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

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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Cardiometabolic Changes in Different Gonadal Female States Caused by Mild Hyperuricemia and Exposure to a High-Fructose Diet

International Journal of Endocrinology ◽

10.1155/2018/6021259 ◽

2018 ◽

Vol 2018 ◽

pp. 1-9 ◽

Cited By ~ 1

Author(s):

J. Soutelo ◽

Y. A. Samaniego ◽

M. C. Fornari ◽

C. Reyes Toso ◽

O. J. Ponzo

Keyword(s):

Uric Acid ◽

Lipid Profile ◽

Wistar Rats ◽

Female Rats ◽

Treatment Control ◽

High Fructose Diet ◽

High Fructose ◽

Metabolic Systems ◽

Female Wistar Rats ◽

Oxonic Acid

Background. The objective of this study is to observe if mild hyperuricemia and a high-fructose diet influence the cardiovascular and metabolic systems in hypogonadic female Wistar rats compared to normogonadic female rats. Methods. Fifty-six (56) adult female Wistar rats were used in the present work. Animals were divided into two groups: normogonadic (NGN) and hypogonadic (HGN). These groups were also divided into four subgroups in accordance with the treatment: control with only water (C), fructose (F), oxonic acid (OA), and fructose + oxonic acid (FOA). Lipid profile, glycemia, uric acid, and creatinine determinations were assessed. Cardiovascular changes were evaluated by measuring blood pressure, myocyte volume, fibrosis, and intima-media aortic thickness. Results. HGN rats had higher levels of total cholesterol (TC) (p<0.01) and noHDLc (p<0.01), in addition to higher levels of uric acid (p<0.05). The OA group significantly increased myocyte volume (p<0.0001) and the percentage of fibrosis as well as the group receiving FOA (p<0.001) in both gonadal conditions, being greater in the HGN group. Hypogonadic animals presented a worse lipid profile. Conclusion. Mild hyperuricemia produces hypertension together with changes in the cardiac hypertrophy, fibrosis, and increased thickness of the intima media in hypogonadic rats fed high-fructose diet.

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Preventive Effect of Bridelia ferruginea Against High-fructose Diet Induced Glucose Intolerance, Oxidative Stress and Hyperlipidemia in Male Wistar Rats

Journal of Pharmacology and Toxicology ◽

10.3923/jpt.2011.249.257 ◽

2011 ◽

Vol 6 (3) ◽

pp. 249-257 ◽

Cited By ~ 14

Author(s):

B. Bakoma ◽

K. Eklu-Gadeg ◽

A. Agbonon ◽

K. Aklikokou ◽

E. Bassene ◽

...

Keyword(s):

Oxidative Stress ◽

Glucose Intolerance ◽

Wistar Rats ◽

Preventive Effect ◽

High Fructose Diet ◽

Bridelia Ferruginea ◽

High Fructose ◽

Male Wistar Rats

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Kupffer cell depletion protects against the steatosis, but not the liver damage, induced by marginal-copper, high-fructose diet in male rats

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00285.2014 ◽

2015 ◽

Vol 308 (11) ◽

pp. G934-G945 ◽

Cited By ~ 8

Author(s):

Ming Song ◽

Dale A. Schuschke ◽

Zhanxiang Zhou ◽

Wei Zhong ◽

Jiayuan Zhang ◽

...

Keyword(s):

