scholarly journals Impact of Gentamicin Coadministration along with High Fructose Feeding on Progression of Renal Failure and Metabolic Syndrome in Sprague-Dawley Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Zaid O. Ibraheem ◽  
Rusliza Basir ◽  
Ahmad Kh. Aljobory ◽  
Omar E. Ibrahim ◽  
Ajwad Alsumaidaee ◽  
...  

The current study evaluates the impact of high fructose feeding in rat model of gentamicin induced nephrotoxicity. Sprague-Dawley rats weighing 180–200 g were randomized into four groups; (C) received standard rodents chow with free access toad libitumdrinking water for 8 weeks and was considered as control, (F) received standard rodents chow with free access to drinking water supplemented with 20% (W/V) fructose for the same abovementioned period, (FG) was fed as group F and was given 80 mg/kg (body weight)/day gentamicin sulphate intraperitoneally during the last 20 days of the feeding period, and (G) was given gentamicin as above and fed as group C. Renal function was assessed at the end of the treatment period through measuring serum creatinine, uric acid and albumin, creatinine clearance, absolute and fractional excretion of both sodium and potassium, twenty-four-hour urinary excretion of albumin, and renal histology. For metabolic syndrome assessment, fasting plasma glucose and insulin were measured and oral glucose tolerance test was performed throughout the treatment period. Results showed that gentamicin enhances progression of fructose induced metabolic syndrome. On the other hand, fructose pretreatment before gentamicin injection produced a comparable degree of renal dysfunction to those which were given fructose-free water but the picture of nephrotoxicity was somewhat altered as it was characterized by higher extent of glomerular congestion and protein urea. Overall, more vigilance is required when nephrotoxic drugs are prescribed for patients with fructose induced metabolic syndrome.

Author(s):  
N.G. Mustafa ◽  
M.K. Hasan

Metabolic syndrome (MS) is a complex condition characterized by insulin resistance, hyperglycemia, dyslipidemia, and obesity. This project aims to induce MS in rat and then a demonstration of the main biochemical parameters. In male, Sprague-Dawley rats, MS has been prompted suitably and relatively by fast (six weeks) approach through a high fructose in drinking water (40%). It has been found that serum urea, creatinine, and total bilirubin raise in MS significantly. Moreover, dyslipidemia has arbitrated via some considerable lipid profile deviations. In addition, BMI, blood glucose, and insulin monitoring evidently ensure achievement of MS. It is concluded that a well-established rat model of MS could be employed by a 40% fructose in drinking water.


2019 ◽  
Vol 8 ◽  
pp. 1250
Author(s):  
Esmat Radmanesh ◽  
Mahin Dianat ◽  
Narges Atefipour

Background: Many risk factors, including nutritional ones, contribute to cardiovascular diseases (CVDs). Increased fructose consumption, for example, can lead to an increase in CVD risk factors, i.e. an increase in blood lipids and the development of insulin resistance. Materials and Methods: In the present study, Sprague Dawley rats were divided into two groups:  control group (free access to tap drinking water for seven weeks), and a group that received fructose 10% in drinking water for seven weeks, (n ═8 per each group). In all groups, before starting the test period and seven weeks after it, electrocardiogram was recorded by Power lab system. Unpaired t-test and two-way ANOVA were used for data analysis. Also, oxidative stress parameters were measured. Results: In the group received high doses of fructose, a significant reduction (P <0.05) was observed in the PR interval (P<0.001) and a significant increase (P<0.05) in the QTc interval. However, there was no significant change in the RR interval and the voltage of the QRS complex. A significant decrease in catalase, superoxide dismutase and glutathione peroxidase (P<0.05) and a significant increase (P<0.05) in malondialdehyde and lactate dehydrogenase were observed in the group that received fructose in comparison with the control group at the end of the experiment. Conclusion: According to our results, the chance of arrhythmias in the rats receiving high doses of fructose was possibly due to the increased oxidative stress in the healthy rats. [GMJ.2019;8:e1250]


2016 ◽  
Vol 310 (10) ◽  
pp. R952-R959 ◽  
Author(s):  
Clare M. Mathes ◽  
Chanel Letourneau ◽  
Ginger D. Blonde ◽  
Carel W. le Roux ◽  
Alan C. Spector

Roux-en-Y gastric bypass surgery (RYGB) decreases caloric intake in both human patients and rodent models. In long-term intake tests, rats decrease their preference for fat and/or sugar after RYGB, and patients may have similar changes in food selection. Here we evaluated the impact of RYGB on intake during a “cafeteria”-style presentation of foods to assess if rats would lower the percentage of calories taken from fat and/or sugar after RYGB in a more complex dietary context. Male Sprague-Dawley rats that underwent either RYGB or sham surgery (Sham) were presurgically and postsurgically given 8-days free access to four semisolid foods representative of different fat and sugar levels along with standard chow and water. Compared with Sham rats, RYGB rats took proportionally fewer calories from fat and more calories from carbohydrates; the latter was not attributable to an increase in sugar intake. The proportion of calories taken from protein after RYGB also increased slightly. Importantly, these postsurgical macronutrient caloric intake changes in the RYGB rats were progressive, making it unlikely that the surgery had an immediate impact on the hedonic evaluation of the foods and strongly suggesting that learning is influencing the food choices. Indeed, despite these dietary shifts, RYGB, as well as Sham, rats continued to select the majority of their calories from the high-fat/high-sugar option. Apparently after RYGB, rats can progressively regulate their intake and selection of complex foods to achieve a seemingly healthier macronutrient dietary composition.


