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Background/Objectives: Menopause induces substantial metabolic changes, including a reduction in metabolic rate and an elevated risk of developing metabolic diseases. Fish oil (FO) supplementation has been shown to ameliorate menopause-associated metabolic risks. Hyperthermia treatment (HT) has recently gained attention for its potential to improve metabolic and immune health. However, it remains to be determined whether HT can confer metabolic benefits comparable to those of FO supplementation or enhance the metabolic benefits of FO supplementation. This study aims to delineate the distinctive and collaborative effects of HT and FO supplementation in mitigating menopause-associated metabolic dysfunction. Methods: Female C57BL/6 ovariectomized (OVX) mice were randomly assigned to four groups (n = 12/group) to evaluate the individual and combined effects of FO supplementation (5% w/w) and HT treatment. For HT, whole-body heat exposure was conducted at 40–41 °C for 30 min, 5 days per week. After 12 weeks, animals were used to evaluate the changes in glucose and lipid metabolism, obesity outcome, and inflammatory markers. The gut microbiome analysis was conducted from cecal content by 16S rRNA sequencing. Acute inflammation was induced by lipopolysaccharide (LPS) injection to evaluate inflammatory responses. Results: HT alone distinctively reduced weight gain, lowered core body temperature, and attenuated insulin resistance comparable to FO supplement in OVX mice. The collaborative effect of FO and HT was not evident in metabolic parameters but more prominent in attenuating proinflammatory responses and microbiota modulation. Conclusions: Our findings suggest that the combined treatment of FO supplementation and HT may serve as an effective strategy to mitigate menopause-associated immune susceptibility and metabolic dysfunction. These benefits are likely mediated, at least in part, through the reduction in inflammation and modulation of the gut microbiota.

Background/Objectives: Global warming and concomitant extreme weather events have markedly increased the incidence of heat stroke. Heat stroke (HS) poses a substantial threat to cerebral health by triggering neuroinflammation and accelerating neurodegenerative processes. The activation of the Nod-like receptor protein 3 (NLRP3) inflammasome for interleukin-1β (IL-1β) secretion has been implicated as a critical mechanism underlying HS-related fatalities. However, the potential role of specific dietary factors to counteract heat stroke-induced neurotoxicity remains largely underexplored. We previously reported that eicosapentaenoic acid (EPA) and urolithin A (UroA), a gut metabolite of ellagic acid, effectively suppress NLRP3 inflammasome activation against metabolic or pathogenic insults. This study aimed to assess the impact of eicosapentaenoic acid (EPA), urolithin A (UroA), and their combination on mitigating heatstroke-mediated NLRP3 inflammasome activation in microglial cells. Methods: In vitro heatstroke conditions were replicated by subjecting murine BV2 microglial cells to a high temperature (41 °C) under hypoxic conditions. To achieve nutrient loading, BV2 cells were preincubated with either EPA (50 µM) or UroA (10 µM). NLRP3 inflammasome activation was evaluated by proinflammatory gene expression, caspase-1 cleavage in cells, and IL-1β secretion to the medium. The caspase-1 activation was determined using a luciferase-based inflammasome and protease activity reporter (iGLuc) assay. Results: Exposure to high temperatures under hypoxia successfully mimicked HS conditions and promoted NLRP3 inflammasome activation in BV2 cells. Both EPA and UroA substantially attenuated the heat stroke-induced priming of proinflammatory genes. More importantly, EPA and UroA demonstrated a synergistic effect in mitigating HS-induced active caspase-1 production, leading to a dramatic decrease in IL-1β secretion. This synergistic effect between EPA and UroA was further confirmed by the iGLuc reporter assay. Conclusions: Dietary enrichment with EPA and UroA precursors may constitute an efficacious strategy for mitigating heat stroke-mediated neuroinflammation and neurodegenerative diseases.

Excess body weight is a major risk factor for type 2 diabetes (T2D) and associated metabolic complications, and weight loss has been shown to improve glycemic control and decrease morbidity and mortality in T2D patients. Weight-loss strategies using dietary interventions produce a significant decrease in diabetes-related metabolic disturbance. We have previously reported that the supplementation of low molecular chitosan oligosaccharide (GO2KA1) significantly inhibited blood glucose levels in both animals and humans. However, the effect of GO2KA1 on obesity still remains unclear. The aim of the study was to evaluate the anti-obesity effect of GO2KA1 on lipid accumulation and adipogenic gene expression using 3T3-L1 adipocytes in vitro and plasma lipid profiles using a Sprague-Dawley (SD) rat model. Murine 3T3-L1 preadipocytes were stimulated to differentiate under the adipogenic stimulation in the presence and absence of varying concentrations of GO2KA1. Adipocyte differentiation was confirmed by Oil Red O staining of lipids and the expression of adipogenic gene expression. Compared to control group, the cells treated with GO2KA1 significantly decreased in intracellular lipid accumulation with concomitant decreases in the expression of key transcription factors, peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding protein alpha (CEBP/α). Consistently, the mRNA expression of downstream adipogenic target genes such as fatty acid binding protein 4 (FABP4), fatty acid synthase (FAS), were significantly lower in the GO2KA1-treated group than in the control group. In vivo, male SD rats were fed a high fat diet (HFD) for 6 weeks to induced obesity, followed by oral administration of GO2KA1 at 0.1 g/kg/body weight or vehicle control in HFD. We assessed body weight, food intake, plasma lipids, levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) for liver function, and serum level of adiponectin, a marker for obesity-mediated metabolic syndrome. Compared to control group GO2KA1 significantly suppressed body weight gain (185.8 ± 8.8 g vs. 211.6 ± 20.1 g, p < 0.05) with no significant difference in food intake. The serum total cholesterol, triglyceride, and low-density lipoprotein (LDL) levels were significantly lower in the GO2KA1-treated group than in the control group, whereas the high-density lipoprotein (HDL) level was higher in the GO2KA1 group. The GO2KA1-treated group also showed a significant reduction in ALT and AST levels compared to the control. Moreover, serum adiponectin levels were significantly 1.5-folder higher than the control group. These in vivo and in vitro findings suggest that dietary supplementation of GO2KA1 may prevent diet-induced weight gain and the anti-obesity effect is mediated in part by inhibiting adipogenesis and increasing adiponectin level.

