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Search Results: 1 - 10 of 18805 matches for " High-fat diet "
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Expression changes of Akt and GSK-3β during vascular inflammatory response and oxidative stress induced by high-fat diet in rats  [PDF]
Jingshang Wang, Huijun Yin, Ye Huang, Chunyu Guo, Chengdong Xia, Lu Zhang
Journal of Biomedical Science and Engineering (JBiSE) , 2013, DOI: 10.4236/jbise.2013.65A001
Abstract:

Aim: To observe the expression changes of Akt and GSK-3β during vascular inflammatory response and oxidative stress induced by high-fat diet in rats. Methods: 20 male Sprague-Dawley rats were separately fed for 18 weeks with two types of diets; a normal diet (control group, CON) or high-fat diet hyperlipidmia group, HLP). Then the body weight, lipid parameter, plasma hepatocyte growth factor (HGF), serum superoxide dismutase (SOD) , malondialdehyde (MDA), Tumor necrosis factor-α (TNF-α), a Soluble intercellular adhesion molecule-1 (sICAM-1), Lectin-like oxidized cellulose low density lipoprotein receptor-1 (LOX-1), as well as aortic endothelial p-GSK-3β, GSK-3β, p-Akt, Akt expressions were determined. Results: In comparison with the control group, the model group showed a significant increase in the levels of serum total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol ( LDL-C) and significant decrease in the level of serum high density lipoprotein cholesterol (HDL-C) after high-fat diet for 18 weeks (p < 0.05 or p < 0.01). Meanwhile, a more obvious increase of plasma HGF, LOX-1 and serum MDA, TNF-α, and sICAM-1 levels were observed relative to the control group (p < 0.05 or p < 0.01). Moreover, high-fat diet significantly increased the phosphorylation of Akt and GSK-3β in rat aorta. Conclusion: Short-term high-fat diet could induce vascular endothelium injury by increasing inflammation and

Hepatic stereology of schistosomiasis mansoni infected-mice fed a high-fat diet
Neves, Renata Heisler;Alencar, Alba Cristina Miranda de Barros;Aguila, Marcia Barbosa;Mandarim-de-Lacerda, Carlos Alberto;Machado-Silva, José Roberto;Gomes, Delir Corrêa;
Memórias do Instituto Oswaldo Cruz , 2006, DOI: 10.1590/S0074-02762006000900039
Abstract: high-fat diets induce weight gain and fatty liver in wild-type mice. schistosomiasis mansoni infection also promotes hepatic injury. this study was designed to quantify hepatic alterations in schistosomiasis mansoni-infected mice fed a high fat-rich chow compared to mice fed a standard rodent chow, using stereology. female sw mice fed each either high-fat diet (29% lipids) or standard chow (12% lipids) over 8 months, and then were infected with schistosoma mansoni cercariae. four experimental groups were studied: infected mice fed a high-fat diet (ihfc) or standard chow (isc), uninfected mice fed a high-fat diet (hfc) or standard chow (sc). mice were sacrificed during early infection (9 weeks from exposure). the following hepatic biometry and the stereology parameters were determined: volume density (hepatocytes [h], sinusoids [s], steatosis [st] and hepatic fibrosis [hf]); numerical density (hepatocyte nuclei - nv[h]); absolute number of total hepatocyte n[h], normal hepatocyte n[nh], and binucleated hepatocyte n[bh], percentage of normal hepatocyte p[nh] and binucleated hepatocyte p[bh]. ihfc and hfc groups exhibited tc, hdl-c, ldl-c, and body mass significantly greater (p < 0.05) than control group. no significant differences were found regards liver volume (p = 0.07). significant differences were observed regards p[nh] (p = 0.0045), p[bh] (p = 0.0045), nv[h] (p = 0.0006), n[h] (p = 0.0125), n[bh] (p = 0.0164) and n[nh] (p = 0.0078). ihfc mice group presented 29% of binucleated hepatocytes compared to hfc group (19%), isc group (17%) and sc (6%). volume density was significantly different between groups: vv[h] (p = 0.0052), vv[s] (p = 0.0025), vv[st] (p = 0.0004), and vv[hf] (p = 0.0007). in conclusion, schistosomiasis mansoni infection with concurrent high-fat diet promotes intensive quantitative changes in hepatic structure, contributing to an increasing on hepatic regeneration.
