Search Results (356)

Callistemon citrinus has shown antioxidant and anti-inflammatory properties in certain tissues. However, its impact on the brain remains unproven. This study investigates the effect of C. citrinus extract and phytosomes on the oxidative status of the brains of rats fed a high-fat–fructose diet (HFD). Fifty-four male Wistar rats were randomly divided into nine groups (n = 6). Groups 1, 2, and 3 received a standard chow diet; Group 2 also received the vehicle, and Group 3 was supplemented with C. citrinus extract (200 mg/kg). Groups 4, 5, 6, 7, 8, and 9 received a high-fat diet (HFD). Additionally, groups 5, 6, 7, 8, and 9 were supplemented with orlistat at 5 mg/kg, C. citrinus extract at 200 mg/kg, and phytosomes loaded with C. citrinus at doses of 50, 100, and 200 mg/kg, respectively. Administration was oral for 16 weeks. Antioxidant enzymes, biomarkers of oxidative stress, and fatty acid content in the brain were determined. A parallel artificial membrane permeability assay (PAMPA) was employed to identify compounds that can cross the intestinal and blood–brain barriers. The HFD group (group 4) increased body weight and adipose tissue, unlike the other groups. The brain fatty acid profile showed slight variations in all of the groups. On the other hand, group 4 showed a decrease in the activities of antioxidant enzymes SOD, CAT, and PON. It reduced GSH level, while increasing GPx activity as well as MDA, 4-HNE, and AOPP levels. C. citrinus extract and phytosomes restore the antioxidant enzyme activities and mitigate oxidative stress in the brain. C. citrinus modulates oxidative stress in brain tissue through 1.8-cineole and α-terpineol, which possess antioxidant and anti-inflammatory properties. Full article

Understanding the components of the diet, food groups, and nutritional strategies that help prevent MASLD (Metabolic Dysfunction-Associated Steatotic Liver Disease) is essential for identifying dietary behaviors that can stop the progression of this condition, which currently affects over one-quarter of the global population. This review highlights the importance of including antioxidant nutrients in the diet, such as vitamins C and E, CoQ10, and polyphenolic compounds. It also emphasizes substances that support lipid metabolism, including choline, alpha-lipoic acid, and berberine. Among food groups, it is crucial to choose those that help prevent metabolic disturbances. Among carbohydrate-rich foods, vegetables, fruits, and high-fiber products are recommended. For protein sources, eggs, fish, and white meat are preferred. Among fat sources, plant oils and fatty fish are advised due to their content of omega-3 and omega-6 fatty acids. Various dietary strategies aimed at preventing MASLD should include elements of the Mediterranean diet or be personalized to provide anti-inflammatory compounds and substances that inhibit fat accumulation in liver cells. Other recommended dietary models include the DASH diet, the flexitarian diet, intermittent fasting, and diets that limit fructose and simple sugars. Additionally, supplementing the diet with spirulina or chlorella, berberine, probiotics, or omega-3 fatty acids, as well as drinking several cups of coffee per day, may be beneficial. Full article

Hypertension is an important risk factor for cardiovascular diseases. High salt intake when consumed with excess fructose enhances hypertension and resultant cardiovascular disease. Usually, the small intestine absorbs dietary fructose, and the proximal tubule of kidney reabsorbs filtered fructose into the circulation with the help of different transporters including SGLT4 and SGLT5. Very recently, SGLT5 mRNA has also been found to be expressed in the heart. High-fructose diet stimulates the sympathetic nervous system and renin–angiotensin–aldosterone (RAAS) activity, of which both are responsible for endothelial dysfunction and are associated with salt-sensitive hypertension. Few studies exist regarding the effects of SGLT4 and SGLT5 on cardiovascular function and blood pressure. However, SGLT4 gene knockout does not alter fructose-associated impact on blood pressure. In contrast, blood pressure does not increase in SGLT5 knockout rats even during fructose consumption. Given that limiting fructose and salt consumption as a public health strategy has proven challenging, we hope that studies into SGLT4 and SGLT5 transporters will open new research initiatives to address salt-sensitive hypertension and cardiovascular disease. This review highlights current information about SGLT4 and SGLT5 on fructose absorption, salt-sensitive hypertension, cardiovascular disease and points the way for the development of therapeutic fructose inhibitors that limit adverse effects. Full article

