Obese Rats Research Articles

Potential benefit of Lactobacillus acidophilus supplementation to rats fed with a high-fat diet on serum lipid profile, kidney amyloid protein and tumor necrosis factor-alpha level

AimIt was aimed to determine the potential effect of Lactobacillus acidophilus supplementation on rats exposed to an experimental high-fat diet on serum lipid profile and kidney total beta amyloid protein (TBAP) and Tumor Necrosis Factor-alpha (TNF-α) levels. Methods24 male Sprague-Dawley rats were used in the study to establish 4 groups. Standard rat food (SD) was provided to Group 1 as the control; Group 2 was fed a high-fat diet (HFD); Group 3 consumed SD and received L. acidophilus probiotics; Group 4 was fed HFD and received L. acidophilus probiotics. Body weights were determined weekly during the 12-week trial period. At the end of the experiment, TBP and TNF-α levels in the serum and kidney tissue of the rats were measured by ELISA method. Serum total cholesterol (TC), triglyceride (TG), HDL, LDL, urea and creatinine levels and paraoxanase, amylase and lipase activities were determined by spectrophotometric method on the analyzer device. ResultsWhen the control (Group 1) group and Group 2 were compared at the end of the experiment, it was found that Group 2 had gained the most weight and that both the blood and kidney tissue levels of TNF-α and TBAP, as well as the quantities of TG, TK, LDL, and urea, were significantly greater (P<0.05). Serum HDL, PON and amylase levels were found to be significantly low (P>0.05). TG, TK, LDL, urea, and the levels of TNF-α and TBAP in serum and renal tissue were shown to be lower in the groups who received L. acidophilus probiotics (Groups 3, 4) when compared to Group 2 (P>0.05). It was observed that HDL, PON and amylase levels increased and approached the control group (P<0.05). ConclusionThe study's findings showed that probiotic supplementation improved blood levels of TG, TC, HDL, LDL, urea, PON, and amylase as well as serum and kidney tissue levels of TNF-α and TBAP in obese rats fed a high-fat diet.

Reoxygenation improves reduced hypothalamic leptin responsiveness induced by intermittent hypoxia in obese rats

To evaluate the effects of intermittent hypoxia-reoxygenation (IHR) on body weight, diet and water intake, circulating metabolites, and responses to central leptin injection in a rat model of diet-induced obesity (DIO). Rat models of DIO established by 12-week high-fat diet (HFD) feeding were randomized into normoxia group (n=15), intermittent hypoxia group (6% O2, 30 cycles/h, 8 h/day for 4 weeks; n=15), and IHR group (2 weeks of intermittent hypoxia followed by 2 weeks of reoxygenation; n=15). Body weight, diet and water intake of the rats were recorded, and circulating leptin, IL-6, and Ang-II levels were detected. After IHR treatment, the rats received intracerebroventricular injection of 4 μg leptin, and the hypothalamus and liver were taken 1 h later for detecting POMC, FRA-1 and FRA-2 expressions in the hypothalamus using immunohistochemistry, POMC, pSTAT3 and LepR expressions in the hypothalamus using Western blotting, and LepR mRNA expression in the hypothalamus and liver using RT-PCR. The rats in intermittent hypoxia group showed significantly increased weight gain, food intake and elevated systemic inflammatory cytokine levels. Intermittent hypoxia obviously inhibited the expression of POMC, lowered the expressions of FRA-1 and pSTAT3, reduced the responsiveness of the rats to exogenous leptin, and downregulated the mRNA and protein expression of LepR. Two weeks of reoxygenation treatment obviously reduced intermittent hypoxia-induced weight gain and metabolic disorder and improved leptin sensitivity of the rats. Prolonged intermittent hypoxia impairs hypothalamic leptin signaling by downregulating LepR expression to promote weight gain in obese rats, which can be improved by reoxygenation treatment.

Capsinoids Increase Antioxidative Enzyme Activity and Prevent Obesity-Induced Cardiac Injury without Positively Modulating Body Fat Accumulation and Cardiac Oxidative Biomarkers.

