Cafeteria Diet-induced Obesity Research Articles

Efficacy of Metformin Course Application Combined with Intranasal Insulin in Treating Rats with Cafeteria Diet-Induced Obesity

Efficacy of Metformin Course Application Combined with Intranasal Insulin in Treating Rats with Cafeteria Diet-Induced Obesity

Weight and Glucose Control in Rats Submitted to Sleeve Gastrectomy with Cafeteria Diet-Induced Obesity.

Introduction: Sleeve gastrectomy (SG) has been widely disseminated as a surgical treatment for obesity and associated comorbidities, and currently it is one of the most performed surgeries in the world. Experimental research is becoming increasingly relevant to characterize the pathophysiological mechanisms induced by it. Objective: The aim of this study was to standardize an experimental model of SG in rats with obesity induced using a cafeteria diet (CAF) and evaluate variations in weight and glycemic control after vertical SG, maintaining the CAF. Materials and Methods: Twenty Rattus norvegicus albinus rats, Wistar strain, with an average weight of 250 g were used. The animals were randomized into two groups and underwent 4 weeks of obesity induction before the procedure. In 10 animals of the SG group, vertical SG was performed, and in 10 animals of the control/sham (C) group, simulated surgery was performed, consisting of laparotomy and bidigital compression of the stomach. The animals were followed for a total of 8 weeks, with the weight assessed weekly and fasting blood glucose assessed before the start of the CAF, at the time of surgery, and after 4 weeks of the postoperative period, when they were sacrificed. Results: Before obesity induction, the average weight was 257.8 g in the SG group 266.1 g in the C group. After obesity induction, the average weight was 384 g in the vertical sleeve gastrectomy group and 374.8 g in the C group. In the fourth postoperative week, the average weight was 391.6 g in the VSG group and 436.6 g in the C group. The average blood glucose levels were 88.7, 101.8, and 91.3 mg/dL in the VSG group and 86.6, 103.1, and 109.4 mg/dL in the C group, respectively, before the start of the diet, in the fourth preoperative week, and in the fourth postoperative week. Conclusions: Vertical SG in rats is feasible and promotes glycemic control in the postoperative period. CAF allows induction of obesity and changes in blood glucose.

Cafeteria diet-induced obesity remodels immune response in acute Trypanosoma cruzi infection

BackgroundObesity is a global problem associated with several conditions, including hypertension, diabetes, arthritis and cardiovascular diseases. With the increase in the prevalence of obesity in recent years, mostly in developing countries, it is important to study its impact on various diseases, including infectious illnesses, such as Chagas disease, caused by the protozoan Trypanosoma cruzi. Considering that a diet rich in salt, sugar, and fat is associated with obesity, this study aimed to evaluate the influence of cafeteria diet (CAF)-induced obesity on immune responses in T. cruzi-infected rats. MethodsMale Wistar Hannover rats were provided with water and food ad libitum (chow group). The CAF-fed groups received a normal rodent diet or CAF. The animals were intraperitoneally infected with 105 trypomastigote forms of the Y strain of T. cruzi present in the whole blood from a previously infected mouse. ResultsCAF-fed rats showed a significant increase in visceral adipose tissue weight compared to chow-fed rats. A significant reduction in CD3+ CD4+ helper splenic T cells was observed in obese-infected rats compared to non-obese-infected rats, as well as CD11b and macrophages. In addition, macrophages from obese animals displayed reduced RT1b levels compared to those from control animals. Moreover, INF-γ, an important factor in macrophage activation, was reduced in obese-infected rats compared with their counterparts. ConclusionsThese results indicate that a CAF can impair the cell-mediated immune response against T. cruzi.

