Omega-3 Attenuates Disrupted Neurotransmission and Partially Protects Metabolic Dysfunction Caused by Obesity in Wistar Rats.

Omega-3 (n3) is a polyunsaturated fatty acid well known for its anti-inflammatory and neuroprotective properties. Obesity is linked to chronic inflammation that disrupts metabolism, the intestine physiology and the central nervous system functioning. This study aims to determine if n3 supplementation can interfere with the effects of obesity on the mitochondrial activity, intestinal barrier, and neurotransmitter levels in the brain of Wistar rats that received cafeteria diet (CAF). We examined adipose tissue, skeletal muscle, plasma, intestine, and the cerebral cortex of four groups: CT (control diet), CTn3 (control diet with n3 supplementation), CAF, and CAFn3 (CAF and n3). Diets were offered for 13 weeks, with n3 supplementation in the final 5 weeks. Adipose tissue Electron Transport Chain complexes I, II, and III showed higher activity in CAF groups, as did complexes III and IV in skeletal muscle. Acetate levels in plasma were reduced in CAF groups, and Lipopolysaccharide (LPS) was higher in the CAF group but reduced in CAFn3 group. Claudin-5 in the intestine was lower in CAF groups, with no n3 supplementation effect. In the cerebral cortex, dopamine levels were decreased with CAF, which was reversed by n3. DOPAC, a dopamine metabolite, also showed a supplementation effect, and HVA, a diet effect. Serotonin levels increased in the CAF group that received supplementation. Therefore, we demonstrate disturbances in mitochondria, plasma, intestine and brain of rats submitted to CAF and the potential benefit of n3 supplementation in endotoxemia and neurotransmitter levels.

Amino acid HPLC-FLD analysis of spirulina and its protective mechanism against the combination of obesity and colitis in wistar rats.

Objective: The cafeteria diet (CD), designed as an experimental diet mimicking the obesogenic diet, may contribute to the pathogenesis of inflammatory bowel diseases (IBD). This study delves into the influence of spirulina (SP) on obesity associated with colitis in Wistar rats. Methods: The amino acids composition of SP was analyzed using HPLC-FLD. Animals were equally separated into eight groups, each containing seven animals and treated daily for eight weeks as follows: Control diet (SD), cafeteria diet (CD) group, CD + SP (500 mg/kg) and SD + SP. Ulcerative colitis was provoked by rectal injection of acetic acid (AA) (3 % v/v, 5 ml/kg b.w.) on the last day of treatment in the following groups: SD + AA, SD + AA + SP, CD + AA, and CD + AA + SP. Results: Findings revealed that UC and/or CD increased the abdominal fat, weights gain, and colons. Moreover, severe colonic alteration, perturbations in the serum metabolic parameters associated with an oxidative stress state in the colonic mucosa, defined by overproduction of reactive oxygen species (ROS) and increased levels of plasma scavenging activity (PSA). Additionally, obesity exacerbated the severity of AA-induced UC promoting inflammation marked by the overexpression of pro-inflammatory cytokines. Significantly, treatment with SP provided notable protection against inflammation severity, reduced histopathological alterations, attenuated lipid peroxidation (MDA), and enhanced antioxidant enzyme activities (CAT, SOD, and GPX) along with non-enzymatic antioxidants (GSH and SH-G). Conclusions: Thus, the antioxidant effects and anti-inflammatory proprieties of SP could be attributed to its richness in amino acids, which could potentially mitigate inflammation severity in obese subjects suffering from ulcerative colitis. These results imply that SP hold promise as a therapeutic agent for managing of UC, particularly in individuals with concomitant obesity. Understanding SP's mechanisms of action may lead novel treatment strategies for inflammatory bowel diseases and hyperlipidemia in medical research.

Gene expression alterations of purinergic signaling components in obesity-associated intestinal low-grade inflammation in type 2 diabetes.