Exercise training performed simultaneously to a high-fat diet reduces the degree of insulin resistance and improves adipoR1-2/APPL1 protein levels in mice
Farias JM,Maggi RM,Tromm CB,Silva LA
Lipids in Health and Disease , 2012, DOI: 10.1186/1476-511x-11-134
Abstract: Background The aim of the present study was to evaluate the protective effect of concurrent exercise in the degree of the insulin resistance in mice fed with a high-fat diet, and assess adiponectin receptors (ADIPOR1 and ADIPOR2) and endosomal adaptor protein APPL1 in different tissues. Methods Twenty-four mice were randomized into four groups (n = 6): chow standard diet and sedentary (C); chow standard diet and simultaneous exercise training (C-T); fed on a high-fat diet and sedentary (DIO); and fed on a high-fat diet and simultaneous exercise training (DIO-T). Simultaneously to starting high-fat diet feeding, the mice were submitted to a swimming exercise training protocol (2 x 30 minutes, with 5 minutes of interval/day), five days per week, for twelve weeks (90 days). Animals were then euthanized 48 hours after the last exercise training session, and adipose, liver, and skeletal muscle tissue were extracted for an immunoblotting analysis. Results IR, IRs, and Akt phosphorylation decreased in the DIO group in the three analyzed tissues. In addition, the DIO group exhibited ADIPOR1 (skeletal muscle and adipose tissue), ADIPOR2 (liver), and APPL1 reduced when compared with the C group. However, it was reverted when exercise training was simultaneously performed. In parallel, ADIPOR1 and 2 and APPL1 protein levels significantly increase in exercised mice. Conclusions Our findings demonstrate that exercise training performed concomitantly to a high-fat diet reduces the degree of insulin resistance and improves adipoR1-2/APPL1 protein levels in the hepatic, adipose, and skeletal muscle tissue.
The contribution of hypothalamic macroglia to the regulation of energy homeostasis
Kate L. J. Ellacott
Frontiers in Systems Neuroscience , 2014, DOI: 10.3389/fnsys.2014.00212
Abstract: The hypothalamus is critical for the regulation of energy homeostasis. Genetic and pharmacologic studies have identified a number of key hypothalamic neuronal circuits that integrate signals controlling food intake and energy expenditure. Recently, studies have begun to emerge demonstrating a role for non-neuronal cell types in the regulation of energy homeostasis. In particular the potential importance of different glial cell types is increasingly being recognized. A number of studies have described changes in the activity of hypothalamic macroglia (principally astrocytes and tanycytes) in response to states of positive and negative energy balance, such as obesity and fasting. This article will review these studies and discuss how these findings are changing our understanding of the cellular mechanisms by which energy homeostasis is regulated.
The Relationship between Cutaneous Wounds Made on Obese Mice or Those with Decreased Body Weight and Serum Leptin Level  [PDF]
Tamae Urai, ? Haryanto, Kanae Mukai, Tatsuhiko Matsushita, Kimi Asano, Yukari Nakajima, Mayumi Okuwa, Junko Sugama, Toshio Nakatani
Health (Health) , 2016, DOI: 10.4236/health.2016.811105
Abstract: Purpose: Not all obese people have hyperglycemia. We wondered about the healing progress in obese people without hyperglycemia. The purpose of this study is to observe the cutaneous wound healing process. Methods: Three-week-old male mice were fed high-fat diets (containing 60% fat) in the diet group, and commercial diets in the control group, ad libitum for 15 weeks. Circle-full-thickness cutaneous wounds were made on the dorsal skin of mice. From day 0 to day 15 after wounding, we analyzed wound healing process. We measured the blood concentration of leptin, and observed the distribution of leptin-positive cells in each wound. Results: Mean body weight, the areas of subcutaneous fat and visceral fat, and the weight of epididymal fat in the diet group were significantly greater than those in the control group at 15 weeks after feeding. The diet group did not feed on the diet after wounding; their body weight decreased remarkably to the level of the control group. The ratio of wound area, re-epithelialization, and collagen fibers did not differ between the diet and control groups on each day. The blood concentration of leptin in the diet group was significantly greater than that in the control group before wounding and until day 6 after wounding (day 0, 10 hour and day 1: p < 0.01, day 6: p < 0.05). Conclusion: The results show that the wound healing process is similar between obese and non-obese mice, and that the decrease in the leptin level in the obese mouse to that in the non-obese mouse may depend on the decrease of body weight of obese mouse.