Processed products from agricultural produce generate a large number of agricultural by-products that contain a number of functional substances. These are often discarded owing to the lack of suitable processing methods. The present study investigated the anti-photoaging properties of fermented rice bran (FRB), soybean cake (FSB) and sesame seed cake (FSC) on ultraviolet B (UVB)-irradiated hairless mouse skin. Results indicated that the oral administration of FRB, FSB and FSC effectively inhibited the UVB irradiation-induced expression of matrix metalloproteinase (MMP)-2, MMP-9, MMP-3 and MMP-13. Reverse transcription-quantitative polymerase chain reaction results also demonstrated that FRB, FSB and FSC significantly inhibited the UVB-induced expression of the genes encoding tumor necrosis factor-α, inducible nitric oxide synthase, interleukin (IL)-6 and IL-1β when compared with the UVB-vehicle group (P<0.05). Additionally, collagen degradation and mast cell infiltration were reduced in hairless mouse skin. Furthermore, UVB-induced wrinkle formation was also significantly reduced in mouse skin compared with the UVB-vehicle group (P<0.05). These results reveal that fermented agricultural by-products may serve as potential functional materials with anti-photoaging activities.

This research investigated the effect of enzymatically digested low molecular weight (MW) chitosan oligosaccharide on type 2 diabetes prevention. Three different chitosan oligosaccharide samples with varying MW were evaluated in vitro for inhibition of rat small intestinal α-glucosidase and porcine pancreatic α-amylase (GO2KA1; <1000 Da, GO2KA2; 1000–10,000 Da, GO2KA3; MW > 10,000 Da). The in vitro results showed that all tested samples had similar rat α-glucosidase inhibitory and porcine α-amylase inhibitory activity. Based on these observations, we decided to further investigate the effect of all three samples at a dose of 0.1 g/kg, on reducing postprandial blood glucose levels in Sprague-Dawley (SD) rat model after sucrose loading test. In the animal trial, all tested samples had postprandial blood glucose reduction effect, when compared to control, however GO2KA1 supplementation had the strongest effect. The glucose peak (Cmax) for GO2KA1 and control was 152 mg/dL and 193 mg/dL, respectively. The area under the blood glucose-time curve (AUC) for GO2KA1 and control was 262 h mg/dL and 305 h mg/dL, respectively. Furthermore, the time of peak plasma concentration of blood glucose (Tmax) for GO2KA1 was significantly delayed (0.9 h) compared to control (0.5 h). These results suggest that GO2KA1 could have a beneficial effect for blood glucose management relevant to diabetes prevention in normal and pre-diabetic individuals. The suggested mechanism of action is via inhibition of the carbohydrate hydrolysis enzyme α-glucosidase and since GO2KA1 (MW < 1000 Da) had higher in vivo effect, we hypothesize that it is more readily absorbed and might exert further biological effect once it is absorbed in the blood stream, relevant to blood glucose management.

Although ginsenosides Rb1 and Rg3 have been identified as the significant ginsenosides found in red ginseng that confer anti-diabetic actions, it is unclear whether insulin-sensitizing effects are mediated by the individual compounds or by their combination. To determine the effect of ginsenosides Rb1 and Rg3 on adipocyte differentiation, 3T3-L1 preadipocytes were induced to differentiate the standard hormonal inducers in the absence or presence of ginsenosides Rb1 or Rg3. Additionally, we determined the effects of Rb1, Rg3, or their combination on the expression of genes related to adipocyte differentiation, adipogenic transcription factors, and the insulin signaling pathway in 3T3-L1 cells using semi-quantitative RT-PCR. Rb1 significantly increased the expression of CEBPα, PPARγ, and aP2 mRNAs. However, Rg3 exerted its maximal stimulatory effect on these genes at 1 μM concentration, while a high concentration (50 μM) showed inhibitory effects. Similarly, treatment with Rb1 and Rg3 (1 μM) increased the expression of IRS-1, Akt, PI3K, GLUT4, and adiponectin. Importantly, co-treatment of Rb1 and Rg3 (9:1) induced the maximal expression levels of these mRNAs. Our data indicate that the anti-diabetic activity of red ginseng is, in part, mediated by synergistic actions of Rb1 and Rg3, further supporting the significance of minor Rg3.