Intestinal low-grade inflammation induced by a high-fat diet has been found to detonate chronic systemic inflammation, which is a hallmark of obesity, and precede the apparition of insulin resistance, a key factor for developing type 2 diabetes (T2D). Aberrant purinergic signaling pathways have been implicated in the pathogenesis of inflammatory bowel disease and other gastrointestinal diseases. However, their role in the gut inflammation associated with obesity and T2D remains unexplored. C57BL/6 J mice were fed a cafeteria diet for 21 weeks and received one injection of streptozotocin in their sixth week into the diet. The gene expression profile of purinergic signaling components in colon tissue was assessed by RT-qPCR. Compared to control mice, the treated group had a significant reduction in colonic length and mucosal and muscular layer thickness accompanied by increased NF-κB and IL-1ß mRNA expression. Furthermore, colonic P2X2, P2X7, and A3R gene expression levels were lower, while the P2Y2, NT5E, and ADA expression levels increased. In conclusion, these data suggest that these purinergic signaling components possibly play a role in intestinal low-grade inflammation associated with obesity and T2D and thus could represent a novel therapeutic target for the treatment of the metabolic complications related to these diseases.

Sex-Dependent Metabolic Effects in Diet-Induced Obese Rats following Intermittent Fasting Compared with Continuous Food Restriction.

Recently, intermittent fasting has gained relevance as a strategy to lose weight and improve health as an alternative to continuous caloric restriction. However, the metabolic impact and the sex-related differences are not fully understood. The study aimed to compare the response to a continuous or intermittent caloric restriction in male and female rats following a previous induction of obesity through a cafeteria diet by assessing changes in body weight, energy intake, metabolic parameters, and gene expression in liver hepatic and adipose tissue. The continuous restriction reduced the energy available by 30% and the intermittent restriction consisted of a 75% energy reduction on two non-consecutive days per week. The interventions reduced body weight and body fat in both sexes, but the loss of WAT in females was more marked in both models of caloric restriction, continuous and intermittent. Both caloric restrictions improved insulin sensitivity, but more markedly in females, which showed a more pronounced decrease in HOMA-IR score and an upregulation of hepatic IRS2 and Sirt1 gene expression that was not observed in males. These findings suggest the fact that females are more sensitive than males to reduced caloric content in the diet.

Cannabidiol improves maternal obesity-induced behavioral, neuroinflammatory and neurochemical dysfunctions in the juvenile offspring.

Maternal obesity is associated with an increased risk of psychiatric disorders such as anxiety, depression, schizophrenia and autism spectrum disorder in the offspring. While numerous studies focus on preventive measures targeting the mothers, only a limited number provide practical approaches for addressing the damages once they are already established. We have recently demonstrated the interplay between maternal obesity and treatment with cannabidiol (CBD) on hypothalamic inflammation and metabolic disturbances, however, little is known about this relationship on behavioral manifestations and neurochemical imbalances in other brain regions. Therefore, here we tested whether CBD treatment could mitigate anxiety-like and social behavioral alterations, as well as neurochemical disruptions in both male and female offspring of obese dams. Female Wistar rats were fed a cafeteria diet for 12 weeks prior to mating, and during gestation and lactation. Offspring received CBD (50 mg/kg) from weaning for 3 weeks. Behavioral tests assessed anxiety-like manifestations and social behavior, while neuroinflammatory and neurochemical markers were evaluated in the prefrontal cortex (PFC) and hippocampus. CBD treatment attenuated maternal obesity-induced anxiety-like and social behavioral alterations, followed by rescuing effects on imbalanced neurotransmitter and endocannabinoid concentrations and altered expression of glial markers, CB1, oxytocin and dopamine receptors, with important differences between sexes. Overall, the findings of this study provide insight into the signaling pathways for the therapeutic benefits of CBD on neuroinflammation and neurochemical imbalances caused by perinatal maternal obesity in the PFC and the hippocampus, which translates into the behavioral manifestations, highlighting the sexual dimorphism encompassing both the transgenerational effect of obesity and the endocannabinoid system.

Changes in reward-induced neural activity upon Cafeteria Diet consumption.

