ABSTRACT
Middle-aged women belong to a risk group for metabolic dysregulation and menopausal symptoms, mainly due to a dramatic hormonal shift. Supplementation with functional compounds or a single nutrient has been dominantly explored as a nutritional approach for improving aging-related health parameters. However, a meal-based approach might be another strategy for promoting the overall health of the target population. This pilot study aimed to develop a meal-based intervention for middle-aged women and to evaluate its potential health benefits. Considering the nutrient intake status of Korean middle-aged women, diets enriched with four major nutrients (isoflavone, omega-3, fiber, and calcium) were designed and provided to forty-nine women aged 50 to 65 with mild levels of menopausal symptoms for 8 weeks. In the post-intervention phase, they showed reduced body weight and body fat, and improved biochemical metabolic parameters with decreased levels of cholesterol, low-density lipoprotein-cholesterol, ApoB, and fasting insulin. Moreover, bone resorption markers and menopause symptoms were lower in the post-intervention phase. In conclusion, the meal-based intervention might be a prominent strategy for overall health promotion in relatively healthy middle-aged women and further investigation is needed to test its efficacy with a randomized controlled study.
Subject(s)
Aging , Diet , Health Promotion , Meals , Female , Humans , Middle Aged , Adipose Tissue , Apolipoproteins B , Pilot Projects , East Asian PeopleABSTRACT
Cancer cachexia is a metabolic disease affecting multiple organs and characterized by loss adipose and muscle tissues. Metabolic dysregulated of adipose tissue has a crucial role in cancer cachexia. ß-Carotene (BC) is stored in adipose tissues and increases muscle mass and differentiation. However, its regulatory effects on adipose tissues in cancer cachexia have not been investigated yet. In this study, we found that BC supplementations could inhibit several cancer cachexia-related changes, including decreased carcass-tumor (carcass weight after tumor removal), adipose weights, and muscle weights in CT26-induced cancer cachexia mice. Moreover, BC supplementations suppressed cancer cachexia-induced lipolysis, fat browning, hepatic gluconeogenesis, and systemic inflammation. Altered diversity and composition of gut microbiota in cancer cachexia were restored by the BC supplementations. BC treatments could reverse the down-regulated adipogenesis and dysregulated mitochondrial respiration and glycolysis in adipocytes and colon cancer organoid co-culture systems. Taken together, these results suggest that BC can be a potential therapeutic strategy for cancer cachexia.
Subject(s)
Colonic Neoplasms , Gastrointestinal Microbiome , Neoplasms , Animals , Mice , Cachexia/etiology , Cachexia/prevention & control , Cachexia/metabolism , beta Carotene/metabolism , Adipose Tissue/metabolism , Neoplasms/metabolism , Colonic Neoplasms/complications , Colonic Neoplasms/metabolism , Muscle, Skeletal/metabolismABSTRACT
College students are vulnerable to diverse mental health disorders. We aimed to investigate whether a meditation class would be an effective means to address students' mental health challenges. Among the college students who registered for the meditation course, 256 participants were enrolled. The meditation course was a 15-week program incorporating mindfulness meditation and Ganhwa Seon (a traditional Buddhist meditation). A questionnaire was administered twice, on the first and last class of the course, collecting information on personal characteristics and six mental health indicators. A paired t-test was used to examine whether the meditation course conferred benefit on the mental health indicators, and logistic regression analyses were run to identify factors associated with mental health outcomes. After completing the meditation course, there were significant improvements for the adult ADHD score (p < 0.01) and ego identity (p = 0.02) but not for the other outcomes. Among college students, meditation practice may have positive effects on the adult ADHD score and ego identity.
ABSTRACT
Light-based phototherapy has been developed for cancer treatment owing to its non-invasiveness and spatiotemporal control. Despite the unique merits of phototherapy, one critical disadvantage of light is its limited penetration depth, which restricts its application in cancer treatment. Although many researchers have developed various strategies to deliver light into deep-seated tumors with two-photon and near-infrared light irradiation, phototherapy encounters the peculiar limitations of light. In addition, high oxygen dependency is another limitation of photodynamic therapy to treat hypoxic tumors. To overcome the drawbacks of conventional treatments, various energy sources have been developed for cancer treatment. Generally, most energy sources, such as ultrasound, chemiluminescence, radiation, microwave, electricity, and magnetic field, are relatively free from the restraint of penetration depth. Combining other strategies or therapies with other energy-source-based therapies improves the strength and compensates for the weakness. This tutorial review focuses on recent advances in the diverse energy sources utilized in cancer treatment and their future perspectives.