VITAMIN D SUPPLEMENTATION DECREASES THE BODY FAT STORES AND PLASMA OXIDATIVE STRESS OF OBESE RATS

The study aimed to verify the effects of vitamin D3 (cholecalciferol) supplementation on thebody fat composition and plasmatic oxidative stress of obese rats. The 21 days old maleWistar rats were acclimatized in the sectorial animal breed until they were 30 days old(CEUA nº 5866200720). Then the obesity induction was initiated using the cafeteria diet(Western Diet; WD). The animals were divided into 2 groups: CTL, rats fed a normal diet;WD, animals fed a WD. After 90 days old, they were subdivided into two other groups: CTL-VD and WD-VD, which received vitamin D3 during 40 days (5.600 UI/week by gavage). At130 days old, blood was collected and the plasma separated for the oxidative stress assays.After, body fat deposits were collected, separated and weighed. The adiposity index of WDrats were higher than CTL and WD-VD animals. The epididymal, retroperitoneal andmesenteric fat deposits of WD were respectively 30%, 46% and 50% higher in WD rats whencompared to WD-VD rats. Body weight gain and abdominal fat were also decreased inanimals supplemented with vitamin D3. Regarding the oxidative stress parameters in theplasma, the levels of carbonyl protein groups were lower, and protein thiol groups and totalantioxidant capacity (TAC) were higher in WD rats when compared to the CTL and WD-VDgroups. In conclusion, treatment with VD3 was able to reduce both fat stores and the levels ofoxidative stress markers in the plasma of rats with cafeteria diet-induced obesity.

Effects of omega-3 supplementation on anxiety-like behaviors and neuroinflammation in Wistar rats following cafeteria diet-induced obesity

ABSTRACT Objetives: Omega-3 (n3) fatty acids have been studied as an option to alleviate the harmful effects of obesity. However, its role in obesity-related behavioral changes is still controversial. This study aimed to evaluate the effects of n3 on behavior and neuroinflammation in obese animals. Methods: Male Wistar rats were divided into four groups: control diet (CT), CT+n3, cafeteria diet (CAF), and CAF+n3. Diet was administered for 13 weeks, and n3 was supplemented during the last 5 weeks. Metabolic and biochemical parameters were evaluated, as well as anxiety-like behaviors. Immunoblots were conducted in the animals’ cerebral cortex and hippocampus to assess changes in neuroinflammatory markers. Results: CAF-fed animals showed higher weight gain, visceral adiposity, fasting glucose, total cholesterol, triglycerides, and insulin levels, and n3 improved the lipid profile and restored insulin sensitivity. CAF-fed rats showed anxiety-like behaviors in the open field and light–dark box tasks but not in the contextual aversive conditioning. Omega-3 did not exert any effect on these behaviors. Regarding neuroinflammation, diet and supplementation acted in a region-specific manner. In the hippocampus, CAF reduced claudin-5 expression with no effect of n3, indicating a brain–blood barrier disruption following CAF. Furthermore, in the hippocampus, the glial fibrillary acidic protein (GFAP) and toll-like receptor 4 (TLR-4) were reduced in treated obese animals. However, n3 could not reverse the TLR-4 expression increase in the cerebral cortex. Discussion: Although n3 may protect against some neuroinflammatory manifestations in the hippocampus, it does not seem sufficient to reverse the increase in anxiolytic manifestations caused by CAF.

Contribution of RAS, ROS and COX-1-derived prostanoids to the contractile profile of perivascular adipose tissue in cafeteria diet-induced obesity

AimsObesity can lead to the loss of the anticontractile properties of perivascular adipose tissue (PVAT). Given that cafeteria (CAF) diet reflects the variety of highly calorie and easily accessible foods in Western societies, contributing to obesity and metabolic disorders, we sought to investigate the impact of CAF diet on PVAT vasoactive profile and the involvement of renin-angiotensin system, oxidative stress, and cyclooxygenase pathway. Main methodsMale Balb/c mice received standard or CAF diet for 4 weeks. Oral glucose tolerance and insulin sensitivity tests were performed, and fasting serum glucose, cholesterol and triglyceride parameters were determined. Vascular reactivity, fluorescence and immunofluorescence analyzes were carried out in intact thoracic aorta in the presence or absence of PVAT. Key findingsCAF diet was effective in inducing obesity and metabolic disorders, as demonstrated by increased body weight gain and adiposity index, hyperlipidemia, hyperglycemia, glucose intolerance and insulin insensitivity. Importantly, CAF diet led to a significant decrease in aortic contractility which was restored in the presence of PVAT, exhibiting therefore a contractile profile. The contractile effect of PVAT was associated with the activation of AT1 receptor, reactive oxygen species, cyclooxygenase-1, thromboxane A2 and prostaglandin E2 receptors. SignificanceThese findings suggest that the contractile profile of PVAT involving the renin-angiotensin system activation, reactive oxygen species and cyclooxygenase-1 metabolites may be a protective compensatory adaptive response during early stage of CAF diet-induced obesity as an attempt to restore the impaired vascular contraction observed in the absence of PVAT, contributing to the maintenance of vascular tone.