Excessive consumption of highly palatable foods rich in sugar and fat, often referred to as "junk" or "fast" foods, plays a central role in the development of obesity. The highly palatable characteristics of these foods activate hedonic and motivational mechanisms to promote food-seeking behavior and overeating, which is largely regulated by the brain reward system. Excessive junk food consumption can alter the functioning of this reward system, but exact mechanisms of these changes are still largely unknown. This study investigated whether long-term junk food consumption, in the form of Cafeteria (CAF) diet, can alter the reward system in adult, female Long-Evans rats, and whether different regimes of CAF diet influence the extent of these changes. To this end, rats were exposed to a 6-week diet with either standard chow, or ad libitum daily access to CAF diet, 30 % restricted but daily access to CAF diet, or one-day-a-week (intermittent) ad libitum access to CAF diet, after which c-Fos expression in the Nucleus Accumbens (NAc), Prefrontal Cortex (PFC), and Ventral Tegmental Area (VTA) following consumption of a CAF reward of choice was examined. We found that all CAF diet regimes decreased c-Fos expression in the NAc-shell when presented with a CAF reward, while no changes in c-Fos expression upon the different diet regimes were found in the PFC, and possibly the VTA. Our data suggests that long-term junk food exposure can affect the brain reward system, resulting in an attenuated activity of the NAc-shell.

Pterostilbene alleviates cafeteria diet-induced obesity and underlying depression in adolescent male Swiss albino mice and affects insulin resistance, inflammation, HPA axis dysfunction and SIRT1 mediated leptin-ghrelin signaling.

Cafeteria diet (CD) model for in-vivo studies mimics the western diet having imbalanced nutritional value, high caloric-density and palatability. Uncontrolled eating leads to the development of childhood obesity, poor self-esteem and depression due to its effects on brain development. Herbal supplements are novel inclusion in the management of obesity and mental well-being. Pterostilbene (PTE) found in blueberries and Pterocarpus marsupium heartwood, is known to prevent obesity in invivo models. Adolescent Swiss albino male mice were fed on CD for 70 days and the development of obesity was assessed by gain in body weight, abdominal circumference. Forced swim and tail suspension test confirmed depression in CD fed mice. Obesity induced depressed (OID) mice were treated with PTE (10, 20, 40 mg/kg), standard antiobesity drug cetilistat (10 mg/kg), antidepressant fluoxetine (10 mg/kg) for 28 days. Post treatment, PTE-treated mice showed reduction in BW and depression-like behavior analysed using paradigms such as sucrose preference, open field, marble burying, and resident intruder test in comparison to the CD group. Insulin resistance, lipid profile, antioxidant enzyme, inflammatory cytokines (NF-κB, IL-6, TNF α) and cortisol levels were mitigated by PTE. It also restored normal cellular architecture of the brain and adipose tissue and increased the Silent mating type information regulation 2 homolog1 (SIRT1), leptin and ghrelin receptors gene expression in the brain. Thus, it can be concluded that PTE might have inhibited OID like behavior in mice via inhibition of IR, modulating neuroinflammation and hypothalamic-pituitary-adrenal axis dysfunction and upregulating SIRT1 mediated leptin-ghrelin signaling.

Lingual Taste Nerve Transection Alters Food Selection, Relative Macronutrient Intake, and Meal Patterns in Rats Consuming a Cafeteria Diet without Changing Total Energy Intake.

The control of ingestive behavior is complex and involves input from many different sources, including the gustatory system. Signals transmitted via the taste nerves trigger responses that promote or discourage ingestion. The lingual taste nerves innervate 70% of taste buds, yet their role in the control of food selection and intake remarkably remains relatively underinvestigated. Here we used our custom five-item Food Choice Monitor to compare postsurgical behavioral responses to chow and a five-choice cafeteria diet (CAF) between male rats that had sham surgery (SHAM) or histologically verified transection of the chorda tympani and glossopharyngeal nerves (2NX). Compared with SHAM rats, 2NX rats ate significantly more of the high-fat CAF foods. The altered food choices led to dramatically increased fat intake and substantially reduced carbohydrate intake by 2NX vs SHAM rats. Furthermore, whether offered chow or CAF, 2NX rats ate fewer, larger meals each day. Eating rates implied that, compared with SHAM, 2NX rats were equally motivated to consume CAF but less motivated to eat chow. Even with these differences, energy intake and weight gain trajectories remained similar between SHAM and 2NX rats. Although some rats experienced CAF before surgery, contrary to our expectations, the effects of prior CAF experience on postsurgical eating were minimal. In conclusion, although total energy intake was unaffected, our results clearly indicate that information from one or both lingual taste nerves has a critical role in food selection, regulation of macronutrient intake, and meal termination but not long-term energy balance.