Capsinoids are potential antioxidant agents capable of reducing oxidative damage and the resulting complications triggered by obesity. Thus, this study aimed to investigate the effects of capsinoids on adiposity and biomarkers of cardiac oxidative stress in obese rats induced by a high-fat diet. Male Wistar rats were exposed to a high-fat diet for 27 consecutive weeks. After the characterization of obesity (week 19), some of the obese animals began to receive capsinoids (10 mg/kg/day) by orogastric gavage. Adiposity and comorbidities were assessed. In the heart, remodeling, injury, and biomarkers of oxidative stress were determined. The treatment did not reduce obesity-induced adiposity but was efficient in reducing cholesterol levels. Capsinoid treatment did not cause a difference in heart and LV mass, despite having reduced troponin I concentrations. Furthermore, capsinoids did not reduce the increase in the advanced oxidation of protein products and carbonylated proteins caused by obesity in cardiac tissue. In addition, obese rats treated with capsinoids presented high levels of malondialdehyde and greater antioxidant enzyme activity compared to untreated obese rats. In conclusion, treatment with capsinoids increases antioxidative enzyme activity and prevents obesity-induced cardiac injury without positively modulating body fat accumulation and cardiac oxidative biomarkers.

Sympathetic innervation of interscapular brown adipose tissue is not a predominant mediator of OT-elicited reductions of body weight gain and adiposity in male diet-induced obese rats.

Recent studies indicate that central administration of oxytocin (OT) reduces body weight (BW) in high fat diet-induced obese (DIO) rodents by reducing energy intake and increasing energy expenditure (EE). Previous studies in our lab have shown that administration of OT into the fourth ventricle (4V; hindbrain) elicits weight loss and stimulates interscapular brown adipose tissue temperature (TIBAT) in DIO rats. We hypothesized that OT-elicited stimulation of sympathetic nervous system (SNS) activation of IBAT contributes to its ability to activate BAT and reduce BW in DIO rats. To test this, we determined the effect of disrupting SNS activation of IBAT on OT-elicited stimulation of TIBAT and reduction of BW in DIO rats. We first confirmed that bilateral surgical SNS denervation to IBAT was successful based on having achieved ≥ 60% reduction in IBAT norepinephrine (NE) content from DIO rats. NE content was selectively reduced in IBAT by 94.7 ± 2.7, 96.8 ± 1.8 and 85.9 ± 6.1% (P<0.05) at 1, 6 and 7-weeks post-denervation, respectively, and was unchanged in liver or inguinal white adipose tissue. We then measured the impact of bilateral surgical SNS denervation to IBAT on the ability of acute 4V OT (1, 5 μg) to stimulate TIBAT in DIO rats. We found that the high dose of 4V OT (5 μg) stimulated TIBAT similarly between sham and denervated rats (P=NS) and that the effects of 4V OT to stimulate TIBAT did not require beta-3 adrenergic receptor signaling. We subsequently measured the effect of bilateral surgical denervation of IBAT on the effect of chronic 4V OT (16 nmol/day) or vehicle infusion to reduce BW, adiposity and energy intake in DIO rats. Chronic 4V OT reduced BW gain by -7.2 ± 9.6 g and -14.1 ± 8.8 g in sham and denervated rats (P<0.05 vs vehicle treatment), respectively, and this effect was similar between groups (P=NS). These effects were associated with reductions in adiposity and energy intake (P<0.05). Collectively, these findings support the hypothesis that sympathetic innervation of IBAT is not required for central OT to increase BAT thermogenesis and reduce BW gain and adiposity in male DIO rats.

The adipose tissue melanocortin 3 receptor is targeted by ghrelin and leptin and may be a therapeutic target in obesity