Investigation of Effect of Polyherbal Mixtures on Cafeteria Diet Induced Obesity in Wistar rats

Investigation of Effect of Polyherbal Mixtures on Cafeteria Diet Induced Obesity in Wistar rats

Contribution of RAS, ROS and COX-1-Derived Prostanoids to the Contractile Profile of Perivascular Adipose Tissue in Cafeteria Diet-Induced Obesity

Contribution of RAS, ROS and COX-1-Derived Prostanoids to the Contractile Profile of Perivascular Adipose Tissue in Cafeteria Diet-Induced Obesity

Evaluation of Antiobesity Activity of Bryophyllum pinnatum (Lam) Oken Leaves Extract in Cafeteria Diet Induced Obesity in Rats

Present study was aimed to scrutinize the antiobesity activity of Bryophyllum pinnatum (Lam) Oken leaves aqueous extract (AEBP) in the cafeteria diet-induced obesity in rats. Female Wistar rats weighing between 100-150 g were allocated in five groups (n=6) i.e. normal control, obesity control, standard drug (Orlistat) treated group, test drug (200 mg/kg and 400 mg/kg AEBP) treated groups. The result revealed that B. pinnatum leaves prevented the increase in BMI, food intake, body weight, glucose, triglycerides and cholesterol level without affecting water intake. This study provides evidence for the antiobesity activity of Bryophyllum pinnatum (Lam) Oken leaves.

Obesity modifies the implantation window and disrupts intrauterine embryo positioning in rats.

Obesity is a chronic disease that impairs female reproduction. When gestation is achieved, maternal obesity can cause offspring's health complications. We intended to evaluate the effects of maternal pre-conceptional obesity on uterine contractile activity, embryo implantation and offspring development. Using cafeteria diet-induced obesity as an animal model, we found that maternal obesity delays embryo transport from the oviduct to the uterus and alters the intrauterine embryo positioning. Adrenergic receptor (AR) signaling is involved in embryo positioning, so all AR isoforms were screened in the pre-implantation uteri. We found that the β2AR is the dominant isoform in the rat uteri and that obesity causes its upregulation. Although β2AR activation is known to induce uterine relaxation, higher spontaneous contractile activity was detected in obese dams. Uteri from obese dams showed a higher sensitivity to salbutamol (a selective agonist of β2AR) than controls, consistent with the higher β2AR levels detected in those animals. Despite this, in obese dams, some embryos were still in the oviduct at the predicted time of initial embryo attachment, embryo implantation is successfully carried out since the total number of fetuses on gd 18.5 were similar between control and obese dams. These findings show that obesity is modifying the implantation window. Moreover, we found that maternal obesity resulted in macrosomia in the offspring, which is an important predictor of fetal programming of postnatal health. Hence, our results show that maternal obesity prior to pregnancy not only disturbs the implantation process, but also affects offspring development.

Proteomic and Structural Manifestations of Cardiomyopathy in Rat Models of Obesity and Weight Loss.

Obesity cardiomyopathy increases the risk of heart failure and death. Obesity is curable, leading to the restoration of the heart phenotype, but it is not clear if there are any after-effects of obesity present after weight loss. We characterize the proteomic landscape of obesity cardiomyopathy with an evaluation of whether the cardiac phenotype is still shaped after weight loss. Cardiomyopathy was validated by cardiac hypertrophy, fibrosis, oversized myocytes, and mTOR upregulation in a rat model of cafeteria diet-induced developmental obesity. By global proteomic techniques (LC-MS/MS) a plethora of molecular changes was observed in the heart and circulation of obese animals, suggesting abnormal utilization of metabolic substrates. This was confirmed by increased levels of cardiac ACSL-1, a key enzyme for fatty acid degradation and decreased GLUT-1, a glucose transporter in obese rats. Calorie restriction and weight loss led to the normalization of the heart’s size, but fibrosis was still excessive. The proteomic compositions of cardiac tissue and plasma were different after weight loss as compared to control. In addition to morphological consequences, obesity cardiomyopathy involves many proteomic changes. Weight loss provides for a partial repair of the heart’s architecture, but the trace of fibrotic deposition and proteomic alterations may occur.