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.

Consumption of a Taiwanese cafeteria diet induces metabolic disorders and fecal flora changes in obese rats.

OBJECTIVES: Among diet-induced obesity animal models, the cafeteria diet, which contains human junk food and processed foods, is a popular experimental animal diets in Western countries. Consumption of a cafeteria diet can lead to the development of obesity and non-alcoholic liver disease in as soon as 2 mo, which more accurately reflects human eating patterns. The aim of this study was to establish a Taiwanese cafeteria diet and compare it with a traditional lard-based, 60% high-fat diet in a 12-wk animal model. METHODS: Six-wk-old male Wistar rats were assigned to the following three groups: control diet (C; LabDiet 5001); high-fat diet (HFD; 60% HFD); and the Taiwanese cafeteria diet (CAF). RESULTS: At the end of the study, weight gain and steatosis were observed in the HF and CAF groups. Compared with the HFD group, rats in the CAF group showed significantly higher plasma triacylglycerol concentrations and insulin resistance, which may have been correlated with increased inflammatory responses. Significantly lower hepatic sterol regulatory element-binding protein-1c and insulin receptor substrate-1 protein expressions were observed in the CAF group compared with the HFD group. Additionally, disruption of the microbiotic composition followed by increased obesity-related bacteria was observed in the CAF group. CONCLUSIONS: The present study confirmed that the Taiwanese cafeteria diet-induced rat model provided a potential platform for investigating obesity-related diseases.

The Nature of Available Choices Affects the Intake and Meal Patterns of Rats Offered a Palatable Cafeteria-Style Diet.

Humans choose which foods they will eat from multiple options. The use of cafeteria-style diets with rodent models has increased our understanding of how a multichoice food environment affects eating and health. However, the wide variances in energy density, texture, and the content of micronutrients, fiber, and protein can be interpretatively problematic when human foodstuffs are used to create rodent cafeteria diets. We minimized these differences with a custom rodent cafeteria diet (ROD) that varied similarly to a previously used human-foods cafeteria diet (HUM) in fat and sugar content. Here, we used our custom Five-Item Food Choice Monitor to compare the intake and meal patterns of rats offered ROD and HUM in a crossover design. Compared with chow, rats consumed more calories, sugar, and fat and less protein and carbohydrate while on either of the choice diets (p < 0.05). While energy intake was similar between HUM and ROD, there were differences in the responses. Rats consumed more of the low-fat, low-sugar choice on the ROD compared with the nutritionally similar choice on the HUM leading to differences in fat and carbohydrate intake between the diets (p < 0.05). The stability of macronutrient intake while on either choice diet suggests macronutrient intake is determined by the available foods and is strongly regulated. Therefore, interpretative consideration must be given to the nature of food choices in the context of available options when interpreting cafeteria-diet intake.

Quinoa (Chenopodium quinoa Willd.) supplemented cafeteria diet ameliorates glucose intolerance in rats.

Quinoa (Chenopodium quinoa Willd.) is a pseudocereal with rich nutritional composition, gluten free, and organoleptic. The primary aim of this study was to elucidate the possible protective roles of quinoa in glucose homeostasis in a model of cafeteria diet-induced obesity. Male Wistar rats (3 weeks of age) were randomly allocated to be fed by; control chow (CON; n = 6), quinoa (QUI; n = 6), cafeteria (CAF; n = 6), or quinoa and cafeteria (CAFQ; n = 6) for 15 weeks. CAFQ resulted in decreased saturated fat, sugar, and sodium intake in comparison with CAF. Compared to CON, CAF increased body weight gain, plasma insulin, plasma glucose, decreased liver IRS-1, AMPK mRNA expressions, and pancreatic ß-cell insulin immunoreactivity, and developed hepatocyte degeneration and microvesicular steatosis. Compared to CAF, QUI lowered body weight, plasma glucose, and plasma insulin, increased liver IRS-1 and AMPK mRNA expressions, and pancreatic ß-cell insulin immunoreactivity. Compared to CAF, CAFQ lowered plasma glucose, increased liver IRS-1 mRNA expressions, increased pancreatic ß-cell insulin immunoreactivity, and lowered hepatocyte degeneration and microvesicular steatosis. Dietary treatments did not influence IRS-2, AKT2, and INSR mRNA expressions. HOMA-IR, HOMA-ß, and QUICKI were also similar between groups. Restoration of insulin in CAFQ islets was as well as that of CON and QUI groups. In conclusion, as a functional food, quinoa may be useful in the prevention of obesity and associated metabolic outcomes such as glucose intolerance, disrupted pancreatic ß-cell function, hepatic insulin resistance, and lipid accumulation.

