hypertension warrants further clinical translation.

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