Subject(s)
Neoplasms , Photochemotherapy , Humans , Luminescence , Neoplasms/drug therapy , Oxygen , PhototherapyABSTRACT
BACKGROUND/OBJECTIVES: Colorectal cancer (CRC) is the third most common cancer worldwide and has a high recurrence rate, which is associated with cancer stem cells (CSCs). ß-carotene (BC) possesses antioxidant activity and several anticancer mechanisms. However, no investigation has examined its effect on colon cancer stemness. MATERIALS/METHODS: CD133+CD44+ HCT116 and CD133+CD44+ HT-29 cells were isolated and analyzed their self-renewal capacity by clonogenic and sphere formation assays. Expressions of several CSCs markers and Wnt/ß-catenin signaling were examined. In addition, CD133+CD44+ HCT116 cells were subcutaneously injected in xenograft mice and analyzed the effect of BC on tumor formation, tumor volume, and CSCs markers in tumors. RESULTS: BC inhibited self-renewal capacity and CSC markers, including CD44, CD133, ALDH1A1, NOTCH1, Sox2, and ß-catenin in vitro. The effects of BC on CSC markers were confirmed in primary cells isolated from human CRC tumors. BC supplementation decreased the number and size of tumors and delayed the tumor-onset time in xenograft mice injected with CD133+CD44+ HCT116 cells. The inhibitory effect of BC on CSC markers and the Wnt/ß-catenin signaling pathway in tumors was confirmed in vivo as well. CONCLUSIONS: These results suggest that BC may be a potential therapeutic agent for colon cancer by targeting colon CSCs.
ABSTRACT
PURPOSE: The agreement between axillary temperature (AT) and rectal temperature (RT) measurements has not been well established in preterm infants. Therefore, our study aimed to evaluate the agreement between AT and RT measurements in very preterm infants. METHODS: Preterm infants <32 weeks of gestational age were prospectively included. The infants' body temperature (BT) was measured twice a day from day 1 to day 6. A paired t-test and the Bland-Altman method were used to analyze the difference between the AT and RT. A linear regression model was used to explore the effects of environmental factors on the differences of BT between the axillary and rectal measurements and to calibrate the RT according to the AT. RESULTS: Eighty infants each underwent 6 paired axillary and rectal measurements. The gestational age varied from 22 to 31 weeks (mean 28 weeks). The birth weight varied from 302 to 1,770 g (mean 1,025 g). The AT was significantly lower than the RT. The difference between the RT and AT significantly increased with increasing RT. The AT and RT demonstrated poor agreement overall; however, the RT can be estimated using the AT with the following equation: RT = -4.033 + 1.116 × AT. Environmental factors, including the incubator temperature, incubator humidity, phototherapy, and application of invasive mechanical ventilation did not affect the differences between the AT and RT measurements. CONCLUSION: AT measurements cannot be interchangeably used with RT measurements in very preterm infants.
Subject(s)
Body Temperature , Infant, Premature , Axilla , Humans , Infant , Infant, Newborn , Infant, Very Low Birth Weight , TemperatureABSTRACT
OBJECTIVE: The present study aimed to evaluate a new tibial nerve stimulation (TNS) modality, which uses interferential currents, in terms of the stimulation electric field penetration efficiency into the body and physiological effectiveness. METHODS: In silico experiments were performed to analyze the penetration efficiency of proposed interferential current therapy (ICT). Based on this, we performed in vivo experiments to measure excitation threshold of ICT for the tibial nerve, which is related to stimulation field near the nerve. Regarding analysis of the physiological effectiveness, in vivo ICT-TNS was performed, and changes in bladder contraction frequency and voiding volume were measured. The penetration efficiency and physiological effectiveness of ICT were evaluated by comparison with those of conventional TNS using transcutaneous electrical nerve stimulation (TENS). RESULTS: Simulation results showed that ICT has high penetration efficiency, thereby generating stronger field than TENS. These results are consistent with the in vivo results that nerve excitation threshold of ICT is lower than that of TENS. Moreover, ICT-TNS decreased contraction frequency and increased voiding volume, and its performance was profound compared with that of TENS-TNS. CONCLUSION: The proposed ICT is more efficient in inducing the stimulation field near the tibial nerve placed deep inside the body compared with conventional TENS and shows a good clinical effectiveness for TNS. SIGNIFICANCE: The high efficiency of ICT increases the safety of noninvasive neurostimulation; therefore, it has clinical potential to become a promising modality for TNS to treat OAB and other peripheral neurostimulations.