The Hepatic Antioxidant System Damage Induced with the Cafeteria (CAF) Diet Is Largely Counteracted Using SCD Probiotics during Development of Male Wistar Rats.

The cafeteria (CAF) diet, reflective of predominant Western dietary behaviors, is implicated in hastening weight gain, subsequently resulting in health complications such as obesity, diabetes, and cancer. To this end, it is vital to notice the deleterious consequences of the CAF regimen prior to the onset of complications, which is fundamental for early intervention in the context of numerous diseases. Probiotic-derived postbiotic metabolites have gained attention for their antioxidative properties, offering a potential countermeasure against oxidative stress. This research sought to discern the protective efficacy of SCD Probiotics against liver glutathione system damage arising from the CAF diet during developmental phases. Male Wistar rats, from weaning on day 21 to day 56, were categorized into four groups: a control on a conventional diet; a group on a standard diet enriched with SCD Probiotics; a mixed-diet group comprising both CAF and standard feed; and a combination diet group supplemented with SCD Probiotics. Through the application of real-time PCR, enzyme activity assessments, and quantitative metabolite analyses, our findings highlight the CAF diet's adverse influence on the liver's antioxidant defenses via shifts in gene expression. Yet, the inclusion of SCD Probiotics mostly ameliorated these harmful effects. Remarkably, the positive regulatory influence of SCD Probiotics on the liver's antioxidant system was consistently observed, independent of the CAF diet's presence.

SCD Probiotics mitigate cafeteria diet-induced liver damage in Wistar rats during development.

BACKGROUND AND AIM: The liver plays a critical role in metabolic homeostasis, and its health is often compromised by poor dietary habits. This study aimed to investigate the therapeutic potential of SCD Probiotics in mitigating adverse liver effects induced by a cafeteria diet in male Wistar rats during their developmental period. METHODS: Four groups of seven male Wistar rats each were subjected to different dietary regimens from day 21 (weaning) to day 56. The groups were as follows: a control group on normal feed; a probiotic-supplemented group on normal feed; a group on a cafeteria diet mixed with normal feed; and a group on a cafeteria diet mixed with normal feed, supplemented with SCD Probiotics. Liver health was assessed using Fourier transform infrared spectroscopy and histopathological evaluations. RESULTS: Rats on the cafeteria diet exhibited significant disruptions in lipid, protein, cholesterol, triglyceride levels, and glycogen/phosphate content. Histopathological abnormalities such as lymphocytic infiltration, steatosis, and necrosis were also observed. However, SCD Probiotics supplementation led to notable improvements in the liver's biomolecular composition and mitigated histopathological abnormalities. Serum liver enzyme levels (AST, ALT, ALP, and LDH) also showed beneficial effects, while serum albumin levels remained stable. CONCLUSIONS: SCD Probiotics demonstrated a promising potential to counteract the adverse liver effects induced by a cafeteria diet in male Wistar rats. The study revealed significant improvements in biomolecular composition, histopathology, and serum enzyme levels. However, these findings are preliminary and necessitate further in vivo studies and clinical trials for validation.

Chromatographic Analyses of Spirulina (Arthrospira platensis) and Mechanism of Its Protective Effects against Experimental Obesity and Hepatic Steatosis in Rats.