ObjectiveObesity is linked to perturbations in energy balance mechanisms, including ghrelin and leptin actions at the hypothalamic circuitry of neuropeptide Y (NPY) and melanocortin. However, information about the regulation of this system in the periphery is still scarce. Our objective was to study the regulation of the NPY/melanocortin system in the adipose tissue (AT) and evaluate its therapeutic potential for obesity and type 2 diabetes. MethodsThe expression of the NPY/melanocortin receptors’ levels was assessed in the visceral AT of individuals with obesity and altered metabolism. Protein levels of these receptors were evaluated in cultured adipocytes incubated with ghrelin (30 and 100 ng/mL) and leptin (1 and 10 nM) and in the AT of an animal model with a mutation in the leptin receptor (ZSF1 rat), to understand their regulation by leptin and ghrelin. The vertical sleeve gastrectomy animal model was used to evaluate the putative therapeutic potential of the NPY/melanocortin system. ResultsIn this study, we unravelled that leptin (1 nM and 10 nM) selectively reduced the levels of NPY5R and MC3R but no other NPYR/MCRs in cultured adipocytes. In turn, acylated ghrelin (100 ng/mL) significantly increased NPY1R, but the inhibition of its receptor also abrogates MC3R levels. However, in the Lepr-deficient ZSF1 rat, both NPY5R and MC3R levels were reduced, along with other NPYRs and MCRs, suggesting that leptin resistance negatively affects NPY and melanocortin signalling. In human adipose tissue, we found a downregulation of genes encoding the NPY and melanocortin receptors in the visceral AT of individuals with obesity and insulin resistance, being correlated with genes regulating metabolic activity. Additionally, diabetic obese rats submitted to vertical sleeve gastrectomy showed increased levels of NPY, melanocortin, ghrelin, and leptin receptors in the AT, including MC3R, suggesting it may constitute a therapeutic target in obesity. ConclusionsOur results suggest that the AT NPY/melanocortin system, particularly the MC3R, may be involved in the neuroendocrine regulation of adipocyte metabolism. Altogether, our work shows MC3R is under the control of the ghrelin/leptin duo, is reduced in patients with obesity and prediabetes, and may constitute a therapeutic target in obesity.

Therapeutic effects of alpha lipoic acid and/or caffeine-loaded chitosan nanoparticles on memory impairment and neurochemical changes in high-fat diet-induced obese rats

The therapeutic effects of alpha lipoic acid (LA) and/or caffeine-loaded chitosan nanoparticles (CCNPs) on obesity-induced memory impairment were evaluated in the present study. Rats were divided into control rats, obese rats induced by high fat diet (HFD) and obese rats treated with LA and/or CCNPs. Obesity was confirmed by measuring the body mass index (BMI). Memory and cognitive functions were evaluated by novel object recognition test (NORT). The levels of serotonin (5-HT), dopamine (DA), norepinephrine (NE), lipid peroxidation (MDA), nitric oxide (NO), reduced glutathione (GSH), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), leptin (LEP) and ghrelin (GHR) and the activities of monoamine oxidase (MAO), acetylcholinesterase (AchE) and Na+,K+,ATPase were determined in the cortex and hippocampus. The cerebral histopathological alterations were examined in obese rats.Obese rats showed impaired memory and exhibited significant neurochemical changes, including decreased levels of 5-HT, DA, GSH, GHR, and Na+,K+-ATPase activity, as well as an increase in AchE, MAO, MDA, NO, IL-1β, TNF-α, and LEP. LA and/or CCNPs treatment reduced BMI and improved memory. LA or CCNPs alleviated the cortical and hippocampal neurochemical changes and histopathological changes induced by obesity. Furthermore, LA and CCNPs exhibited antioxidant and anti-inflammatory properties, which likely contributed to their effects. However, no synergistic effect was observed between LA and CCNPs. These findings suggest that LA or CCNPs may be a potential therapy against obesity and its adverse effects on memory, mediated by their ability to restore monoamine levels and exhibit antioxidant and anti-inflammatory properties.

Combined Aerobic Exercise Training and Chlorella Intake Reduces Arterial Stiffness through Enhanced Arterial Nitric Oxide Production in Obese Rats.

This study aimed to assess the effect of a combination of aerobic exercise training (ET) and Chlorella (CH) intake on arterial nitric oxide (NO) production and arterial stiffness in obese rats. Twenty-week-old obese male rats were randomly grouped into four (n = 6): OBESE-SED (sedentary control), OBESE-ET (treadmill 25 m/min, 1 h, 5 d/week), OBESE-CH (0.5% Chlorella powder in normal diet), and OBESE-ET+CH (combination of ET and CH intake) groups. The carotid-femoral pulse wave velocity (cfPWV), an index of arterial stiffness, was significantly lesser in the OBESE-ET, OBESE-CH, and OBESE-ET+CH groups than in the OBESE-SED group, and in the OBESE-ET+CH group significantly further enhanced these effects compared with the OBESE-ET and OBESE-CH groups. Additionally, arterial nitrate/nitrite (NOx) levels were significantly greater in the OBESE-ET, OBESE-CH, and OBESE-ET+CH groups than in the OBESE-SED group, and the OBESE-ET+CH group compared with the OBESE-ET and OBESE-CH groups. Furthermore, arterial NOx levels were positively correlated with arterial endothelial NO synthase phosphorylation levels (r = 0.489, p < 0.05) and negatively correlated with cfPWV (r = -0.568, p < 0.05). In conclusion, a combination of ET and CH intake may reduce arterial stiffness via an enhancement of the arterial NO signaling pathway in obese rats.

