Diet-induced endothelial dysfunction in the rat is independent of the degree of increase in total body weight

A growing number of studies indicate an association between obesity, insulin resistance, dyslipidaemia and cardiovascular disorders, collectively known as Syndrome X. In this study we have aimed to produce a model of Syndrome X by voluntary feeding of Wistar rats with a highly palatable cafeteria diet, and examined its effects on metabolic changes and vascular reactivity of Wistar rats. At the end of the experiment, the cafeteria-diet fed group was divided into two groups of low weight gain (LWG) and high weight gain (HWG). Both LWG and HWG groups had significantly (P < 0.01) higher fat-pad mass than their chow-fed counterparts, while gastrocnemius muscle mass were comparable. All cafeteria-diet fed rats had significantly (P < 0.01) raised plasma triacylglycerol (TG) levels whereas plasma non-esterified fatty acids, glucose and insulin levels were similar between chow-fed and cafeteria-diet fed rats. Vasorelaxation responses to acteylcholine, insulin and sodium nitroprusside were significantly (P < 0.01) attenuated in cafeteria-diet fed animals; however, there were no differences in contractile responses of the mesenteric arteries to noradrenaline or KCl between the groups. Multiple regression analysis showed a significant (P < 0.05) negative association between plasma TG levels and reduction in acetylcholine-induced vasorelaxation. Acetylcholine-induced vasorelaxation was also significantly (P < 0.05) associated with the amount of fat-pad mass. These data suggest that diet-induced vascular dysfunction can occur in the absence of insulin resistance, and that plasma TGs may have a detrimental effect on vascular reactivity.

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Eicosapentaenoic acid actions on adiposity and insulin resistance in control and high-fat-fed rats: role of apoptosis, adiponectin and tumour necrosis factor-α

British Journal Of Nutrition ◽

10.1017/s0007114507207627 ◽

2007 ◽

Vol 97 (2) ◽

pp. 389-398 ◽

Cited By ~ 131

Author(s):

Patricia Pérez-Matute ◽

Nerea Pérez-Echarri ◽

J. Alfredo Martínez ◽

Amelia Marti ◽

María J. Moreno-Aliaga

Keyword(s):

Gene Expression ◽

Insulin Resistance ◽

Body Weight ◽

Adipose Tissue ◽

Weight Gain ◽

Body Weight Gain ◽

Control Diet ◽

Cafeteria Diet ◽

High Fat ◽

Beneficial Effects

n-3 PUFA have shown potential anti-obesity and insulin-sensitising properties. However, the mechanisms involved are not clearly established. The aim of the present study was to assess the effects of EPA administration, one of the n-3 PUFA, on body-weight gain and adiposity in rats fed on a standard or a high-fat (cafeteria) diet. The actions on white adipose tissue lipolysis, apoptosis and on several genes related to obesity and insulin resistance were also studied. Control and cafeteria-induced overweight male Wistar rats were assigned into two subgroups, one of them daily received EPA ethyl ester (1 g/kg) for 5 weeks by oral administration. The high-fat diet induced a very significant increase in both body weight and fat mass. Rats fed with the cafeteria diet and orally treated with EPA showed a marginally lower body-weight gain (P = 0·09), a decrease in food intake (P < 0·01) and an increase in leptin production (P < 0·05). EPA administration reduced retroperitoneal adipose tissue weight (P < 0·05) which could be secondary to the inhibition of the adipogenic transcription factor PPARγ gene expression (P < 0·001), and also to the increase in apoptosis (P < 0·05) found in rats fed with a control diet. TNFα gene expression was significantly increased (P < 0·05) by the cafeteria diet, while EPA treatment was able to prevent (P < 0·01) the rise in this inflammatory cytokine. Adiposity-corrected adiponectin plasma levels were increased by EPA. These actions on both TNFα and adiponectin could explain the beneficial effects of EPA on insulin resistance induced by the cafeteria diet.