Effectiveness of Telmisartan as an Adjunct to Metformin in Treating Type II Diabetes Mellitus in Rats  [PDF]
Rania M. Salama, Mona F. Schaalan, Moushira E. Ibrahim, Amani E. Khalifa, Alaaeldin A. Elkoussi
Open Journal of Endocrine and Metabolic Diseases (OJEMD) , 2013, DOI: 10.4236/ojemd.2013.33026
Abstract:

The monitoring reports of most patients with type II diabetes mellitus (T2DM) revealed that monotherapy with metformin could not achieve long-term glycemic control. Thus, we designed this study aiming to investigate the effect of telmisartan, a unique AT1 receptor antagonist and a partial agonist of peroxisome-proliferator activated receptor gamma (PPARγ), individually and as an adjunct to metformin, on a rat model that simulates the metabolic characteristics of human T2DM. Adult male Wistar rats were fed high-fat, high-fructose diet (HFFD) for 8 weeks followed by a single low dose of streptozotocin (STZ) (35 mg/kg/day, i.p.) rendering them diabetic and insulin resistant. The effectiveness of both drugs and their combination was tested by assessing the changes in the levels of serum glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR) index, lipid profile and adiponectin. In addition, the level of reduced glutathione (GSH) in the liver, was investigated. Results showed that the addition of telmisartan to metformin successfully restored serum glucose back to normal levels and corrected the altered serum total cholesterol (TC), triglycerides (TG) and adiponectin, emphasizing the potential role of telmisartan as an adjunct to metformin.

Impact of high-fat diet on antioxidant status, vascular wall thickening and cardiac function in adult female LDLR–/– mice  [PDF]
Stéphanie Delemasure, Carole Richard, Ségolène Gambert, Jean-Claude Guilland, Catherine Vergely, Patrick Dutartre, Luc Rochette, Jean-Louis Connat
World Journal of Cardiovascular Diseases (WJCD) , 2012, DOI: 10.4236/wjcd.2012.23031
Abstract: Background: Western diet, rich in saturated fatty acids and cholesterol, is associated with increased cardiovascular risk. We thus investigated in female mice the influence of this diet on plasma antioxidant status, vascular wall thickening and cardiac function. Methods and Results: Adult female C57BL/6J wild type (WT) and LDLR–/– mice were fed a normal diet (ND) or a high-fat diet (HFD) for 17 weeks. HFD induced an increase in plasma lipids and vitamin C (Vit C) levels in both groups but at a much higher level in LDLR–/– and a decrease in plasma ascorbyl free radical levels to Vit C ratio (an endogenous oxidative stress index) in LDLR–/–. We only found a slight decrease in circulating antioxidant status evaluated by the Oxygen Radical Absorbance Capacity (ORAC) assay in WT, but not in LDLR–/–. Echocardiography evidenced an increase in arterial wall thickness in aortic arch at atherosclerosis predilection sites in HFD LDLR–/– as compared to ND LDLR–/– and HFD WT. This result was confirmed by histology. Further-more, histological examination of aortic valves showed an increase in atherosclerotic lesions. Our study, using echocardiography, show that chronic HFD does not induce any major modifications of systolic function in the both mice groups. Conclusions: High-fat intake in mice causes serious disturbances in lipid plasma levels associated to variations of circulating antioxidant status due, at least in part, to an increase in Vit C. At this stage, atherosclerotic lesions, observed in aortic arch and valve, do not impair cardiac function in HFD-fed mice.
Diet-induced metabolic syndrome model in rats
Reza Homayounfar,Elham Ehrampoush,Seyyed Amin Koohpaye,Mohammad Hasan Meshkibaf
Journal of Fasa University of Medical Sciences , 2013,
Abstract: Background & Objective: Risk for heart disease, diabetes, and stroke increases with the number of the metabolic risk factors. In general, a person who has the metabolic syndrome is twice as likely to develop heart disease and five times as likely to develop diabetes as someone who does not have the metabolic syndrome. High-calorie-diet rodent models have contributed significantly to the analysis of the pathophysiology of the metabolic syndrome, but their phenotype varies distinctly between different studies and maybe is not very similar to a model of the metabolic syndrome in humans. We sought to create a model in this study close to the disease in humans. Materials & Methods: Twenty male, Wistar rats were randomly assigned to the high-calorie diet group with 416 calories per 100 grams (researcher made) or the control diet group for 12 weeks. Weight changes, lipid profile, glucose, insulin levels, and QUICKI index (an indicator of insulin sensitivity) were measured. Weight changes were compared using the repeated measures and the independent t-test, and serum factors were compared using the independent t-test. Results: There was a significant change in weight, glucose, insulin, and lipid profile except for HDL at the end of the study. The QUICKI index (0.34 ± 0.02 vs. 0.40 ± 0.01; p value <0.0001) suggested that insulin resistance had been created in the high-calorie diet group. Conclusion: The present study demonstrates the ability to make diet-induced metabolic syndrome domestically.