Cafeteria diet-induced obesity reduces leptin-stimulated NADPH-diaphorase reactivity in the hypothalamic arcuate nucleus of rats

Leptin is an adipokine that plays an important role in the regulation of energy homeostasis. The failure of endogenous and exogenous leptin to mediate its effects (for example, at suppressing appetite and decreasing body weight) has been termed leptin resistance. Hyperleptinemia and leptin resistance can be well demonstrated in animals in which obesity is induced by consumption of a palatable, high-calorie diet (e.g., cafeteria diet-induced obesity). Since leptin receptor signaling is known to be impaired in the hypothalamic arcuate nucleus (ARC) of obese rodents, we investigated the effect of leptin on nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) reactivity in the ARC of male Wistar rats with cafeteria diet-induced obesity. Our results have shown that after intraperitoneal administration of leptin, the number of NADPH-d positive neurons in the ARC was significantly lower in obese rats compared with that observed in normal weight rats. Additionally, we have found that leptin-induced NADPH-d staining in ARC neurons and the adjacent ependyma was decreased in obese rats. The results presented here suggest that the ability of leptin to activate nitric oxide synthase in neurons within the ARC as well as tanycytes and ependymal cells of the third ventricle is reduced in rats made obese by a cafeteria diet. We speculate that impairment in leptin-induced NO production presents a potential mechanism, involved in the pathogenesis of obesity and obesity-related disease states.

The Role of Mitochondria in Sex-Dependent Differences in Hepatic Steatosis and Oxidative Stress in Response to Cafeteria Diet-Induced Obesity in Mice.

Female mice fed a cafeteria diet (FCaf) develop higher liver steatosis and oxidative stress than males (MCaf) as a consequence of unresolved ER stress. Here, we investigated whether mitochondria play a role in this sex difference. The isolated mitochondria from FCaf showed more signs of oxidative stress than those of MCaf, correlated with a reduced content of GSH, increased amount of reactive oxygen species (ROS), and lower activities of enzymes involved in ROS neutralisation. Mitochondria from FCaf and MCaf livers exhibited lower rates of succinate-driven state III respiration and reduced ATPase activity in intact coupled mitochondria compared to their controls fed a standard diet (FC and MC), with no differences between the sexes. Fatty acid oxidation in mitochondria and peroxisomes was higher in MCaf and FCaf compared to their respective controls. In the intact perfused liver, there was no difference between sex or diet regarding the fatty acid oxidation rate. These results indicated that cafeteria diet did not affect mitochondrial energy metabolism, even in FCaf livers, which have higher steatosis and cellular oxidative stress. Nevertheless, the increase in mitochondrial ROS generation associated with a decrease in the antioxidant defence capacity, probably contributes to inducing or reinforcing the ER stress in FCaf livers.

Sex differences in the development of hepatic steatosis in cafeteria diet-induced obesity in young mice

The present study was planned to improve our understanding about sex differences in the development of hepatic steatosis in cafeteria diet-induced obesity in young mice. Female (FCaf) and male (MCaf) mice fed a cafeteria diet had similar body weight gain and adiposity index, but FCaf had a more extensive steatosis than MCaf. FCaf livers exhibited a higher non-alcoholic fatty liver disease activity score, elevated lipid percentage area (+34%) in Sudan III staining and increased TG content (+25%) compared to MCaf. Steatosis in FCaf was not correlated with changes in the transcript levels of lipid metabolism-related genes, but a reduced VLDL release rate was observed. Signs of oxidative stress were found in FCaf livers, as elevated malondialdehyde content (+110%), reduced catalase activity (−36%) and increased Nrf2 and Hif1a mRNA expression compared to MCaf. Interestingly, fibroblast growth factor 21 (Fgf21) mRNA expression was found to be exclusively induced in MCaf, which also exhibited higher FGF21 serum levels (+416%) and hepatic protein abundance (+163%) than FCaf. Moreover, cafeteria diet increased Fgfr1, Fsp27 and Ucp1 mRNA expression in brown adipose tissue of males (MCaf), but not females (FCaf). FGF21 hepatic production by male mice seems to be part of a complex network of responses to the nutritional stress of the cafeteria diet, probably related to the unfolded protein response activation. Although aimed at the restoration of hepatic metabolic homeostasis, the branch involving Fgf21 upregulation seems to be impaired in females, rendering them incapable of reducing the hepatic lipid content and cellular oxidative stress.