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Sweet taste of saccharin induces weight gain without increasing caloric intake, not related to insulin-resistance in Wistar rats

Appetite ◽

10.1016/j.appet.2015.11.003 ◽

2016 ◽

Vol 96 ◽

pp. 604-610 ◽

Cited By ~ 19

Author(s):

Kelly Carraro Foletto ◽

Bruna Aparecida Melo Batista ◽

Alice Magagnin Neves ◽

Fernanda de Matos Feijó ◽

Cíntia Reis Ballard ◽

...

Keyword(s):

Insulin Resistance ◽

Weight Gain ◽

Wistar Rats ◽

Caloric Intake ◽

Sweet Taste

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Cafeteria diet intake for fourteen weeks can cause obesity and insulin resistance in Wistar rats

Revista de Nutrição ◽

10.1590/s1415-52732012000300001 ◽

2012 ◽

Vol 25 (3) ◽

pp. 313-319 ◽

Cited By ~ 8

Author(s):

Danilo Antônio Corrêa Pinto Júnior ◽

Patricia Monteiro Seraphim

Keyword(s):

Insulin Resistance ◽

Fat Mass ◽

Wistar Rats ◽

Soft Drink ◽

Strong Predictor ◽

Liver Weight ◽

Progressive Increase ◽

Obese Group ◽

Cafeteria Diet ◽

Control Group

OBJECTIVE: Obesity is a strong predictor of some kinds of diseases. High intake of high-fat foods contributes significantly to the growth of the obese population globally. The aim of this study was to verify if consumption of a cafeteria diet for fourteen weeks could increase white fat mass, body weight and skeletal muscle mass and promote insulin resistance in male Wistar rats. METHODS: Twenty animals were divided into two groups: control and obese. Both were fed standard chow and water ad libitum. Additionally, a cafeteria diet consisting of bacon, bologna sausage, sandwich cookies and soft drink was given to the obese group. RESULTS: The obese group was significantly heavier (p<0.0001) than controls from the second week until the end of the cafeteria-diet intervention. Absolute and relative fat mass, liver weight and Lee Index increased significantly (p<0.05) in the obese group. Furthermore, the obese group had lower (p<0.05) insulin sensitivity than the control group. CONCLUSION: In conclusion, fourteen weeks of cafeteria diet promoted a progressive increase of fat mass and insulin resistance. Therefore, this is a great and inexpensive diet-induced insulin resistance model.

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Evaluation of Polyherbal Formulation (Kemite) on Cafeteria Diet-induced Obesity in Wistar Rats

International Journal of Pharmaceutical Sciences Review and Research ◽

10.47583/ijpsrr.2021.v70i01.020 ◽

2021 ◽

Vol 70 (1) ◽

Author(s):

GNANGORAN Boua Narcisse ◽

Traoré Moussa ◽

YAPO Angoué Paul

Keyword(s):

Body Weight ◽

Food Intake ◽

Aqueous Extract ◽

Wistar Rats ◽

Risk Index ◽

The Body ◽

Cafeteria Diet ◽

Atherogenic Index ◽

Coronary Risk ◽

Fat Pad

Obesity is a chronic disorder of global prevalence and associated with morbidity and mortality. This pathology is a real public health problem. The work was undertaken to evaluate the antiobesity efficacy of aqueous extract of Kemite in cafeteria diet induced obese Wistar rats for a period of 28 days. Aqueous extract of Kemite (AEK) was prepared by hot extraction method. Female Wistar rats weighing 124-170 g were divided into different groups i.e. Normal control, cafeteria control and aqueous extract of Kemite at dose of 200 mg/kg bw. The antiobesity activity is estimated in terms of body weight gain, food intake, serum triglycerides (TG), Total cholesterol (TC), LDL cholesterol (LDL-C), HDL cholesterol (HDL-C), VLDL cholesterol (VLDL-C), blood glucose (BG), ASAT and ALAT activities, atherogenic index, coronary risk index and liver and fat pad weights. Results showed Cafeteria diet fed rats for 28 successive days significantly increased the body weight, food intake, ASAT and ALAT activities, liver and fat pad weights, atherogenic index, coronary risk index TG, TC, LDL, VLDL, BG and not influenced HDL levels. Rats treated with extract for 28 successive days along with cafeteria diet reversed the effects induced by cafeteria diet. In conclusion, this study revealed that AEK may be a natural and safe remedy for the prevention and control of obesity.