2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Ji Hun Park ◽  
Min Chul Kho ◽  
Hye Yoom Kim ◽  
You Mee Ahn ◽  
Yun Jung Lee ◽  
...  

Increased fructose ingestion has been linked to obesity, hyperglycemia, dyslipidemia, and hypertension associated with metabolic syndrome. Blackcurrant (Ribes nigrum; BC) is a horticultural crop in Europe. To induce metabolic syndrome, Sprague-Dawley rats were fed 60% high-fructose diet. Treatment with BC (100 or 300 mg/kg/day for 8 weeks) significantly suppressed increased liver weight, epididymal fat weight, C-reactive protein (CRP), total bilirubin, leptin, and insulin in rats with induced metabolic syndrome. BC markedly prevented increased adipocyte size and hepatic triglyceride accumulation in rats with induced metabolic syndrome. BC suppressed oral glucose tolerance and protein expression of insulin receptor substrate-1 (IRS-1) and phosphorylated AMP-activated protein kinase (p-AMPK) in muscle. BC significantly suppressed plasma total cholesterol, triglyceride, and LDL content. BC suppressed endothelial dysfunction by inducing downregulation of endothelin-1 and adhesion molecules in the aorta. Vascular relaxation of thoracic aortic rings by sodium nitroprusside and acetylcholine was improved by BC. The present study provides evidence of the potential protective effect of BC against metabolic syndrome by demonstrating improvements in dyslipidemia, hypertension, insulin resistance, and obesityin vivo.


Author(s):  
Pedram Shokouh ◽  
Per Bendix Jeppesen ◽  
Kjeld Hermansen ◽  
Christoffer Laustsen ◽  
Hans Stødkilde-Jørgensen ◽  
...  

Literature is inconsistent as to how coffee affects the features of the metabolic syndrome (MetS), and which bioactive compounds are responsible for its metabolic effects. We aimed to compare the in-vivo effects of unfiltered coffee with a selected mixture of its compounds on diet-induced MetS. 24 male Sprague-Dawley rats were fed a high-fat (35% W/W) food plus 20% W/W fructose in drinking water for 14 weeks, and were randomized into three groups: control, coffee, or nutraceuticals (5-O-caffeoylquinic acid, caffeic acid, and trigonelline). Coffee or nutraceuticals were provided in drinking water in a dosage equal to 4 cups/day in a human. Compared to the controls, only coffee supplementation decreased total food intake, weight gain, and estimated average plasma glucose. Surrogate measures of insulin resistance (fasting insulin, HOMA-IR, and oral glucose tolerance) were improved at endpoint in the coffee group. Circulating triglyceride levels were also reduced by coffee. Histopathological and quantitative measurements indicated lower grades of liver steatosis after long-term coffee consumption. In conclusion, a combination of phenolic acids and trigonelline was not as effective as coffee per se in improving the components of the MetS. This points to the role of other coffee chemicals and a potential synergism between compounds.


2021 ◽  
pp. 1-21
Author(s):  
M.E. Ragi ◽  
R. El-Haber ◽  
F. El-Masri ◽  
O.A. Obeid

Abstract The ingestion of non-caloric sweeteners from food and/or drink was intended to reduce caloric intake without compromising palatability. However, the inconclusive relation between non-caloric sweeteners and body weight may partially relate to their form of ingestion (solid or liquid). Thus, two paralleled experiments (Aspartame and Sucralose) were conducted. In each, Sprague Dawley rats (7-week-old male) were randomly divided into 4 groups. In experiment 1, aspartame (0.05%) was added to the diet (AD) or drinking water (AW) or both diet and water (ADW), and a control group (C) was given a non-sweetened diet with plain water. In experiment 2, sucralose (0.016%) was similarly provided in the diet (SD) or drinking water (SW) or both diet and water (SDW), with a control group (C). All rats had free access to food and water for 7 weeks. Energy intake, body weight, and body composition were monitored and blood metabolites were determined. Results showed that aspartame ingestion significantly increased body weight and fat mass mainly due to an increase in energy efficiency. The effect was related to the amount rather than the form of ingestion. Additionally, aspartame ingestion was associated with glucose intolerance. Sucralose ingestion had a similar impact to that of aspartame though to a lesser extent. In conclusion, 7-week ingestion of aspartame and sucralose had adverse effects on body measures that were not related to the form of ingestion.