Effects of Kimchi Intake on the Gut Microbiota and Metabolite Profiles of High-Fat-Induced Obese Rats.

With rising global obesity rates, the demand for effective dietary strategies for obesity management has intensified. This study evaluated the potential of kimchi with various probiotics and bioactive compounds as a dietary intervention for high-fat diet (HFD)-induced obesity in rats. Through a comprehensive analysis incorporating global and targeted metabolomics, gut microbiota profiling, and biochemical markers, we investigated the effects of the 12-week kimchi intake on HFD-induced obesity. Kimchi intake modestly mitigated HFD-induced weight gain and remarkably altered gut microbiota composition, steroid hormones, bile acids, and metabolic profiles, but did not reduce adipose tissue accumulation. It also caused significant shifts in metabolomic pathways, including steroid hormone metabolism, and we found substantial interactions between dietary interventions and gut microbiota composition. Although more research is required to fully understand the anti-obesity effects of kimchi, our findings support the beneficial role of kimchi in managing obesity and related metabolic disorders.

Protective Role of Ovothiol-A against Muscle and Kidney Injuries in Obese Rats

Background: Obesity is a serious chronic metabolic disease impairing health damaging many organs such as kidneys and muscles. Ovothiol-A (Ovo-A) has been found to keep the redox balance normal in sea urchins indicating its antioxidant characteristics. Aim: This study aims to investigate the protective effects of Ovo-A on kidneys and muscles in obese rats. objective: Investigation of the protective effect of Ovo-A on kidneys and muscles in obese rats. Methods: In-silco studies were performed on lactate dehydrogenase (LDH) and creatine kinase (CK) with Ovo-A to compute their binding affinities. Obesity was induced by high-fat diet (HFD) for 4 weeks. Wistar rats were used in this study as 6 rats per group as control, HFD, Ovo-A (200 and 400 mg/Kg, p.o) groups. Results: Docking results have revealed that Ovo-A has affinities to bind to LDH (-8.5 kcal/mol) and CK (-17.7 kcal/mol). Ovo-A reduced the levels of uric acid, urea, creatinine, LDH, CK, malondialdehyde (MDA), and nitric oxide (NO), while increasing the levels of glutathione (GSH), catalase (CAT), and glutathione-S-transferase (GST). Histopathological investigations have revealed that Ovo-A restored the renal and muscular structure. Conclusion: The current study showed that Ovo-A has a protective effect on kidneys and muscles in obese rats. Ovo-A enhances renal and muscular functions by inhibiting LDH and CK activities and improving the antioxidant system. Ovo-A is more effective in the high dose.

Inhibition of 5-alpha reductase attenuates cardiac oxidative damage in obese and aging male rats via the enhancement of antioxidants and the p53 protein suppression

In aging and metabolic syndrome oxidative stress is a causative factor in the cardiovascular pathology. Upregulation of 5-⍺ reductase is associated with cardiac hypertrophy but how inhibition of 5-⍺ reductase affects cardiometabolic function during oxidative damage under those conditions is unclear. Our hypothesis was that Finasteride (Fin), a 5-⍺ reductase inhibitor, promotes an antioxidant response, leading to an improvement in cardiac function in obese and aging rats. Male rats were divided into 3 groups including normal diet (ND) fed rats, ND-fed rats treated with d-galactose (D-gal) to induce aging, and high-fat diet (HFD) fed rats to induce obesity. Rats received their assigned diet or D-gal for 18 weeks. At week 13, rats in each group were divided into 2 subgroups and received either a vehicle or Fin (5 mg/kg/day, oral gavage). Cardiometabolic and molecular parameters were subsequently investigated. Both D-gal and HFD successfully induced cardiometabolic dysfunction, oxidative stress, mitochondrial dysfunction, and DNA fragmentation. Fin treatment did not affect metabolic disturbances; however, it reduced cardiac sympathovagal imbalance, cardiac dysfunction through the inhibition of oxidative stress and promoted antioxidants, resulting in reduced p53 protein levels and DNA fragmentation. Surprisingly, Fin induced insulin resistance in ND-fed rats. Fin effectively improved cardiac function in both models by enhancing antioxidant levels, suppressing oxidative stress and DNA fragmentation. However, Fin treatment did not confer any beneficial effects on metabolic status. Fin administration effectively improved cardiac sympathovagal balance and cardiac function in rats with oxidative damage induced by either D-gal or HFD.