Retinal degeneration is associated with dietary factors and environmental light exposure. This study investigated the effects of a high-fructose high-fat (HFHF) diet on susceptibility to blue light (BL)-induced retinal damage. Male ICR mice were randomized into three groups: control, BL alone, and BL plus HFHF diet (BL + HFHF). The BL + HFHF group consumed the HFHF diet for 40 weeks, followed by 8 weeks of low-intensity BL exposure (465 nm, 37.7 lux, 0.8 μW/cm²) for 6 h daily. The BL group underwent the same BL exposure while kept on a standard diet. Histopathological analysis showed that, under BL exposure, the HFHF diet significantly reduced the number of photoreceptor nuclei and the thickness of the outer nuclear layer and inner/outer segments compared to the BL group (p < 0.05). While BL exposure alone caused oxidative DNA damage, rhodopsin loss, and Müller cell activation, the combination with an HFHF diet significantly amplified the oxidative DNA damage and Müller cell activation. Moreover, the HFHF diet increased blood–retinal barrier permeability and triggered apoptosis under BL exposure. Mechanistically, the BL + HFHF group exhibited increased retinal advanced glycated end product (AGE) deposition, accompanied by the activation of the receptor for AGE (RAGE), NFκB, and the NLRP3 inflammasome-dependent IL-1β pathway. In conclusion, this study underscores that unhealthy dietary factors, particularly those high in fructose and fat, may intensify the hazard of BL and adversely impact visual health. Full article

Oxidative stress can be caused by bad nutrition, psychoemotional stress, or other external influences in everyday life. The aim of this study is to develop and verify biological models using male Wistar rats that allow reproducing oxidative stress in vivo, in particular: food (diet with high cholesterol and fructose content), medical (injection of CCl₄), and physiological (immobilization stress). Diet with 1% cholesterol and fructose had the greatest impact on the antioxidant status of animals: a significant increase in serum malondialdehyde (by 1.8 times) and superoxide dismutase (by 2.4 times) as well as a significant decrease in the Cat gene expression by 35% were shown. The immobilization led only to a significant decrease in serum lipid peroxides by 29%. A single intraperitoneal administration of CCl₄ was accompanied by a significant increase in the blood lipid peroxides (by 1.3 times) and catalase (by 1.6 times), as well as a significant decrease in the Cat mRNA by 33% and Gpx1 by 48%. The obtained data can be used to study the effectiveness of drugs, biologically active food supplements and functional nutrition in vivo. Full article

Background/Objective: Metabolic dysfunction-associated fatty liver disease (MAFLD) is defined by the presence of hepatic steatosis, and is associated with obesity, diabetes, and other metabolic alterations. Feeding rats with a high-fat high-fructose (HFHF) diet is a reproducible experimental model of obesity/metabolic syndrome and the related MAFLD. Aronia melanocarpa, Rosa canina, and Alchemilla vulgaris are polyphenol-rich plants with proven health benefits. The aim of this study was to reveal the effects of four Aronia melanocarpa-based fruit juices (AMBFJs) in HFHF-fed rats. Methods: The AMBFJs were AM20 and AM60 (produced from aronia berries at 20 °C and 60 °C, respectively), AMRC (aronia juice with Rosa canina), and AMAV (aronia juice with Alchemilla vulgaris). Male Wistar rats were allocated to 6 groups. Except for the Control, the rest of the groups were fed an HFHF diet for 60 days. Throughout the experiment, each of the AMBFJs was administered to one HFHF-fed group. Results: HFHF-fed rats had an increased calorie intake on the background of increased liquid and decreased food consumption. At the end of the experiment, they had similar body weights, slightly increased fat indices, increased levels of blood lipids and liver enzymes, as well as typical histopathological changes in liver and adipose tissue. AMBFJs-treated animals showed improvement in most of these parameters, especially in triglyceride levels, liver enzymes, and the histopathological changes in the liver and fat. AMAV, the juice with the highest polyphenolic content, had the highest effect on adiposity. Conclusion: In HFHF-fed rats, AMBFJs exerted beneficial effects on MAFLD probably due to their polyphenolic ingredients. Full article