Fatty Liver ◽

Regulatory Element ◽

Critical Role ◽

Deionized Water ◽

Male Rats ◽

Sprague Dawley ◽

Deficient Diet ◽

High Fructose Diet ◽

Triglyceride Accumulation ◽

High Fructose

High-fructose feeding impairs copper status and leads to low copper availability, which is a novel mechanism in obesity-related fatty liver. Copper deficiency-associated hepatic iron overload likely plays an important role in fructose-induced liver injury. Excess iron in the liver is distributed throughout hepatocytes and Kupffer cells (KCs). The aim of this study was to examine the role of KCs in the pathogenesis of nonalcoholic fatty liver disease induced by a marginal-copper high-fructose diet (CuMF). Male weanling Sprague-Dawley rats were fed either a copper-adequate or a marginally copper-deficient diet for 4 wk. Deionized water or deionized water containing 30% fructose (wt/vol) was also given ad libitum. KCs were depleted by intravenous administration of gadolinium chloride (GdCl3) before and/or in the middle of the experimental period. Hepatic triglyceride accumulation was completely eliminated with KC depletion in CuMF consumption rats, which was associated with the normalization of elevated plasma monocyte chemoattractant protein-1 (MCP-1) and increased hepatic sterol regulatory element binding protein-1 expression. However, hepatic copper and iron content were not significantly affected by KC depletion. In addition, KC depletion reduced body weight and epididymal fat weight as well as adipocyte size. Plasma endotoxin and gut permeability were markedly increased in CuMF rats. Moreover, MCP-1 was robustly increased in the culture medium when isolated KCs from CuMF rats were treated with LPS. Our data suggest that KCs play a critical role in the development of hepatic steatosis induced by marginal-copper high-fructose diet.

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High-fructose diet during periadolescent development increases depressive-like behavior and remodels the hypothalamic transcriptome in male rats

Psychoneuroendocrinology ◽

10.1016/j.psyneuen.2015.08.025 ◽

2015 ◽

Vol 62 ◽

pp. 252-264 ◽

Cited By ~ 25

Author(s):

Constance S. Harrell ◽

Jillybeth Burgado ◽

Sean D. Kelly ◽

Zachary P. Johnson ◽

Gretchen N. Neigh

Keyword(s):

Male Rats ◽

High Fructose Diet ◽

High Fructose

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Role of Nitric Oxide in the Early Renal Changes Induced by High Fructose Diet in Rats

Kidney & Blood Pressure Research ◽

10.1159/000068694 ◽

2002 ◽

Vol 25 (6) ◽

pp. 363-369 ◽

Cited By ~ 8

Author(s):

Alessandro Cosenzi ◽

Elena Bernobich ◽

Michela Bonavita ◽

Furio Gris ◽

Giulio Odoni ◽

...

Keyword(s):

Nitric Oxide ◽

High Fructose Diet ◽

High Fructose ◽

Renal Changes

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Endothelin-1 blockade prevents COX2 induction and TXA2 production in the fructose hypertensive ratThis paper is one of a selection of papers published in this Special Issue, entitled The Cellular and Molecular Basis of Cardiovascular Dysfunction, Dhalla 70th Birthday Tribute.

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y06-088 ◽

2007 ◽

Vol 85 (3-4) ◽

pp. 422-429 ◽

Cited By ~ 11

Author(s):

Jihong Jiang ◽

Linda Tran ◽

Harish Vasudevan ◽

Zhengyuan Xia ◽

Violet G. Yuen ◽

...

Keyword(s):

Insulin Resistance ◽

Control Level ◽

Total Duration ◽

Endothelin 1 ◽

High Fructose Diet ◽

Thromboxane Synthase Inhibitor ◽

High Fructose ◽

Male Wistar Rats ◽

Synthase Inhibitor

Feeding rats with a high fructose diet results in insulin resistance and hypertension. Fructose-hypertensive rats (FHR) have increased vascular levels of endothelin-1 (ET-1) and thromboxane (TXA2). We have previously shown that chronic treatment with either the dual endothelin receptor blocker, bosentan, or the thromboxane synthase inhibitor, dazmegrel, prevented fructose-induced increases in blood pressure, suggesting that both ET-1 and TXA2 play important roles in the development of hyperinsulinemia/insulin resistance-associated hypertension. In this study, we investigated the potential interrelationship between ET-1 and TXA2 in the development of fructose-induced hypertension in vivo. Male Wistar rats were fed on a high fructose diet for 9 weeks. Either bosentan or dazmegrel treatment (daily by oral gavage) was initiated 3 weeks after the start of fructose feeding for a total duration of 6 weeks. At the end of drug treatment, blood and aorta were collected from each animal. Plasma thromboxane B2 (TXB2), a stable TXA2 metabolite, increased significantly in FHR and was reduced to control level by both chronic bosentan and dazmegrel treatment. Protein expression of cyclooxygenase 2 (COX2) was elevated significantly in FHR aortas and treatment with bosentan and dazmegrel corrected these changes. These results indicate that the actions of ET-1 in the aorta of FHR may be mediated through COX2-derived TXA2. Bosentan may prevent the development of hypertension in fructose-fed rats through inhibition of COX2 induction and subsequently the reduction in plasma TXA2.

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