ИЗМЕНЕНИЕ СООТНОШЕНИЯ ОРЕКСИГЕННЫХ И АНОРЕКСИГЕННЫХ ФАКТОРОВ В ГИПОТАЛАМУСЕ КРЫС С ОЖИРЕНИЕМ, ВЫЗВАННЫМ КАФЕТЕРИЙ-ДИЕТОЙ, "Российский физиологический журнал им. И.М. Сеченова"

The hypothalamus controls food behavior, and the abnormalities in this regulation induce obesity. This is largely due to the changes in the balance of the hypothalamic factors, such as ore-xigenic factors, including orexin (OR), agouti-like peptide (AgRP) and neuropeptide Y (NPY), and anorexigenic factors including the melanocortin peptides generated from pro-opiomelanocortin (POMC). The data on the expression and the ratio of these factors in obesity induced by the high-calorie diet are few and contradictory. The aim was to study the expression of POMC, OR of the A-type (OR-A), AgRP and NPY in the hypothalamic structures of male rats with cafeteria diet-induced obesity as compared to control animals. Starting the 26-day-old age, the rats consumed a cafeteria diet for 12 weeks, which leads to obesity, insulin resistance, the changes in the carbohydrate and lipid metabolism, and hyperleptinemia. In the perifornical area of the hypothalamus of obese rats, a significant decrease in the number of OR-A and the mRNA expression for the gene encoding pre-proorexin, the OR-A precursor, was shown. In the hypothalamic arcuate nuclei of obese rats, the expression of the gene for AgRP, the antagonist of type 4 melanocortin receptor, was decreased, the expression of the gene for POMC was increased, and the expression of the gene for NPY changed to a small extent. Thus, in different areas of the hypothalamus of rats with cafeteria diet-induced obesity, the compensatory processes are triggered to increase anorexigenic effects and suppress orexigenic effects, which should weaken hyperphagia and prevent the negative metabolic and hormonal changes caused by excessive caloric intake

Cafeteria diet-induced obesity causes oxidative damage in white adipose

Obesity continues to be one of the most prominent public health dilemmas in the world. The complex interaction among the varied causes of obesity makes it a particularly challenging problem to address. While typical high-fat purified diets successfully induce weight gain in rodents, we have described a more robust model of diet-induced obesity based on feeding rats a diet consisting of highly palatable, energy-dense human junk foods – the “cafeteria” diet (CAF, 45–53% kcal from fat). We previously reported that CAF-fed rats became hyperphagic, gained more weight, and developed more severe hyperinsulinemia, hyperglycemia, and glucose intolerance compared to the lard-based 45% kcal from fat high fat diet–fed group. In addition, the CAF diet-fed group displayed a higher degree of inflammation in adipose and liver, mitochondrial dysfunction, and an increased concentration of lipid-derived, pro-inflammatory mediators. Building upon our previous findings, we aimed to determine mechanisms that underlie physiologic findings in the CAF diet. We investigated the effect of CAF diet-induced obesity on adipose tissue specifically using expression arrays and immunohistochemistry. Genomic evidence indicated the CAF diet induced alterations in the white adipose gene transcriptome, with notable suppression of glutathione-related genes and pathways involved in mitigating oxidative stress. Immunohistochemical analysis indicated a doubling in adipose lipid peroxidation marker 4-HNE levels compared to rats that remained lean on control standard chow diet. Our data indicates that the CAF diet drives an increase in oxidative damage in white adipose tissue that may affect tissue homeostasis. Oxidative stress drives activation of inflammatory kinases that can perturb insulin signaling leading to glucose intolerance and diabetes.