Metabolic dysfunction-associated steatotic liver disease (MASLD) and its progressive form, metabolic dysfunction-associated steatohepatitis (MASH), are growing global health concerns. However, pharmacological therapies for MASLD/MASH have not yet been established. Dietary interventions and their bioactive components have been explored as strategies to mitigate MASLD and MASH progression. Although specific nutrients and bioactive compounds have exhibited potential therapeutic benefits, they also exacerbate adverse outcomes. In this comprehensive review, we synthesize the protective and exacerbating or sometimes dual effects of key macronutrients, including fatty acids (saturated, unsaturated, and trans fats) and carbohydrates (fructose, glucose, and sucrose), and bioactive compounds and micronutrients, in the context of MASLD management. The evidence suggests that coffee-derived compounds, such as caffeine and chlorogenic acid, may attenuate liver injury. However, the effects on MASLD severity are inconsistent. Diets high in saturated fatty acids exacerbate MASLD pathogenesis, whereas moderate intake (7–10% of total energy) may confer metabolic benefits. Other bioactive compounds and micronutrients have been explored for their diverse roles in hepatic lipid metabolism and insulin sensitivity. Although current evidence supports the therapeutic potential of specific dietary nutrients and bioactive compounds in the management of MASLD, inconsistencies in results highlight the need for more robust, well-controlled studies, including clinical trials, to clarify the preventive and therapeutic standards for balanced food interventions in MASLD management. In particular, well-designed clinical trials are necessary before clinical application. Although this is a narrative review and the literature retrieval may be biased, we covered a wide variety of substances. Full article

Background/Objectives: Neurodegenerative disorders have a complex multifactorial pathogenesis that develop decades before the initial symptoms occur. One of the crucial factors in the development of neurodegenerative disorders is an unbalanced diet. A pediatric animal model of diet-induced metabolic dysfunction-associated steatotic liver disease (MASLD) was established by feeding juvenile Iberian pigs a diet high in fat and fructose for 10 weeks. The aim of this study was to investigate the initial molecular imbalances in the frontal cortex (FC) of diet-induced juvenile MASLD pig model and determine whether these changes are associated with neuronal loss. Methods: Eighteen 15-day-old Iberian pigs were randomly assigned to either a standard diet (SD) or a Western diet (WD) for 10 weeks. A short-term recognition memory test and animal activity was recorded during the study. Animals were euthanized in week 10, and the FC and hippocampus (HIP) tissue samples were collected for immunohistochemistry and transcriptomics analyses. Results: WD-fed pigs developed MASLD. There were no significant differences in animals’ activity or recognition memory between WD and SD. To identify and quantify mature neurons, NeuN immunostaining intensity was measured, which was significantly lower in the FC of WD than SD (p ≤ 0.05), but it did not change in HIP (p ≥ 0.05). The Wnt/β-catenin pathway, which promotes neuronal survival and neurogenesis, was downregulated in FC of WD-fed pigs (p ≤ 0.05). Similarly, cytoskeleton organization and extracellular matrix biological processes were downregulated in FC of WD-fed pigs (p ≤ 0.05), whereas the mitochondrial respiratory chain complex and mitochondrion increased in FC of WD compared with SD (p ≤ 0.01). There were several other significantly modulated pathways including signal transduction, cell migration, axon guidance, and calcium ion binding. Conclusions: The high-fructose, high-fat diet led to neuronal loss in the frontal cortex of MASLD pigs and dysregulated gene expression of the Wnt/β-catenin signaling pathway, cytoskeleton organization, extracellular matrix, and mitochondrial respiratory chain—all pathways that are found deregulated in neurodegnerative diseases. Full article