Postprandial blood glucose lowering effect of vitamin B 6 (pyridoxine) was evaluated in healthy individuals with normal blood glucose levels. Blood glucose levels were measured every 30 min for 2 h after oral sugar administration with or without 50 mg of pyridoxine. Pyridoxine significantly lowered the postprandial blood glucose levels at 30 min (from 165.95 ± 17.19 to 138.36 ± 20.43, p  < 0.01) and 60 min (from 131.40 ± 17.20 to 118.50 ± 15.95) after administration. In addition, the area under the concentration–time curve (AUC t ) was reduced by about 8.3% (from 257.08 ± 22.38 to 235.71 ± 12.33, p  < 0.05) and the maximum concentration of blood glucose (C max ) was reduced by about 13.8% (from 165.95 ± 17.19 to 143.07 ± 11.34, p  < 0.01) when compared with those of the control group. Our findings suggest that pyridoxine supplementation may be beneficial for controlling postprandial hyperglycemia.

Sesame is an important oilseed crop, which has been used as a traditional health food to ameliorate the prevention of various diseases. We evaluated the changes in the anti-allergic activities of sesame by bioconversion. SDS-PAGE of non-fermented sesame proteins showed major allergen bands, while that of fermented sesame showed only a few protein bands. Additionally, we investigated the effectiveness of fermented sesame by bioconversion in tumor necrosis factor-α (TNF-α)- and interferon-γ (IFN-γ)-induced HaCaT cells. In HaCaT cells, fermented sesame inhibited the mRNA expression of interleukin-6 (IL-6) and interleukin-1β (IL-1β), thymus and macrophage-derived chemokine (MDC/CCL22), activation-regulated chemokine (TARC/CCL17), and intercellular adhesion molecule-1 (ICAM-1). Moreover, fermented sesame inhibited the activation of nuclear factor-κB (NF-κB) and signal transducer and activator of transcription 1 (STAT1). Fermented sesame exerts anti-allergic effects by suppressing the expression of chemokines and cytokines via blockade of NF-κB and STAT1 activation.

Endocrine disrupting chemicals (EDCs) disrupt the physiological metabolism, thus playing an important role in the development of obesity. EDCs, the so-called ‘obesogens’, might predispose some individuals to gain weight. This study investigated the effects of bisphenol A (BPA) and its alternatives (BPS and BPF) on adipocyte differentiation and the effects of the leaves of Potentilla rugulosa Nakai extract (LPE) as a functional food ingredient on obesogen-induced lipid production and adipogenesis in 3T3-L1 cells. The results showed that LPE has high total phenolic and flavonoid contents (77.58 ± 0.57 mg gallic acid equivalents (GAE)/g and 57.31 ± 1.72 mg quercetin equivalents (QE)/g, respectively). In addition, LPE exerted significant antioxidant effects in terms of DPPH radical scavenging activity, reducing power, ferric-ion reducing antioxidant power, and oxygen radical absorbance capacity. BPA, BPS, and BPF increased lipid accumulation, protein expressions of adipogenic transcription factors (PPAR-γ, C/EBP-α, and aP2), and reactive oxygen species (ROS) production in 3T3-L1 cells. However, LPE suppressed the BPA-, BPS-, and BPF-induced effects on adipogenesis. Therefore, LPE has potential as a functional food supplement that can prevent bisphenol-induced lipid metabolism disorders.

Background/Aims: Previously, we demonstrated that soy protein ameliorates the diabetic phenotype in several rodent models of obesity and metabolic syndrome (MS). This study was designed to further elucidate factors related to adiposity, glycemic control, and renal function in male Zucker Diabetic Fatty (ZDF/Lepr(fa)) rats. Methods: Animals were randomly assigned to one of four diets: control, casein (C); low isoflavone (LIS) soy protein; high isoflavone (HIS) soy protein, or casein + rosiglitazone (CR) for 11 weeks. At sacrifice, physiological, biochemical, and molecular parameters were determined. Results: Body weight and total adiposity were higher in LIS and CR diet groups despite lower food intake. Additionally, these animals exhibited differential regulation of adipose-specific proteins (PPAR-gamma and GLUT4) and enzyme activity (FAS and GPDH). HIS-fed animals had reduced total and liver adiposity. Glycemic control was prolonged in both soy-based and rosiglitazone (RGZ) groups. Renal dysfunction was significantly reduced in soy-fed and RGZ-treated rodents as demonstrated by lower levels of proteinuria and dilated tubules with proteinaceous casts. Conclusion: Collectively, these data provide evidence that soy protein with low or high isoflavone content may have therapeutic significance in reducing severity of diabetes, MS, and renal disease as demonstrated in this preclinical model.