Maternal high-fructose intake induces hypertension through activating histone codes on the (pro)renin receptor promoter

2020 ◽  
Vol 527 (3) ◽  
pp. 596-602 ◽  
Author(s):  
Hyun Min Cho ◽  
InKyeom Kim
Keyword(s):  
Fructose Intake ◽  
High Fructose ◽  
Histone Codes

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 The Role of Perivascular Adipose Tissue in Early Changes in Arterial Function during High-Fat Diet and Its Combination with High-Fructose Intake in Rats

Biomedicines ◽  
2021 ◽  
Vol 9 (11) ◽  
pp. 1552
Author(s):  
Jozef Torok ◽  
Anna Zemancikova ◽  
Zuzana Valaskova ◽  
Peter Balis
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Control Diet ◽  
Sympathetic Nerves ◽  
High Fat ◽  
Perivascular Adipose Tissue ◽  
Fructose Intake ◽  
High Fructose ◽  
Wistar Kyoto ◽  
Isolated Arteries

The aim of the current study was to evaluate the influence of a high-fat diet and its combination with high-fructose intake on young normotensive rats, with focus on the modulatory effect of perivascular adipose tissue (PVAT) on the reactivity of isolated arteries. Six-week-old Wistar–Kyoto rats were treated for 8 weeks with a control diet (10% fat), a high-fat diet (HFD; 45% fat), or a combination of the HFD with a 10% solution of fructose. Contractile and relaxant responses of isolated rat arteries, with preserved and removed PVAT for selected vasoactive stimuli, were recorded isometrically by a force displacement transducer. The results demonstrated that, in young rats, eight weeks of the HFD might lead to body fat accumulation and early excitation of the cardiovascular sympathetic nervous system, as shown by increased heart rate and enhanced arterial contractile responses induced by endogenous noradrenaline released from perivascular sympathetic nerves. The addition of high-fructose intake deteriorated this state by impairment of arterial relaxation and resulted in mild elevation of systolic blood pressure; however, the increase in arterial neurogenic contractions was not detected. The diet-induced alterations in isolated arteries were observed only in the presence of PVAT, indicating that this structure is important in initiation of early vascular changes during the development of metabolic syndrome.

scholarly journals High fructose intake induces cardiac diastolic dysfunction in rats

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Iara Cristina Araujo ◽  
Cristiano Mostarda ◽  
Polyana Souza Lima ◽  
Larissa Naomi Yamane ◽  
Marina Soares Souza ◽  
...  
Keyword(s):  
Diastolic Dysfunction ◽  
Fructose Intake ◽  
High Fructose

High fructose intake and the route towards cardiometabolic diseases

Life Sciences ◽  
2020 ◽  
Vol 259 ◽  
pp. 118235
Author(s):  
Deborah de Farias Lelis ◽  
João Marcus Oliveira Andrade ◽  
Camila Cruz Pereira Almenara ◽  
Gilson B. Broseguini-Filho ◽  
José Geraldo Mill ◽  
...  
Keyword(s):  
Cardiometabolic Diseases ◽  
Fructose Intake ◽  
High Fructose

scholarly journals Insulin Resistance Promotes Early Atherosclerosis via Increased Proinflammatory Proteins and Oxidative Stress in Fructose-Fed ApoE-KO Mice

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Beatriz Cannizzo ◽  
Agustín Luján ◽  
Natalia Estrella ◽  
Carina Lembo ◽  
Montserrat Cruzado ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Vascular Remodeling ◽  
Oxidase Activity ◽  
Fructose Intake ◽  
High Fructose ◽  
Study Results ◽  
Apoe Ko Mice ◽  
And Oxidative Stress ◽  
Apoe Ko

High fructose intake induces an insulin resistance state associated with metabolic syndrome (MS). The effect of vascular inflammation in this model is not completely addressed. The aim of this study was to evaluate vascular remodeling, inflammatory and oxidative stress markers, and atheroma development in high-fructose diet-induced insulin resistance of ApoE-deficient mice (ApoE-KO). Mice were fed with either a normal chow or a 10% w/v fructose (HF) in drinking water over a period of 8 weeks. Thereafter, plasma metabolic parameters, vascular remodeling, atheroma lesion size, inflammatory markers, and NAD(P)H oxidase activity in the arteries were determined. HF diet induced a marked increase in plasma glucose, insulin, and triglycerides in ApoE-KO mice, provoked vascular remodeling, enhanced expression of vascular cell-adhesion molecule-1 (VCAM-1) and matrix metalloprotease 9 (MMP-9) and enlarged atherosclerotic lesion in aortic and carotid arteries. NAD(P)H oxidase activity was enhanced by fructose intake, and this effect was attenuated by tempol, a superoxide dismutase mimetic, and losartan, an Angiotensin II receptor antagonist. Our study results show that high-fructose-induced insulin resistance promotes a proinflammatory and prooxidant state which accelerates atherosclerotic plaque formation in ApoE-KO mice.

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