Inulin supplementation prevents high fructose diet-induced hypertension in rats

2008 ◽  
Vol 27 (2) ◽  
pp. 276-282 ◽  
Author(s):  
Marie-Hélène Rault-Nania ◽  
Céline Demougeot ◽  
Elyett Gueux ◽  
Alain Berthelot ◽  
Stanislaw Dzimira ◽  
...  
Keyword(s):  
High Fructose Diet ◽  
High Fructose ◽  
Induced Hypertension

Possible Involvement of Up-regulated Salt Dependent Glucose Transporter-5 (SGLT5) in High-fructose Diet-induced Hypertension

2021 ◽  
Author(s):  
Hiroaki Hara ◽  
Kaori Takayanagi ◽  
Taisuke Shimizu ◽  
Takatsugu Iwashita ◽  
Akira Ikari ◽  
...  
Keyword(s):  
Glucose Transporter ◽  
Salt Intake ◽  
Extracellular Fluid ◽  
Sodium Reabsorption ◽  
High Fructose Diet ◽  
Fructose Metabolism ◽  
High Fructose ◽  
Induced Hypertension ◽  
Underlying Mechanisms ◽  
Salt Sensitive Hypertension

Abstract Excessive fructose intake causes a variety of adverse conditions (e.g., obesity, hepatic steatosis, insulin resistance and uric acid overproduction). Particularly, high fructose-induced hypertension is the most common and significant pathological setting, however, its underlying mechanisms are not established. We investigated these mechanisms in 7-week-old male SD rats fed a diet containing 60% glucose (GLU) or 60% fructose (FRU) for 3, 6, or 12 weeks. Daily food consumption was measured to avoid between-group discrepancies in caloric/salt intake, adjusting for feeding amounts. The FRU rats' mean blood pressure was significantly higher and fractional sodium excretion (FENa) was significantly lower, indicating that the high-fructose diet caused salt retention. The FRU rats' kidney weight and glomerular surface area were greater, suggesting that the high-fructose diet induced an increase in extracellular fluid volume. The GLUT5 and ketohexokinase expressions, an enzyme required for fructose metabolism, were up-regulated in FRU. Cortical ATP levels were significantly lower in FRU, which might indicate ATP consumption due to fructose metabolism. Unlike previous reports, the high-fructose diet did not affect NHE3 expression. A gene chip analysis conducted to identify susceptible molecules revealed that only Slc5a10 (corresponding to SGLT5) in FRU showed >2-fold up-regulation versus GLU. RT-PCR and in situ hybridization confirmed the SGLT5 up-regulation. Our findings may indicate that the high-fructose diet increased sodium reabsorption principally through up-regulated SGLT5, finally causing salt-sensitive hypertension.

Green Tea Polyphenol Extract Regulates the Expression of Genes Involved in Glucose Uptake and Insulin Signaling in Rats Fed a High Fructose Diet

2007 ◽  
Vol 55 (15) ◽  
pp. 6372-6378 ◽  
Author(s):  
Heping Cao ◽  
Isabelle Hininger-Favier ◽  
Meghan A. Kelly ◽  
Rachida Benaraba ◽  
Harry D. Dawson ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Green Tea ◽  
Insulin Signaling ◽  
Tea Polyphenol ◽  
High Fructose Diet ◽  
Expression Of Genes ◽  
High Fructose ◽  
Green Tea Polyphenol

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 Dietary Interventions to Prevent High Fructose Diet-associated Worsening of Colitis and Colitis-associated Tumorigenesis in Mice

2021 ◽  
Author(s):  
Ryohei Nishiguchi ◽  
Srijani Basu ◽  
Hannah A Staab ◽  
Naotake Ito ◽  
Xi Kathy Zhou ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Control Diet ◽  
Experimental Colitis ◽  
Protective Effects ◽  
Diet Change ◽  
Chronic Colitis ◽  
Acute Colitis ◽  
High Fructose Diet ◽  
High Consumption ◽  
High Fructose

Abstract Diet is believed to be an important factor in the pathogenesis of Inflammatory Bowel Disease. High consumption of dietary fructose has been shown to exacerbate experimental colitis, an effect mediated through the gut microbiota. This study evaluated whether dietary alterations could attenuate the detrimental effects of a high fructose diet (HFrD) in experimental colitis. First, we determined whether the pro-colitic effects of a HFrD could be reversed by switching mice from a HFrD to a control diet. This diet change completely prevented HFrD-induced worsening of acute colitis, in association with a rapid normalization of the microbiota. Second, we tested the effects of dietary fiber, which demonstrated that psyllium was the most effective type of fiber for protecting against HFrD-induced worsening of acute colitis, compared to pectin, inulin or cellulose. In fact, supplemental psyllium nearly completely prevented the detrimental effects of the HFrD, an effect associated with a shift in the gut microbiota. We next determined whether the protective effects of these interventions could be extended to chronic colitis and colitis-associated tumorigenesis. Using the azoxymethane/dextran sodium sulfate model, we first demonstrated that HFrD feeding exacerbated chronic colitis and increased colitis-associated tumorigenesis. Using the same dietary changes tested in the acute colitis setting, we also showed that mice were protected from HFrD-mediated enhanced chronic colitis and tumorigenesis, upon either diet switching or psyllium supplementation. Taken together, these findings suggest that high consumption of fructose may enhance colon tumorigenesis associated with long-standing colitis, an effect that could be reduced by dietary alterations.