Background and Objectives: Obesity is currently a major health problem due to fatty acid accumulation and excess intake of energy, which leads to an increase in oxidative stress, particularly in the liver. The main goal of this study is to evaluate the protective effects of spirulina (SP) against cafeteria diet (CD)-induced obesity, oxidative stress, and lipotoxicity in rats. Materials and Methods: The rats were divided into four groups and received daily treatments for eight weeks as follows: control group fed a standard diet (SD 360 g/d); cafeteria diet group (CD 360 g/d); spirulina group (SP 500 mg/kg); and CD + SP group (500 mg/kg, b.w., p.o.) according to body weight (b.w.) per oral (p.o.). Results: Our results show that treatment with a CD increased the weights of the body, liver, and abdominal fat. Additionally, severe hepatic alteration, disturbances in the metabolic parameters of serum, and lipotoxicity associated with oxidative stress in response to the CD-induced obesity were observed. However, SP treatment significantly reduced the liver alteration of CD feed and lipid profile disorder associated with obesity. Conclusions: Our findings suggest that spirulina has a marked potential therapeutic effect against obesity and mitigates disturbances in liver function parameters, histological alterations, and oxidative stress status.

Maternal cafeteria diet influences kisspeptin (Kiss1), kisspeptin receptor(Gpr54), and sirtuin (Sirt1) genes, hormonal and metabolic profiles, and reproductive functions in rat offspring in a sex-specific manner†.

Kisspeptin (KP, encoded by Kiss1, binding to the Gpr54 receptor) is a neuropeptide conveying information on the metabolic status to the hypothalamic-pituitary-gonadal axis. KP acts together with dynorphin A (encoded by Pdyn) and neurokinin B (encoded by Tac2) to regulate reproduction. KP is crucial for the onset of puberty and is under the control of sirtuin (encoded by Sirt1). We hypothesize that the maternal cafeteria (CAF) diet has adverse effects on the offspring's hormonal, metabolic, and reproductive functions due to sex-specific alterations in the expression of Kiss1, Gpr54, Pdyn, Tac2, and Sirt1 in the hypothalamus, and Kiss1, Gpr54, and Sirt1 in the liver. Rats were fed a CAF diet before pregnancy, during pregnancy, and during lactation. The vaginal opening was monitored. Offspring were sacrificed in three age points: PND 30, PND 35, and PND 60 (females) and PND 40, PND 45, and PND 60 (males). Their metabolic and hormonal status was assessed. mRNA for Kiss1, Gpr54, Pdyn, Tac2, and Sirt1 were measured by real-time PCR in the hypothalamus and/or livers. We found that CAF offspring had lower weight and altered body composition; increased cholesterol and triglyceride levels, sex-specific changes in glucose and insulin levels; sex-dependent changes in Sirt1/Kiss1 mRNA ratio in the hypothalamus; sex-specific alterations in Kiss1 and Sirt1 mRNA in the liver with more diversity in males; and a delayed puberty onset in females. We concluded that the mother's CAF diet leads to sex-specific alterations in metabolic and reproductive outcomes via Kiss1/Gpr54 and Sirt1 systems in offspring.

Rhythm and ROS: Hepatic Chronotherapeutic Features of Grape Seed Proanthocyanidin Extract Treatment in Cafeteria Diet-Fed Rats.

Polyphenols play a key role in the modulation of circadian rhythms, while the cafeteria diet (CAF) is able to perturb the hepatic biological rhythm and induce important ROS production. Consequently, we aimed to elucidate whether grape seed proanthocyanidin extract (GSPE) administration recovers the CAF-induced hepatic antioxidant (AOX) misalignment and characterize the chronotherapeutic properties of GSPE. For this purpose, Fischer 344 rats were fed a standard diet (STD) or a CAF and concomitantly treated with GSPE at two time-points (ZT0 vs. ZT12). Animals were euthanized every 6 h and the diurnal rhythms of hepatic ROS-related biomarkers, hepatic metabolites, and AOX gene expression were examined. Interestingly, GSPE treatment was able to recover the diurnal rhythm lost due to the CAF. Moreover, GSPE treatment also increased the acrophase of Sod1, as well as bringing the peak closer to that of the STD group. GSPE also corrected some hepatic metabolites altered by the CAF. Importantly, the differences observed at ZT0 vs. ZT12 due to the time of GSPE administration highlight a chronotherapeutic profile on the proanthocyanin effect. Finally, GSPE could also reduce diet-induced hepatic oxidative stress not only by its ROS-scavenging properties but also by retraining the circadian rhythm of AOX enzymes.