Subject(s)
Electric Stimulation Therapy , Transcutaneous Electric Nerve Stimulation , Urinary Bladder, Overactive , Humans , Tibial Nerve , Urinary Bladder, Overactive/therapyABSTRACT
BACKGROUND/OBJECTIVES: Brain senescence causes cognitive impairment and neurodegeneration. It has also been demonstrated that curcumin (Cur) and hesperetin (Hes), both antioxidant polyphenolic compounds, mediate anti-aging and neuroprotective effects. Therefore, the objective of this study was to investigate whether Cur, Hes, and/or their combination exert anti-aging effects in D-galactose (Dg)-induced aged neuronal cells and rats. MATERIALS/METHODS: SH-SY5Y cells differentiated in response to retinoic acid were treated with Cur (1 µM), Hes (1 µM), or a combination of both, followed by 300 mM Dg. Neuronal loss was subsequently evaluated by measuring average neurite length and analyzing expression of ß-tubulin III, phosphorylated extracellular signal-regulated kinases, and neurofilament heavy polypeptide. Cellular senescence and related proteins, p16 and p21, were also investigated, including their regulation of antioxidant enzymes. In vivo, brain aging was induced by injecting 250 mg/kg body weight (b.w.) Dg. The effects of supplementing this model with 50 mg/kg b.w. Cur, 50 mg/kg b.w. Hes, or a combination of both for 3 months were subsequently evaluated. Brain aging was examined with a step-through passive avoidance test and apoptosis markers were analyzed in brain cortex tissues. RESULTS: Cur, Hes, and their combination improved neuron length and cellular senescence by decreasing the number of ß-gal stained cells, down-regulated expression of p16 and p21, and up-regulated expression of antioxidant enzymes, including superoxide dismutase 1, glutathione peroxidase 1, and catalase. Administration of Cur, Hes, or their combination also tended to ameliorate cognitive impairment and suppress apoptosis in the cerebral cortex by down-regulating Bax and poly (ADP-ribose) polymerase expression and increasing Bcl-2 expression. CONCLUSIONS: Cur and Hes appear to attenuate Dg-induced brain aging via regulation of antioxidant enzymes and apoptosis. These results suggest that Cur and Hes may mediate neuroprotective effects in the aging process, and further study of these antioxidant polyphenolic compounds is warranted.
ABSTRACT
Physical inactivity and high-fat diet, especially high saturated fat containing diet are established risk factors for breast cancer that are amenable to intervention. High-fat diet has been shown to induce tumor growth and metastasis by alteration of inflammation but steady exercise has anti-tumorigenic effects. However, the mechanisms underlying the effects of physical activity on high-fat diet stimulated breast cancer initiation and progression are currently unclear. In this study, we examined how the intensity of physical activity influences high fat diet-stimulated breast cancer latency and progression outcomes, and the possible mechanisms behind these effects. Five-week-old female Balb/c mice were fed either a control diet or a high-fat diet for 8 weeks, and then 4T1 mouse mammary tumor cells were inoculated into the mammary fat pads. Exercise training occurred before tumor cell injection, and tumor latency and tumor volume were measured. Mice with a high-fat diet and low-intensity exercise (HFLE) had a longer tumor latency period, slower tumor growth, and smaller tumor volume in the final tumor assessment compared with the control, high-fat diet control (HFDC), and high-fat diet with moderate-intensity exercise (HFME) groups. Steady low- and moderate-intensity exercise had no effect on cell proliferation but induced apoptosis by activating caspase-3 through the alteration of Bcl-2, Bcl-xL, and Bax expression. Furthermore, steady exercise reduced M2 macrophage polarization in breast tumor tissue, which has been linked to tumor growth. The myokine, myostatin, reduced M2 macrophage polarization through the inhibition of the JAK-STAT signaling pathway. These results suggest that steady low-intensity exercise could delay breast cancer initiation and growth and reduce tumor volume through the induction of tumor cell apoptosis and the suppression of M2 macrophage polarization.