scholarly journals High-Fructose Diet Increases Inflammatory Cytokines and Alters Gut Microbiota Composition in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Yong Wang ◽  
Wentao Qi ◽  
Ge Song ◽  
Shaojie Pang ◽  
Zhenzhen Peng ◽  
...  
Keyword(s):  
Uric Acid ◽  
Inflammatory Response ◽  
Gut Microbiota ◽  
Inflammatory Cytokines ◽  
Proinflammatory Cytokines ◽  
Lipid Accumulation ◽  
Fasting Blood Glucose ◽  
High Fructose Diet ◽  
Fructose Intake ◽  
High Fructose

High-fructose diet induced changes in gut microbiota structure and function, which have been linked to inflammatory response. However, the effect of small or appropriate doses of fructose on gut microbiota and inflammatory cytokines is not fully understood. Hence, the abundance changes of gut microbiota in fructose-treated Sprague-Dawley rats were analyzed by 16S rRNA sequencing. The effects of fructose diet on metabolic disorders were evaluated by blood biochemical parameter test, histological analysis, short-chain fatty acid (SCFA) analysis, ELISA analysis, and Western blot. Rats were intragastrically administered with pure fructose at the dose of 0 (Con), 2.6 (Fru-L), 5.3 (Fru-M), and 10.5 g/kg/day (Fru-H) for 20 weeks. The results showed that there were 36.5% increase of uric acid level in the Fru-H group when compared with the Con group. The serum proinflammatory cytokines (IL-6, TNF-α, and MIP-2) were significantly increased ( P < 0.05 ), and the anti-inflammatory cytokine IL-10 was significantly decreased ( P < 0.05 ) with fructose treatment. A higher fructose intake induced lipid accumulation in the liver and inflammatory cell infiltration in the pancreas and colon and increased the abundances of Lachnospira, Parasutterella, Marvinbryantia, and Blantia in colonic contents. Fructose intake increased the expressions of lipid accumulation proteins including perilipin-1, ADRP, and Tip-47 in the colon. Moreover, the higher level intake of fructose impaired intestinal barrier function due to the decrease of the expression of tight junction proteins (ZO-1 and occludin). In summary, there were no negative effects on body weight, fasting blood glucose, gut microbiota, and SCFAs in colonic contents of rats when fructose intake is in small or appropriate doses. High intake of fructose can increase uric acid, proinflammatory cytokines, intestinal permeability, and lipid accumulation in the liver and induce inflammatory response in the pancreas and colon.

scholarly journals Influence of Normo- and Hypogonadal Condition, Hyperuricemia, and High-Fructose Diet on Renal Changes in Male Rats

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Jimena Soutelo ◽  
Yanina Alejandra Samaniego ◽  
Elsa Zotta ◽  
María Cecilia Fornari ◽  
Carlos Reyes Toso ◽  
...  
Keyword(s):  
Gender Disparity ◽  
Male Rats ◽  
Renal Lesion ◽  
Treatment Control ◽  
High Fructose Diet ◽  
High Fructose ◽  
Renal Changes ◽  
Male Wistar Rats ◽  
Progression Of Renal Disease ◽  
Oxonic Acid

Background. There is a gender disparity in the incidence, prevalence, and progression of renal disease. The object of this paper is to evaluate the presence and type of renal lesion in normogonadic and hypogonadic male rats in a mild hyperuricemia induced condition and exposed to a high-fructose diet. Methods. 56 adult male Wistar rats were used. Animals were divided into two groups, one normogonadic (NGN) and one hypogonadic (HGN), and each group was divided into four subgroups in accordance with the treatment: control with only water (C), fructose (F), oxonic acid (OA), and fructose + oxonic acid (FOA). Renal changes were evaluated by measuring glomerulosclerosis, fibrosis, and arteriolar media/lumen (M/L) ratio.Results. The OA and FOA groups presented significantly hypertension (p<0.001). The OA group significantly increased (p<0.05) the percentage of glomerulosclerosis as well as the FOA group (p<0.001). When comparing NGN versus HGN, we observed a trend to a lower glomerulosclerosis in the latter. A higher arteriolar M/L ratio was observed in the OA (p<0.05) and FOA (p<0.001). Conclusion. Hyperuricemia conditions and a high-fructose diet favor blood pressure increase together with changes in the arteriolar media/lumen ratio and renal glomerular damage. These changes were more apparent in normogonadic animals.

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