Differential Effects of High-Carbohydrate and High-Fat Diet Composition on Metabolic Control and Insulin Resistance in Normal Rats
Jorge L. Ble-Castillo,María A. Aparicio-Trapala,Isela E. Juárez-Rojop,Jorge E. Torres-Lopez,Jose D. Mendez,Hidemi Aguilar-Mariscal,Viridiana Olvera-Hernández,Leydi C. Palma-Cordova,Juan C. Diaz-Zagoya
International Journal of Environmental Research and Public Health , 2012, DOI: 10.3390/ijerph9051663
Abstract: The macronutrient component of diets is critical for metabolic control and insulin action. The aim of this study was to compare the effects of high fat diets (HFDs) vs. high carbohydrate diets (HCDs) on metabolic control and insulin resistance in Wistar rats. Thirty animals divided into five groups (n = 6) were fed: (1) Control diet (CD); (2) High-saturated fat diet (HSFD); (3) High-unsaturated fat diet (HUFD); (4) High-digestible starch diet, (HDSD); and (5) High-resistant starch diet (HRSD) during eight weeks. HFDs and HCDs reduced weight gain in comparison with CD, however no statistical significance was reached. Calorie intake was similar in both HFDs and CD, but rats receiving HCDs showed higher calorie consumption than other groups, ( p < 0.01). HRSD showed the lowest levels of serum and hepatic lipids. The HUFD induced the lowest fasting glycemia levels and HOMA-IR values. The HDSD group exhibited the highest insulin resistance and hepatic cholesterol content. In conclusion, HUFD exhibited the most beneficial effects on glycemic control meanwhile HRSD induced the highest reduction on lipid content and did not modify insulin sensitivity. In both groups, HFDs and HCDs, the diet constituents were more important factors than caloric intake for metabolic disturbance and insulin resistance.
Fenugreek with reduced bitterness prevents diet-induced metabolic disorders in rats
Etsuko Muraki, Hiroshige Chiba, Keiko Taketani, Shohei Hoshino, Nobuaki Tsuge, Nobuyo Tsunoda, Keizo Kasono
Lipids in Health and Disease , 2012, DOI: 10.1186/1476-511x-11-58
Abstract: Forty Sprague–Dawley rats were fed with high-fat high-sucrose (HFS) diet for 12 week to induce mild glucose and lipid disorders. Afterwards, the rats were divided into 5 groups. In the experiment 1, each group (n?=?8) was fed with HFS, or HFS containing 2.4% fenugreek, or HFS containing 1.2%, 2.4% and 4.8% FRB, respectively, for 12 week. In the experiment 2, we examined the effects of lower doses of FRB (0.12%, 0.24% and 1.2%) under the same protocol (n?=?7 in each groups).In the experiment 1, FRB dose-dependently reduced food intake, body weight gain, epididymal white adipose tissue (EWAT) and soleus muscle weight. FRB also lowered plasma and hepatic lipid levels and increased fecal lipid levels, both dose-dependently. The Plasma total cholesterol levels (mmol/L) in the three FRB and Ctrl groups were 1.58?±?0.09, 1.45?±?0.05*, 1.29?±?0.07* and 2.00?±?0.18, respectively (*; P?<?0.05 vs. Ctrl). The Hepatic total cholesterol levels (mmol/g liver) were 0.116?±?0.011, 0.112?±?0.006, 0.099?±?0.007* and 0.144?±?0.012, respectively (*; P?<?0.05 vs. Ctrl). The calculated homeostasis model assessment as an index of insulin resistance (HOMA-IR) indicated 0.52?±?0.04*, 0.47?±?0.06*, 0.45?±?0.05* and 1.10?±?0.16, respectively (*; P?<?0.05 vs. Ctrl). None of the FRB groups showed any adverse effect on the liver, kidney or hematological functions. In the experiment 2, no significant difference of food intake was observed, while the 1.2% FRB group alone showed nearly the same effects on glucose and lipid metabolism as in the experiment 1.Thus we have demonstrated that FRB (1.2?~?4.8%) prevents diet-induced metabolic disorders such as insulin resistance, dyslipidemia and fatty liver.
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