Cafeteria diet-induced obesity causes oxidative damage in white adipose

Cafeteria diet-induced obesity causes oxidative damage in white adipose

Effect of Coleus forskohliiextract on cafeteria diet-induced obesity in rats

Background:Obesity is a metabolic disorder that can lead to adverse metabolic effects on blood pressure, cholesterol, triglycerides and insulin resistance and also increases the risk of coronary heart disease, ischemic stroke and type 2 diabetes mellitus. This study was designed to determine the effect of Coleus forskohlii on obesity and associated metabolic changes in rats fed with cafeteria diet.Objective:The aim of this study was to evaluate antiobesogenic and metabolic benefits of C. forskohlii in cafeteria diet induced obesity rat model.Materials and Methods:Rats were randomly divided into five groups of six animals in each group and as follows: Normal pellet diet group; cafeteria diet group; cafeteria diet followed by 50 mg/kg/d Coleus forskohlii extract (CFE), 100 mg/kg/d CFE and 45 mg/kg/d orlistat groups, respectively. Indicators of obesity such as food intake, body weight and alteration in serum lipid profiles were studied.Results:Feeding of cafeteria diet induced obesity in rats. Administration of CFE significantly halted increase in food intake and weight gain associated with cafeteria diet. Development of dyslipidemia was also significantly inhibited.Conclusion:The observed effects validate that supplementation of CFE with cafeteria diet could curb the appetite and mitigate the development of dyslipidemia.

Effects of food pattern change and physical exercise on cafeteria diet-induced obesity in female rats

Obesity affects a large number of people around the world and appears to be the result of changes in food intake, eating habits and physical activity levels. Changes in dietary patterns and physical exercise are therefore strongly recommended to treat obesity and its complications. The present study tested the hypothesis that obesity and metabolic changes produced by a cafeteria diet can be prevented with dietary changes and/or physical exercise. A total of fifty-six female Wistar rats underwent one of five treatments: chow diet; cafeteria diet; cafeteria diet followed by a chow diet; cafeteria diet plus exercise; cafeteria diet followed by a chow diet plus exercise. The duration of the experiment was 34 weeks. The cafeteria diet resulted in higher energy intake, weight gain, increased visceral adipose tissue and liver weight, and insulin resistance. The cafeteria diet followed by the chow diet resulted in energy intake, body weight, visceral adipose tissue and liver weight and insulin sensitivity equal to that of the controls. Exercise increased total energy intake at week 34, but produced no changes in the animals' body weight or adipose tissue mass. However, insulin sensitivity in animals subjected to exercise and the diet was similar to that of the controls. The present study found that exposure to palatable food caused obesity and insulin resistance and a diet change was sufficient to prevent cafeteria diet-induced obesity and to maintain insulin sensitivity at normal levels. In addition, exercise resulted in normal insulin sensitivity in obese rats. These results may help to develop new approaches for the treatment of obesity and type 2 diabetes mellitus.

Anti-obesity effect of Stellaria media methanolic extract in the murine model of cafeteria diet induced obesity

Context: The whole plant of Stellaria media Linn (family Caryophyllaceae) is used by the local people of Dibrugarh district of Assam state, India, as a dietary supplement for the treatment of overweight and is also mentioned in the traditional system of Indian medicine as a remedy for obesity. Moreover phytoconstituents like flavonoid, saponin, and sitosterol have already been reported for their anti-obesity activity, and the extract of S. media also contains the same constituents in its extracts. With this background, this study was carried out. Objective: The anti-obesity activity of the alcoholic and methanolic extracts of Stellaria media was evaluated against the cafeteria diet-induced obesity model in female Wistar rats. Materials and Methods: Obesity was induced by feeding a cafeteria diet for 48 days to female Wistar rats, although one group was kept on a normal chow diet to evaluate the effect of Stellaria media on body weight changes, exploratory behavior, theromogenesis, lipid metabolism, effect on White Adipose Tissue (WAT), and histology of the fat pad. Results: Among these two extracts, the methanolic extract of Stellaria media (MESM) has shown a strong anti-obesity effect compared to the alcoholic extract of Stellaria media (AESM); may be because of its multiple mechanisms. The LD 50 value was found to be more than 5000 mg/kg. Discussion and Conclusion: These findings suggest that the anti-obesity activity produced by MESM may be because of the flavonoid and saponin contents, which have thermogenic and appetite-suppressant properties or it may be due to the β-sitosterol content. With this study we conclude that MESM is beneficial for the suppression of obesity and its associated complications.