The effects of brown rice as functional food on Lee Index, adipose tissues and PRDM16 levels in obesity model &lt;i&gt;Rattus norvegicus&lt;/i&gt;

Brown rice is a functional food known to improve the Lee Index, influencing PRDM16 levels in obesity conditions. Therefore, this study aims to determine the differences in Lee Index, Brown Adipose Tissue (BAT) weight, White Adipose Tissue (WAT) weight, BeAT weight, total body fat, and PRDM16 levels of obese model rats with the intervention of brown and white rice, as well as ℽ-oryzanol. A true experimental method was used with a post-test-only control group in vivo design. The obesity model was constructed with male Sprague Dawley rats (Rattus norvegicus), divided into five diet groups namely standard and HFHF diet control, as well as HFHF + brown rice, HFHF + white rice, and HFHF + ℽ-oryzanol combination diet. The experiment was carried out for 26 weeks, with details of 14 weeks to form an obese model and 12 weeks for the intervention. Before statistical correlation was tested, Lee index values, adipose tissues, and PRDM16 were analyzed. The anthropometric data collection method was carried out by weighing before and after the intervention, while adipose tissue was collected by weighing after sacrifice. The immunofluorescence method was used to collect the expression of PRDM16 and the mean of PRDM16 levels was analyzed in the ImageJ application. After the data collection process, analysis was performed using SPSS to determine possible differences in each group. Normally distributed data were analyzed using One-Way ANOVA, while those without normal distribution were assessed using the Kruskall-Walis method and the Mann Whitney-U advanced test, with a p-value of &lt;0.05 considered significantly different.The result showed that there were differences among several groups regarding total body fat (p=0.012), WAT (p=0.026), and BAT (p=0.025). However, no differences were found between all groups regarding the Lee index (p=0.275), BeAT (p=0.079), and PRDM16 level (p=0.292). In conclusion, brown rice intervention did not significantly affect Lee index values, the expression of PRDM16, and adipose tissue weights at the end of the intervention.

Корекція пробіотиком пародонтального синдрому у тварин за умов ожиріння і хронічного стресу

The aim of this study was to investigate the effect of obesity and chronic stress on periodontal tissues, both separately and in the combined comorbidity of these conditions in rats, and the role of the probiotic Lactobacillus casei in the correction of periodontal syndrome under these conditions. Methods. The development of periodontal syndrome and the effectiveness of the probiotic Lactobacillus casei IMV B-7280, administered to rats from one month of age intragastrically in a volume of 1 mL (5 · 108 CFU) in two-week courses with breaks of 2 weeks, were studied in a model of glutamate-induced obesity and chronic stress - in combination and separately. In periodontal tissues, the total proteolytic and antitryptic activity, free fucose and glycosaminoglycans (GAG) content, catalase activity, thiobarbiturate active products (TBA reagents), and the content of oxidatively modified proteins (OMP) and molecules of average mass (AMM) were determined; in bone tissue, the molar root exposure coefficient was calculated. The anthropometric parameters of the animals and the Selye triad were studied. Results. We have substantiated the development of periodontal syndrome in animals with glutamate-induced obesity against the background of chronic stress, as evidenced by the activation of free radical oxidation of lipids and proteins, depolymerization of fucoproteins and proteoglycans of periodontal connective tissue, which causes exposure of molar roots by almost 65%. The administration of the probiotic Lactobacillus casei in two-week courses with intervals of 2 weeks to obese rats with chronic stress prevented the development of obesity, as evidenced by a significant decrease in visceral fat mass, Li index, and BMI, as well as the severity of stress syndrome, as evidenced by a decrease in ulcer formation, thymus involution, and adrenal hypertrophy. The periodontoprotective effect of Lactobacillus casei under the combined influence of obesity and chronic stress was proved by significant changes in oxidative stress, free fucose, and GAG content and a 1.5-times decrease in the molar root exposure ratio. Conclusions. Periodic administration of Lactobacillus casei to rats treated with sodium glutamate in the neonatal period against the background of chronic stress prevented the development of obesity, the severity of stress syndromeб and damage to periodontal tissues, as evidenced by the prevention of oxidative stress, increased catabolism of extracellular connective tissue proteins and antiresorptive effect.