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Effect of Physical Preconditioning on Vascular Reactivity and Metabolic Parameters of Wistar Rats Treated with Cafeteria Diet

Medicine & Science in Sports & Exercise ◽

10.1249/00005768-200605001-00907 ◽

2006 ◽

Vol 38 (Supplement) ◽

pp. S3-S4

Author(s):

Angelina Zanesco ◽

Camila de Moraes ◽

Mario Angelo Claudino ◽

Carla Franco Penteado ◽

Emerielle C. Vanzela ◽

...

Keyword(s):

Wistar Rats ◽

Vascular Reactivity ◽

Cafeteria Diet ◽

Metabolic Parameters

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Dietary obesity in the rat induces endothelial dysfunction without causing insulin resistance: a possible role for triacylglycerols

Clinical Science ◽

10.1042/cs1010499 ◽

2001 ◽

Vol 101 (5) ◽

pp. 499-506 ◽

Cited By ~ 19

Author(s):

Ebrahim K. NADERALI ◽

Michael J. BROWN ◽

Lucy C. PICKAVANCE ◽

John P.H. WILDING ◽

Patrick J. DOYLE ◽

...

Keyword(s):

Insulin Resistance ◽

Insulin Sensitivity ◽

Endothelial Dysfunction ◽

Mesenteric Arteries ◽

Maximal Response ◽

Fat Pad ◽

Metabolic Disturbances ◽

Response Curves ◽

No Donor ◽

Obese Rats

Impaired arterial vasorelaxation, due primarily to endothelial dysfunction, is associated with obesity. To clarify the relationship with insulin resistance and other metabolic disturbances, we studied endothelial-dependent and -independent vascular responses in rats with dietary-induced obesity. Dietary-obese rats had significantly higher body weights (10-32%; P < 0.001) and fat-pad masses (220-280%; P < 0.001) than lean controls, together with raised plasma levels of triacylglycerols (15-80%; P < 0.001), non-esterified fatty acids (13-38%; P < 0.05) and leptin (85-180%; P < 0.001). However, measures of insulin sensitivity (including the hyperinsulinaemic-euglycaemic clamp in a parallel experiment) were comparable with those in controls. Contractions induced in mesenteric arteries by noradrenaline (0.5-8μmol/l) were comparable in lean and obese groups, but vasorelaxation in noradrenaline-preconstricted arteries was markedly reduced in dietary-obese rats of both sexes. Concentration-response curves to endothelium-dependent vasorelaxants (acetylcholine, A23187 and insulin) showed significant reductions in maximal relaxation (20-95% less than in leans; P < 0.001) and significant rightward shifts in EC40 (concentration giving 40% of maximal response) (P < 0.01). Relaxation in response to the direct NO donor, sodium nitroprusside, showed a lesser impairment (12%; P < 0.01) in dietary-obese rats. Maximal relaxation to acetylcholine was correlated inversely in both sexes with fat-pad mass (r2 = 0.37, P < 0.05) and plasma triacylglycerols (r2 = 0.51, P < 0.01), and with leptin in males only (r2 = 0.35, P < 0.05). Independent determinants of acetylcholine-induced relaxation were fat mass and plasma triacylglycerols; plasma insulin and insulin sensitivity had no effect. Dietary-induced obesity severely impaired arterial relaxation in both sexes, particularly at the endothelial level. This is not attributable to insulin resistance, but may be related to moderate hypertriglyceridaemia.

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Cafeteria diet decreases sucrose preference and increases the sensitivity of risperidone in the caloric intake of Wistar rats

Nutrition & Food Science ◽

10.1108/nfs-05-2021-0148 ◽

2021 ◽

Vol ahead-of-print (ahead-of-print) ◽

Author(s):

Jéssica Sena Gonçalves ◽

Arthur Rocha-Gomes ◽

Amanda Escobar Teixeira ◽

Alexandre Alves da Silva ◽

Mayara Rodrigues Lessa ◽

...