Subject(s)
Diet, High-Fat , Neoplasms , Animals , Cell Proliferation , Diet, High-Fat/adverse effects , Female , Inflammation , Macrophages , Mice , Mice, Inbred BALB CABSTRACT
Emerging evidence has shown that flavonoids extracted from Artemisia have beneficial effects on metabolic disorders. However, whether and how jaceosidin ameliorates insulin resistance and diabetic nephropathy in type 2 diabetes mellitus is largely unknown. For 8 weeks, db/db diabetic mice were fed with or without jaceosidin. Oral jaceosidin supplementation reduced fasting blood glucose levels and insulin resistance through the upregulation of insulin receptor downstream pathways in the liver and skeletal muscles. While jaceosidin did not noticeably alter kidney filtration function, this dietary intervention contributed to attenuating the accumulation of advanced glycation end products in diabetic kidneys. The levels of VEGF-a (vascular endothelial growth factor-a) proteins in the diabetic kidneys were markedly diminished by jaceosidin treatments, which increased the expression and activity of Cu (copper) and Zn-SOD (zinc-superoxide dismutase). Therefore, it is suggested that jaceosidin supplementation elicits antidiabetic effects and treats diabetic nephropathy by augmenting insulin signaling, suppressing fibrosis, and enhancing antioxidant activity.
Subject(s)
Diabetes Mellitus, Experimental , Diabetes Mellitus, Type 2 , Diabetic Nephropathies , Flavonoids/therapeutic use , Insulin Resistance , Animals , Antioxidants/metabolism , Diabetes Mellitus, Experimental/drug therapy , Diabetes Mellitus, Type 2/drug therapy , Diabetic Nephropathies/drug therapy , Kidney/drug effects , Mice , Receptor, Insulin/genetics , Signal Transduction , Vascular Endothelial Growth Factor AABSTRACT
In this work, iron (oxyhydr)oxide nanoparticle-doped expanded graphite (IO/EG-1 and IO/EG-2) was prepared via a hydrothermal reaction and applied for the phosphorus adsorption in the aqueous solutions. The analysis of scanning electron microscopy (SEM) and X-ray diffraction (XRD) verified the successful fabrication of IO/EGs, and iron (oxyhydr)oxide nanoparticles became more crystalized according to the calcination at high temperature (IO/EG-2). The maximum adsorption capacity of IO/EG-1 was considerably higher (7.30 mg/g) than that of IO/EG-2 (0.70 mg/g) mainly due to the electrostatic interaction between the negatively charged phosphate ions with iron (oxyhydr)oxides. At the neutral pH, IO/EG-1 exhibited more positively charged than IO/EG-2, which the iso-electric points (IEP) were pH of 9.1 and 6.0, respectively. The thermodynamic study also suggested that the phosphorus adsorption energy of IO/EG-1was considerably favorable (-12.13 kJ/mol) than that of IO/EG-2 (-7.43 kJ/mol). The regeneration of IO/EG-1 were efficiently achieved by a simple extraction using an alkaline solution such as NaOH. Overall, our study suggested that the prepared IO/EGs could be used as good adsorbents for the phosphorus recovery from aqueous solutions.
Subject(s)
Graphite/chemistry , Phosphorus/chemistry , Water Pollutants, Chemical/chemistry , Adsorption , Hydrogen-Ion Concentration , Iron/chemistry , Nanoparticles , Oxides , Phosphates , Thermodynamics , X-Ray DiffractionABSTRACT
The tumor microenvironment (TME), consisting of stromal fibroblasts, immune cells, cancer cells and other cell types, plays a crucial role in cancer progression and metastasis. M2 macrophages and activated fibroblasts (AFs) modulate behavior of cancer cells in the TME. Since nutritional effects on cancer progression, including colorectal cancer (CRC), may be mediated by alterations in the TME, we determined the ability of ß-carotene (BC) to mediate anti-cancer effects through regulation of macrophage polarization and fibroblast activation in CRC. The M2 macrophage phenotype was induced by treating U937 cells with phorbol-12-myristate-13-acetate and interleukin (IL)-4. Treatment of these M2 macrophages with BC led to suppression of M2-type macrophage-associated markers and of the IL-6/STAT3 signaling pathway. In separate experiments, AFs were induced by treating CCD-18Co cells with transforming growth factor-ß1. BC treatment suppressed expression of fibroblast activation markers. In addition, conditioned media from BC-treated M2 macrophages and AF inhibited cancer stem cell markers, colon cancer cell invasiveness and migration, and the epithelial-mesenchymal transition (EMT). In vivo, BC supplementation inhibited tumor formation and the expression of M2 macrophage markers in an azoxymethane/dextran sodium sulfate-induced colitis-associated CRC mouse model. To our knowledge, the present findings provide the first evidence suggesting that the potential therapeutic effects of BC on CRC are mediated by the inhibition of M2 macrophage polarization and fibroblast activation.