Corrigendum: Impact of short and long exposure to cafeteria diet on food intake and white adipose tissue lipolysis mediated by glucagon-like peptide 1 receptor.

[This corrects the article DOI: 10.3389/fendo.2023.1164047.].

Taurine supplementation reduces adiposity and hepatic lipid metabolic activity in adult offspring following maternal cafeteria diet.

Maternal taurine supplementation has been shown to exert protective effects following a maternal obesogenic diet on offspring growth and metabolism. However, the long-term effects of maternal cafeteria diet on adiposity, metabolic profile, and hepatic gene expression patterns following supplementation of taurine in adult offspring remains unclear. In this study, we hypothesized that exposure to maternal taurine supplementation would modulate the effects of maternal cafeteria diet by reducing adiposity and hepatic gene expression patterns involved in lipid metabolism in adult offspring. Female Wistar rats were fed a control diet, control diet supplemented with 1.5% taurine in drinking water, cafeteria diet (CAF) or CAF supplemented with taurine (CAFT) from weaning. After 8 weeks, all animals were mated and maintained on the same diets during pregnancy and lactation. After weaning, all offspring were fed with control chow diet until the age of 20 weeks. Despite similar body weights, CAFT offspring had significantly lower fat deposition and body fat when compared with CAF offspring. Microarray analysis revealed that genes (Akr1c3, Cyp7a1, Hsd17b6, Cd36, Acsm3, and Aldh1b1) related to steroid hormone biosynthesis, cholesterol metabolism, peroxisome proliferator-activated receptor signaling pathway, butanoate metabolism, and fatty acid degradation were down-regulated in CAFT offspring. The current study shows that exposure to maternal cafeteria diet promoted adiposity and taurine supplementation reduced lipid deposition and in both male and female offspring and led to alterations in hepatic gene expression patterns, reducing the detrimental effects of maternal cafeteria diet.

The cardioprotective effects of secoisolariciresinol diglucoside (flaxseed lignan) against cafeteria diet-induced cardiac fibrosis and vascular injury in rats: an insight into apelin/AMPK/FOXO3a signaling pathways.

Introduction: Fast food is a major risk factor for atherosclerosis, a leading cause of morbidity and mortality in the Western world. Apelin, the endogenous adipokine, can protect against cardiovascular disease via activating its receptor, APJ. Concurrently, secoisolariciresinol diglucoside (SDG), a flaxseed lignan extract (FLE), showed a therapeutic impact on atherosclerosis. The current study aimed to examine the effect of SDG on cafeteria diet (CAFD)-induced vascular injury and cardiac fibrosis via tracking the involvement of the apelin/APJ pathway. Methods: Thirty male rats were allocated into control, FLE-, CAFD-, CAFD/FLE-, and CAFD/FLE/F13A-treated rats, where F13A is an APJ blocker. All treatments lasted for 12 weeks. Results and discussion: The CAFD-induced cardiovascular injury was evidenced by histological distortions, dyslipidemia, elevated atherogenic indices, cardiac troponin I, collagen percentage, glycogen content, and apoptotic markers. CAFD increased both the gene and protein expression levels of cardiac APJ, apelin, and FOXO3a, in addition to increasing endothelin-1, VCAM1, and plasminogen activator inhibitor-1 serum levels and upregulating cardiac MMP-9 gene expression. Moreover, CAFD reduced serum paraoxonase 1 and nitric oxide levels, cardiac AMPK, and nuclear Nrf2 expression. FLE attenuated CAFD-induced cardiovascular injury. Such effect was reduced in rats receiving the APJ blocker, implicating the involvement of apelin/APJ in FLE protective mechanisms. Conclusion: FLE supplementation abrogated CAFD-induced cardiac injury and endothelial dysfunction in an apelin/APJ-dependent manner.