Keyword(s):

Adipose Tissue ◽

Weight Gain ◽

Food Intake ◽

Energy Intake ◽

Wistar Rats ◽

Cafeteria Diet ◽

Sucrose Preference ◽

Control Group ◽

Lactation Period ◽

Content Type

Purpose The purpose of this study was to evaluate the increase in sensitivity of a single risperidone administration in relation to energy intake of Wistar rats treated with cafeteria diet from birth to adulthood (119 days). Design/methodology/approach During the lactation period, six litters of Wistar rats (dam + 8 pups each litter) were fed one of the following two diets: Control (n = 3) or Cafeteria (n = 3) diets and water ad libitum. After weaning, the males were placed in individual cages, receiving the same diet offered to their respective dams (Control = 18; or Cafeteria = 18) until adulthood (119 postnatal days). The following parameters were evaluated: food and energy intake; macronutrient intake; weight gain; adipose tissue relative weight; sucrose preference; food intake after an administration of risperidone (0.1 mg/kg body weight). Findings The Cafeteria group showed a higher energy intake in relation to the Control group (p < 0.001). The consumption of energy beyond the individual needs can be understood as a hyperphagic condition. Also, the Cafeteria group reported greater weight gain (p = 0.048) and accumulation of adipose tissue (p < 0.001) with respect to the Control group. These results indicate that the cafeteria diet generated obesity in animals. The Cafeteria group showed reduced sucrose preference (p = 0.031), which is associated with the development of anhedonia-like behavior. In the food intake test, risperidone showed a greater sensitivity in Cafeteria animals, promoting a decrease in their energy intake in relation to the Control group that received risperidone (p = 0.040). Originality/value The cafeteria diet promoted hyperphagia, anhedonia-like behavior and obesity in animals. Acute risperidone administration showed greater sensitivity in the Cafeteria group, with a decrease in energy intake. The reported effects may be related to a downregulation of the dopaminergic system in the NAc region.

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Dose-dependent and time-dependent metabolic, hemodynamic, and redox disturbances in dexamethasone-treated Wistar rats

Journal of Basic and Clinical Physiology and Pharmacology ◽

10.1515/jbcpp-2020-0365 ◽

2021 ◽

Vol 0 (0) ◽

Author(s):

Elvine P. Nguelefack-Mbuyo ◽

Fernande P. Peyembouo ◽

Christian K. Fofié ◽

Télesphore B. Nguelefack

Keyword(s):

Insulin Resistance ◽

Body Weight ◽

Catalase Activity ◽

Wistar Rats ◽

Chronic Treatment ◽

Body Weight Loss ◽

Redox Status ◽

Duration Of Treatment ◽

Renal Hypertrophy ◽

Subchronic Treatment

Abstract Objectives Dexamethasone is used experimentally to induce insulin resistance and type 2 diabetes. However, data concerning the dose, the duration of treatment, and the associated comorbidities are inconsistent. The aim of this study was to compare the effects of different doses of dexamethasone and the duration of treatment necessary for the development of a model of insulin resistance that mimics the clinical condition with the associated comorbidities. Methods Dexamethasone was administered intramuscularly to male Wistar rats, at doses of 500 and 1,000 µg/kg/day for the subchronic treatment (eight consecutive days) and at doses of 5, 25, 50, and 100 µg/kg/day in chronic treatment (28 consecutive days). Effects on body weight, metabolism, hemodynamics, renal function, and redox status were evaluated. Results Both treatments induced a progressive body weight loss that was drastic in subchronic treatment, improved glucose tolerance without affecting fasting glycemia. Doses of 1,000 and 100 µg/kg were associated with hypertriglyceridemia, hypertension, and increased heart rate, cardiac and renal hypertrophy. Increased creatinemia associated with reduced creatinuria were observed in sub-chronic treatment while increased proteinuria and reduced creatinuria were noticed in chronic treatment. 1,000 µg/kg dexamethasone caused an increase in hepatic, and renal malondialdehyde (MDA) and glutathione (GSH) coupled with a reduction in catalase activity. The dose of 100 µg/kg induced a rise in GSH and catalase activity but reduced MDA levels in the kidney. Conclusions Doses of 1,000 µg/kg for subchronic and 100 µg/kg for chronic treatment exhibited similar effects and are the best doses to respective time frames to induce the model.

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