1995 ◽  
Vol 83 (6) ◽  
pp. 1220-1232 ◽  
Author(s):  
K. A. Keller ◽  
C. Callan ◽  
P. Prokocimer ◽  
L. Delgado-Herrera ◽  
M. B. Friedman ◽  
...  

Abstract Background Under certain circumstances in the clinical setting, contact of the anesthetic sevoflurane with a CO2absorbant (e.g., soda lime, Baralyme) leads to the formation of a degradant designated as pentafluoroisopropenyl fluoromethyl ether (PIFE; Compound A). Previous studies have shown that the kidney is the primary target organ for toxicity in the rat. This study was designed to determine the impact of PIFE on rat renal histology correlated with functional changes. The findings are discussed in terms of probable mechanism of action and relevance to humans.


Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1547 ◽  
Author(s):  
Pedram Shokouh ◽  
Per Jeppesen ◽  
Kjeld Hermansen ◽  
Christoffer Laustsen ◽  
Hans Stødkilde-Jørgensen ◽  
...  

The literature is inconsistent as to how coffee affects metabolic syndrome (MetS), and which bioactive compounds are responsible for its metabolic effects. This study aimed to evaluate the effects of unfiltered coffee on diet-induced MetS and investigate whether or not phenolic acids and trigonelline are the main bioactive compounds in coffee. Twenty-four male Sprague‒Dawley rats were fed a high-fat (35% W/W) diet plus 20% W/W fructose in drinking water for 14 weeks, and were randomized into three groups: control, coffee, or nutraceuticals (5-O-caffeoylquinic acid, caffeic acid, and trigonelline). Coffee or nutraceuticals were provided in drinking water at a dosage equal to 4 cups/day in a human. Compared to the controls, total food intake (p = 0.023) and mean body weight at endpoint (p = 0.016) and estimated average plasma glucose (p = 0.041) were lower only in the coffee group. Surrogate measures of insulin resistance including the overall fasting insulin (p = 0.010), endpoint HOMA-IR (p = 0.022), and oral glucose tolerance (p = 0.029) were improved in the coffee group. Circulating triglyceride levels were lower (p = 0.010), and histopathological and quantitative (p = 0.010) measurements indicated lower grades of liver steatosis compared to controls after long-term coffee consumption. In conclusion, a combination of phenolic acids and trigonelline was not as effective as coffee per se in improving the components of the MetS. This points to the role of other coffee chemicals and a potential synergism between compounds.


Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Emily Henson ◽  
Gustavo Ares ◽  
Mohammed Haque ◽  
Pablo Ortiz

Consumption of fructose as a sweetener has increased in the past three decades. A high-fructose diet has been implicated in the epidemic of diabetes, obesity, and hypertension. A third of the US population consumes 20-40% of their caloric intake from added sugars, with half of those calories from fructose. Little is known about the role of high fructose intake in renal salt handling and blood pressure regulation during high salt intake. In genetic models of salt-sensitive hypertension, the Na/K/2Cl cotransporter NKCC2 plays an important role by reabsorbing NaCl in the thick ascending limb (TAL). We hypothesized that 20% fructose in drinking water stimulates NKCC2 and sensitizes normal rats to high salt induced hypertension. Adult Sprague-Dawley rats were given 20% fructose or 20% glucose in drinking water for 1 week after which a high salt diet (4% Na in chow) was started. Systolic blood pressure (SBP) was measured every other day by tail cuff after 2 weeks of training. After one week of fructose or glucose alone, SBP did not change. In rats fed fructose, adding a 4% NaCl diet increased SBP to 128±6 mmHg by day 2 (p<0.01 vs glucose) and continued to increase up to 144±18 mmHg after 2 weeks on high salt (p<0.01 vs baseline; p<0.01 vs glucose). In glucose-fed rats high salt did not increase SBP (from 122±6 to 116±9 mmHg). 20% fructose alone for 3 weeks, or high salt alone did not change SBP. NKCC2 phosphorylation at Thr96,101 is associated with enhanced TAL NaCl reabsorption. We found that NKCC2 phosphorylation at Thr96,101 (normalized to total NKCC2) was higher in TALs isolated from rats fed fructose plus salt for 2 weeks compared to high salt alone (high-salt: 100%; fructose + high-salt: 250±40%, p<0.05). We concluded that a high fructose but not high glucose diet induces salt-sensitive hypertension in Sprague Dawley rats. This effect occurs within 1 week of a high fructose diet. In addition, a high fructose diet may stimulate NKCC2 activity by enhancing its phosphorylation. These data suggest that high fructose intake may increase blood pressure by preventing appropriate renal NaCl excretion during high dietary salt intake.


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