Background/Objectives: The consumption of fructose-sweetened beverages, especially when combined with a high-fat (HF) diet, substantially contributes to obesity, diabetes, and metabolic dysfunction-associated steatotic liver disease. Ectopic fat accumulation in skeletal muscles is a critical factor in the development of insulin resistance, a key feature of these metabolic disorders. We aimed to investigate the effects of the rare sugar, d-allulose, on fructose-induced insulin resistance. Methods: Male Wistar rats were randomly assigned to fructose-free control diet (CD), HF/fructose-free diet (HF), or HF/fructose diet (HFF) groups. After 4 weeks, an intraperitoneal glucose tolerance test (IPGTT) was performed, followed by a two-step hyperinsulinemic–euglycemic clamp (HE-clamp) test at 5 weeks. Blood, skeletal muscle, and liver samples were collected after 6 weeks, and triglyceride (TG) levels were measured. Additionally, Western blot was performed on skeletal muscle samples. The same protocol was repeated for the HFF group supplemented with either 5% d-allulose or 5% cellulose. Results: Compared to the CD and HF groups, the HFF group exhibited increased blood glucose levels during the IPGTT and greater systemic and skeletal muscle insulin resistance in the HE-clamp. Furthermore, plasma, liver, and muscle TG levels were significantly elevated in the HFF group. However, d-allulose supplementation improved insulin resistance in the HFF group and reduced blood, liver, and muscle TG levels. Additionally, insulin-stimulated AKT phosphorylation and acetyl-CoA carboxylase phosphorylation were enhanced in the skeletal muscle following d-allulose administration. Conclusions: d-allulose may improve insulin resistance by reducing TG accumulation in the skeletal muscle, potentially independent of its anti-obesity properties. Full article

Fats play a key role in the rheological and textural properties of meat products. However, growing awareness of the link between diet and disease has stimulated research on fat replacers that can replicate these functional properties. Inulin, a β-D-fructose polymer available in various degrees of polymerization (DP), is promising as a fat replacer due to its gel-forming ability in aqueous systems and its neutral sensory profile. This study focused on optimizing the formulation of inulin gel-based fat replacers for producing reduced-fat beef burgers. A D-optimal mixture-process design was employed, considering inulin with high-DP (HDP) and low-DP (LDP). The aim was to determine the optimal amount of inulin, water, and guar gum to achieve gels with rheological properties (η, shear viscosity; K, consistency index) similar to beef fat. The optimal formulations consisted of 51.52% inulin, 48.48% water, 1.50% guar gum for LDP gel, and 39.12% inulin, 60.88% water, 1.50% guar gum for HDP gel. These gels demonstrated shear viscosity and consistency indices comparable to beef fat. While rheological behavior at constant temperatures was similar, inulin gels showed increasing viscoelastic moduli (G′ and G″) with temperature, in contrast to the melting behavior of animal fat. When used in beef burger formulations, the optimized gels resulted in improved cooking yields, reduced shrinkage, and better dimensional stability compared to conventional controls. These benefits are attributed to the hydrophilic and stabilizing properties of inulin. The findings support the use of inulin-based gels as effective fat replacers, offering a promising strategy to reduce fat content in meat products without compromising functional quality. Full article

Biochemical alterations linked to metabolic syndrome (MetS), type 2 diabetes (T2DM), and metabolic dysfunction-associated steatotic liver disease (MASLD) may be brought on by the Western diet. Based on research conducted over the past decade, fructose is one of the main culprits. Over 80% of ingested fructose is metabolized by the liver at first pass, where it stimulates de novo lipogenesis (DNL) to drive hepatic triglyceride (TG) synthesis, which contributes to MASLD, hepatic insulin resistance (IR), and dyslipidemia. Fructose reduction produces quick and significant amelioration in these metabolic disturbances. We hereby propose potential overarching processes that can link these pathways to signaling disruption by the critical metabolic sensor AMP-activated protein kinase (AMPK). We proffer that when large amounts of fructose and glucose enter the liver, triose fluxes may be sufficient to produce transient increases in methylglyoxal (MG), allowing steady-state concentrations between its production and catabolism by glyoxalases to be high enough to modify AMPK-sensitive functional amino acid residues. These reactions would transiently interfere with AMPK activation by both AMP and aldolase. Such a sequence of events would boost the well-documented lipogenic impact of fructose. Given that MG adducts are irreversible, modified AMPK molecules would be less effective in metabolite sensing until they were replaced by synthesis. If proven, this mechanism provides another avenue of possibilities to tackle the problem of fructose in our diet. We additionally discuss potential multimodal treatments and future research avenues for this apparent hepatic AMPK malfunction. Full article