Abstract MP32: Megalin and lysosomal disruption in the kidney epithelial cells of high salt diet fed rats: protective role of angiotensin II type 2 receptor

Earlier we have reported that 2-days high salt diet (HSD) feeding caused proteinuria in obese rats and the AT 2 R agonist treatment prevented proteinuria. Since HSD feeding for 2 days and the AT 2 R activation did not affect blood pressure, GFR, glomerular structure, and inflammation, the mechanism responsible for proteinuria remains unknown. Megalin is a proximal tubule epithelial cells endocytic receptor responsible for filtered protein reabsorption. The absorbed proteins are directed to lysosomes for degradation. Lysosomes is a nutrient sensing subcellular compartment and a critical part of the endocytic machinery and cellular trafficking. We hypothesized that high salt intake caused lysosomal stress, which negatively impacted megalin-protein cellular trafficking and thus caused proteinuria. Therefore, we evaluated the markers of lysosomal stress and megalin expression in the proximal tubules of HSD fed obese Zucker rats. Urinary excretion of N-acetyl-glucosaminidase (NAG), which is a marker of lysosomal injury and oxidative stress, was significantly increased in HSD fed rats compared with normal salt diet (NSD: 16.6 vs HSD: 40.5 RFU/hr/µg Cr). This increase was associated with an increase in another oxidative stress marker H 2 O 2 in the urine (NSD: 0.37 vs HSD: 1.72 ΔRFU/min). Confocal analysis revealed that megalin was localized in the lysosomes in HSD fed rats, as megalin was co-localized with the lysosomal marker LAMP-1 in the proximal tubules. Moreover, in HSD fed rats there was a remarkable increase (2-fold) in the lysosomal size (fig) and number per tubule (NSD: 18 vs HSD: 48). The AT 2 R agonist C21 (0.3 mg/Kg/day, i.p.) treatment of HSD-fed rats restored surface megalin expression, reduced urinary NAG and H 2 O 2 and the lysosomal number and size. Our in vitro studies performed in OK cells (proximal tubule epithelial cells) treated with high NaCl (100 mM) without/with the AT 2 R agonist C21 (1µM) also revealed that compared to NSD, high NaCl reduced megalin surface expression and C21 treatment prevented it. We conclude that high salt intake causes lysosomal stress. Particularly, large lysosomal size potentially is affecting endocytic machinery, including impairing megalin-protein dissociation and megalin recycling, thus causing proteinuria.

Study the Potential Effect of Dietary Intervention with Strawberry and Cauliflower Leaves on Oxidative Stress, Inflammation, Insulin Resistance and Histological Alterations in Diet-Induced Obese Rat

Study the Potential Effect of Dietary Intervention with Strawberry and Cauliflower Leaves on Oxidative Stress, Inflammation, Insulin Resistance and Histological Alterations in Diet-Induced Obese Rat

The Effects of 1-Kestose on the Abundance of Inflammation-Related Gene mRNA in Adipose Tissue and the Gut Microbiota Composition in Rats Fed a High-Fat Diet.