This study aimed to evaluate the protective effects of peach leaf extract (Prunus persica L.) against metabolic syndrome and oxidative stress in Wistar rats subjected to a high-fructose diet. The Wistar rats were divided into groups and fed a high-fructose diet, with or without supplementation of peach leaf extract. The extract was characterized by its bioactive compounds, including an organic acid yield of 53.8%, total phenolic content (TPC) of 273.36 ± 1.929 mg GAE/g DW, flavonoid content (TFC) at 149.02 ± 57.47 mg QE/g DW, condensed tannins (TCT) at 2.34 ± 0.171 mg CE/g DW, and flavonols at 81.67 ± 0.497 mg DE/g DW. In vitro tests showed significant antioxidant potential, with a total antioxidant capacity (TAC) of 44.11 ± 6.328 mg AAE/g DW, DPPH radical scavenging activity (IC₅₀ = 4.89 mg/mL), and reducing power assay (FRAP, IC₅₀ = 0.525 mg/mL). The results indicated that the extract significantly reduced body weight gain, plasma insulin levels (0.30 ± 0.00 U(IU)/mL), glycemia (0.955 ± 0.068 g/L), total cholesterol (0.555 ± 0.177 g/L), and triglycerides (0.720 ± 0.141 g/L). Regarding oxidative stress markers, the extract decreased levels of malondialdehyde (MDA, 4567 ± 121 μmol/L), hydroperoxides (1304 ± 288 μmol/L), and carbonylated proteins (0.029 ± 0.020 μmol/L), while increasing levels of vitamin C (25.84 ± 3.00 mg AAE/L), Oxygen Radical Absorbance Capacity (ORAC, 6.043 ± 0.345 UA), and catalase activity (0.0052 ± 0.00008 μL/mL). These findings suggest that P. persica L. may alleviate impairments related to metabolic syndrome by improving metabolic profiles and reducing oxidative stress in rats fed a high-fructose diet, making it a potential dietary supplement for managing metabolic syndrome. Full article

Metabolic dysfunction-associated fatty liver disease (MAFLD) is a significant global public health issue. Luteolin possesses several beneficial biological properties, including antioxidation and anti-inflammation. This study investigated luteolin’s effect and potential mechanisms on MAFLD in high-fat diet (HFD)-fed rats. Rats were administered an HFD supplemented with fructose for 12 weeks to induce MAFLD. After that, the HFD-fed rats were given either luteolin (50 or 100 mg/kg/day) or metformin (100 mg/kg/day) for 4 weeks. Luteolin improved metabolic parameters induced by the HFD, since it decreased body weight, blood pressure, fasting blood glucose, serum insulin, free fatty acids, cholesterol, and triglyceride levels (p < 0.05). Luteolin reduced hepatic injury and inflammatory markers in HFD-fed rats (p < 0.05). Additionally, HFD-fed rats treated with luteolin showed reduced malondialdehyde and raised catalase activity in plasma (p < 0.05). Luteolin attenuated hepatic steatosis compared to the untreated rats (p < 0.05). Luteolin also increased plasma adiponectin levels accompanied by upregulation of adiponectin receptor 1 (AdipoR1), AMP-activated protein kinase (AMPK), and peroxisome proliferator-activated receptor γ (PPAR-γ) protein expression in liver (p < 0.05). These findings revealed that luteolin ameliorated HFD-induced MAFLD in rats, possibly by reducing metabolic alterations and oxidative stress and restoring AdipoR1, AMPK, and PPARγ protein expression in HFD-fed rats. Full article

Background/Objectives: Disrupted intracellular calcium (Ca²⁺_i) regulation and renin–angiotensin system (RAS) activation are pathogenetic factors in diabetic cardiomyopathy, a major complication of type 1 (T1D) and type 2 (T2D) diabetes. This study explored their potential link in diabetic rat hearts. Methods: Experiments were conducted on T1D and T2D Sprague-Dawley rats induced by streptozotocin and fructose-rich diet, respectively. In T1D, rats were treated with Enalapril (Ena) or Losartan (Los) for six weeks, whereas T2D animals received high-dose (HD) or low-dose (LD) Ena for 8 weeks. Heart function was assessed via echocardiography, Ca²⁺_i transients by Indo-1 fluorometry in Langendorff-perfused hearts, and key Ca²⁺_i cycling proteins by Western blot. Data: mean ± SD. Results: Diabetic hearts exhibited reduced contractile performance that was improved by RAS inhibition both in vivo (ejection fraction (%): T1D model: Control: 79 ± 7, T1D: 54 ± 11, T1D + Ena: 65 ± 10, T1D + Los: 69 ± 10, n = 18, 18, 15, 10; T2D model: Control: 73 ± 8, T2D: 52 ± 6, T2D + LDEna: 62 ± 8, T2D + HDEna: 76 ± 8, n = 9, 8, 6, 7) and ex vivo (+dPressure/dt_max (mmHg/s): T1D model: Control: 2532 ± 341, T1D: 2192 ± 208, T1D + Ena: 2523 ± 485, T1D + Los: 2643 ± 455; T2D model: Control: 2514 ± 197, T2D: 1930 ± 291, T2D + LDEna: 2311 ± 289, T2D + HDEna: 2614 ± 268). Analysis of Ca²⁺_i transients showed impaired Ca²⁺_i release and removal dynamics and increased diastolic Ca²⁺_i levels in both models that were restored by Ena and Los treatments. We observed a decrease in sarcoendoplasmic reticulum Ca²⁺-ATPase2a (SERCA2a) expression, accompanied by a compensatory increase in 16Ser-phosphorylated phospholamban (P-PLB) in T2D that was prevented by both LD and HD Ena (expression level (% of Control): SERCA2a: T2D: 36 ± 32, T2D + LDEna: 112 ± 32, T2D + HDEna: 106 ± 30; P-PLB: T2D: 557 ± 156, T2D + LDEna: 129 ± 38, T2D + HDEna: 108 ± 42; n = 4, 4, 4). Conclusions: The study highlights the critical role of RAS activation, most likely occurring at the tissue level, in disrupting Ca²⁺_i homeostasis in diabetic cardiomyopathy. RAS inhibition with Ena or Los mitigates these disturbances independent of blood pressure effects, underlining their importance in managing diabetic heart failure. Full article

Excessive high-fat diet (HFD) intake can precipitate metabolic dysfunction-associated fatty liver disease (MAFLD). Tangeretin is a citrus flavonoid possessing many biological properties. We examined the impact of tangeretin on MAFLD and its underlying mechanism. Rats were given HFD plus 15% fructose solution for four months to produce metabolic syndrome. Metabolic syndrome rats were administered 100 mg/kg of metformin or 25 mg/kg of tangeretin for the last four weeks. HFD-induced increased body weight, liver weight, adipose tissue weight, fasting blood glucose, serum insulin, total triglyceride, total cholesterol, and free fatty acids and reduced adiponectin and high-density lipoprotein cholesterol levels in metabolic syndrome, which were alleviated by tangeretin (p < 0.05). Tangeretin stabilized alanine transaminase activity, liver catalase, and inflammatory and oxidative stress markers in HFD rats compared to untreated HFD rats (p < 0.05). Tangeretin reduced hepatic steatosis induced by HFD. Downregulation of hepatic insulin receptor substrate-1 (IRS-1) and protein kinase B (Akt) protein expression in metabolic syndrome rats was recovered by tangeretin (p < 0.05). Metformin, an antihyperglycemic drug, produced comparable effects to tangeretin. In conclusion, tangeretin attenuates metabolic disorders and fatty liver induced by HFD in rats. The underlying mechanisms involve reducing oxidative stress, and inflammation and enhancing insulin sensitivity. Full article