Chronic inflammation in adipose tissue is thought to contribute to insulin resistance, which involves the gut microbiota. Our previous studies have demonstrated that ingestion of 1-kestose can alter the gut microbiota composition, increase cecal butyrate levels, and improve insulin resistance in Otsuka Long-Evans Tokushima Fatty (OLETF) rats. Additionally, we found that 1-kestose supplementation ameliorated insulin resistance in obese rat models fed a high-fat diet (HFD), although the effects of 1-kestose on the abundance of inflammation-related gene in adipose tissue and gut microbiota composition in these rats were not explored. This study aimed to investigate the impact of 1-kestose on these parameters in HFD-fed rats, compared to OLETF rats. Male Sprague-Dawley rats were divided into two dietary groups, control or HFD, for 19 wk. Each group was further subdivided to receive either tap water or tap water supplemented with 2% (w/v) 1-kestose throughout the study. We evaluated gene expression in adipose tissue, as well as short-chain fatty acids (SCFAs) levels and microbial composition in the cecum contents. 1-Kestose intake restored the increased relative abundance of tumor necrosis factor (Tnf) mRNA in adipose tissue and the reduced level of butyrate in the cecum contents of HFD-fed rats to those observed in control diet-fed rats. Additionally, 1-kestose consumption changed the composition of the gut microbiota, increasing Butyricicoccus spp., decreasing UGC-005 and Streptococcus spp., in the cecum contents of HFD-fed rats. Our findings suggest that 1-kestose supplementation reduces adipose tissue inflammation and increases butyrate levels in the gut of HFD-fed rats, associated with changes in the gut microbiota composition, distinct from those seen in OLETF rats.

Effects of semaglutide, peptide YY3-36 and empagliflozin on metabolic dysfunctionsassociated fatty steatotic liver disease in diet-induced obese rats with chronic nitric oxide synthase-inhibition

Effects of semaglutide, peptide YY3-36 and empagliflozin on metabolic dysfunctionsassociated fatty steatotic liver disease in diet-induced obese rats with chronic nitric oxide synthase-inhibition

Mitigating Cold Ischemic Injury: HTK, UW and IGL-2 Solution's Role in Enhancing Antioxidant Defence and Reducing Inflammation in Steatotic Livers.

Liver transplantation remains the only definitive treatment for end-stage liver diseases. However, the increasing prevalence of fatty liver disease among potential donors exacerbates the shortage of suitable organs. This study evaluates the efficacy of the preservation solution Institut Georges Lopez-2 (IGL-2) compared to Histidine-Tryptophan-Ketoglutarate (HTK) and University of Wisconsin (UW) preservation solutions in mitigating ischemia-reperfusion injury (IRI) in steatotic livers. Using Zucker Obese rat livers, we assessed the impact of 24-h static cold storage (SCS) with each solution on transaminase release, glutathione redox balance, antioxidant enzyme activity, lipoperoxidation, and inflammation markers. IGL-2 and UW solutions demonstrated reduced transaminase and lactate levels compared to HTK, indicating better preservation of liver integrity. IGL-2 maintained a higher reduced glutathione/oxidized glutathione (GSH/GSSG) ratio, suggesting more effective management of oxidative stress. Antioxidant enzyme activities catalase, superoxide dismutase, and glutathione peroxidase (CAT, SOD, GPX) were higher in IGL-2 preserved livers, contributing to decreased oxidative damage. Lipid peroxidation markers and inflammatory markers were lower in IGL-2 than in HTK, indicating reduced oxidative stress and inflammation. Additionally, improved mitochondrial function was observed in the IGL-2 group, correlating with reduced reactive oxygen species (ROS) production and lipid peroxidation. These findings suggest that IGL-2 offers superior preservation of liver viability, reduces oxidative stress, and minimizes inflammation compared to HTK and UW solutions. By maintaining a higher ratio of reduced glutathione and antioxidant enzyme activity, IGL-2 effectively mitigates the harmful effects of ischemia-reperfusion injury. The reduced lipid peroxidation and inflammation in the IGL-2 group further underscore its potential in improving liver transplant outcomes. These results highlight the importance of optimizing preservation solutions to enhance the viability and functionality of donor organs, potentially expanding the donor pool and improving the success rates of liver transplantation. Future research should focus on refining preservation techniques and exploring additional protective agents to further improve organ preservation and transplant outcomes.

Whole tomato lipidic extract improved sperm quality in obese rats induced by a high-carbohydrate diet.

Obesity represents a risk in the development of metabolic and oxidative stress (OS), as well as in male infertility. There is still no pharmacological treatment for obesity-induced male infertility, but the use of natural antioxidants has been proposed as a treatment. The aim of this work is to evaluate the effect of a whole tomato lipid extract on rats that decreased their fertility and spermatogenesis after being induced obese with a high carbohydrate diet. One hundred fourteen male Wistar rats of 12weeks of age were used. Two groups were randomly formed non-obese control group (C, n=54) and obese group (Ob, n=54) that received 30% w/v sucrose solution for 3 months. Subsequently, the C and Ob group were divided into two groups: vehicle (C-Vh and Ob-Vh) that received corn oil as vehicle and tomato lipid extract (C-Ex and Ob-Ex) that received whole tomato lipid extract. The groups that received a hypercaloric diet had a gain in visceral and retroperitoneal adipose tissue, an increase in total cholesterol and triglyceride levels, increased OS in the testis, and lesions in testicular histology, as well as a reduction in testicular size and sperm quality parameters (motility, viability, and concentration). Treatment with whole tomato lipid extract significantly decreased the weight of gonadal adipose tissue and OS, maintained testicular size, showed a significant increase in sperm quality parameters and improved histology of seminiferous tubules. These results demonstrate a greater therapeutic and beneficial effect of the tomato lipid extract on sperm quality parameters in obese rats and therefore on fertility.

Paternal high-fat diet affects weight and DNA methylation of their offspring

Obesity poses a public health threat, reaching epidemic proportions. Our hypothesis suggests that some of this epidemic stems from its transmission across generations via paternal epigenetic mechanisms. To investigate this possibility, we focused on examining the paternal transmission of CpG methylation. First-generation male Wistar rats were fed either a high-fat diet (HF) or chow and were mated with females fed chow. We collected sperm from these males. The resulting offspring were raised on a chow diet until day 35, after which they underwent a dietary challenge. Diet-induced obese (DIO) male rats passed on the obesogenic trait to both male and female offspring. We observed significant hypermethylation of the Pomc promoter in the sperm of HF-treated males and in the hypothalamic arcuate nucleus (Arc) of their offspring at weaning. However, these differences in Arc methylation decreased later in life. This hypermethylation is correlated with increased expression of DNMT3B. Further investigating genes in the Arc that might be involved in obesogenic transgenerational transmission, using reduced representation bisulfite sequencing (RRBS) we identified 77 differentially methylated regions (DMRs), highlighting pathways associated with neuronal development. These findings support paternal CpG methylation as a mechanism for transmitting obesogenic traits across generations.

The potency of Thymus vulgaris seed extract in alleviating obesity complications and iron overload in obese rats

Natural products have long been recognized as valuable sources of bioactive compounds in therapeutic agents. Thymus vulgaris, commonly known as thyme and belonging to the Lamiaceae family, is widely distributed and extensively used in Egyptian folk medicine for its antibroncholitic, antispasmodic, carminative, and diuretic properties. However, there is a lack of research on the effects of T. vulgaris seed extract in mitigating obesity-induced iron overload in rats. Given its potent bioactive constituents, this study aimed to investigate the impact of T. vulgaris seed extract on iron overload associated with obesity by evaluating lipid profiles, iron status parameters—including plasma ferritin, total iron-binding capacity (TIBC), plasma transferrin, transferrin saturation percentage (TS%), and hepcidin gene expression in adipose tissue. About 30 flavonoids were identified in T. vulgaris seed extract using LC-MS. Among these, methoxyflavonoids were the most abundant metabolites. The administration of T. vulgaris seed extract to obese rats resulted in significant reductions in anthropometric features, hepcidin gene expression, cholesterol, triglycerides, low-density lipoprotein (LDL), TIBC, plasma ferritin, leptin, and iron and copper content in adipose tissue. Moreover, treatment with T. vulgaris extract led to a notable decrease in interleukin-6 (IL-6) levels (76.33 ± 4.31 ng/L and 40.83 ± 1.82 ng/L for low and high doses, respectively) compared to the obese control group (110.83 ± 5.82 ng/L). Conversely, plasma adiponectin levels were significantly increased with T. vulgaris supplementation (123.6 ± 7.9 µg/L and 217.4 ± 6.1 µg/L for low and high doses, respectively) compared to the obese group (54.6 ± 4.9 µg/L). Additionally, adipose tissue zinc levels were significantly elevated in response to T. vulgaris supplementation (2.54 ± 0.20 µg/g and 3.75 ± 0.14 µg/g for low and high doses, respectively) compared to the obese group (1.45 ± 0.23 µg/g). Our findings suggest that T. vulgaris could be a promising novel therapeutic agent for managing obesity-induced iron overload.