Subject(s)
Antineoplastic Agents/pharmacology , Colonic Neoplasms/drug therapy , Fibroblasts/metabolism , Macrophages/metabolism , beta Carotene/pharmacology , Animals , Antineoplastic Agents/administration & dosage , Cell Movement/drug effects , Cell Proliferation/drug effects , Colonic Neoplasms/metabolism , Colonic Neoplasms/pathology , Epithelial-Mesenchymal Transition/drug effects , Female , HCT116 Cells , Humans , Interleukin-6/metabolism , Male , Mice , Mice, Inbred BALB C , Neoplasm Invasiveness , Neoplastic Stem Cells/metabolism , STAT3 Transcription Factor/metabolism , Signal Transduction/drug effects , Tumor Microenvironment/drug effects , U937 Cells , beta Carotene/administration & dosageABSTRACT
PURPOSE: Walnut phenolic extract (WPE) reduces proliferation and enhances differentiation of colon cancer stem cells (CSCs). The present study investigated the metabolic influence of WPE on the mitochondrial function of colon CSCs to determine its underlying mechanism. METHODS: CD133+CD44+ HCT116 colon cancer cells were selected by fluorescence-activated cell sorting and were treated with or without 40 µg/mL WPE. RNA-sequencing (RNA-Seq) was performed to identify differentially expressed genes (DEGs), which were further validated with RT-PCR. WPE-induced alterations in mitochondrial function were investigated through a mitochondrial stress test by determining cellular oxygen consumption rate (OCR), an indicator of mitochondrial respiration, and extracellular acidification rate (ECAR), an indicator of glycolysis, which were further confirmed by glucose uptake and lactate production tests. RESULTS: RNA-Seq analysis identified two major functional clusters: metabolic and mitochondrial clusters. WPE treatment shifted the metabolic profile of cells towards the glycolysis pathway (ΔECAR = 36.98 mpH/min/ptn, p = 0.02) and oxidative pathway (ΔOCR = 29.18 pmol/min/ptn, p = 0.00001). Serial mitochondrial stimulations using respiration modulators, oligomycin, carbonyl cyanide-4 (trifluoromethoxy) phenylhydrazone, and rotenone/antimycin A, found an increased potential of mitochondrial respiration (ΔOCR = 111.5 pmol/min/ptn, p = 0.0006). WPE treatment also increased glucose uptake (Δ = 0.39 pmol/µL, p = 0.002) and lactate production (Δ = 0.08 nmol/µL, p = 0.005). CONCLUSIONS: WPE treatment shifts the mitochondrial metabolism of colon CSC towards more aerobic glycolysis, which might be associated with the alterations in the characteristics of colon CSC.
Subject(s)
Colonic Neoplasms/metabolism , Juglans/metabolism , Mitochondria/metabolism , Neoplastic Stem Cells/metabolism , Plant Extracts/metabolism , Cell Differentiation , Cell Proliferation , Cells, Cultured , Energy Metabolism , Glycolysis , Humans , Oxygen ConsumptionABSTRACT
PURPOSE: Walnuts (Juglans regia) are known to have anti-cancer and immunomodulatory effects. However, little information is available on the effects of walnut phenolic extract (WPE) on intestinal inflammation and colitis-associated colon cancer. METHODS: COLO205 cells were pretreated with WPE and then stimulated with tumor necrosis factor (TNF)-α. In the acute colitis model, wild type mice (C57BL/6) were administered 4% dextran sulfate sodium (DSS) for 5 days. In the chronic colitis model, interleukin (IL)-10-/- mice were administered with either the vehicle or WPE (20 mg/kg) by oral gavage daily for 2 weeks. In an inflammation-associated tumor model, wild type mice were administered a single intraperitoneal injection of azoxymethane followed by three cycles of 2% DSS for 5 days and 2 weeks of free water consumption. RESULTS: WPE significantly inhibited IL-8 and IL-1α expression in COLO205 cells. WPE attenuated both the TNF-α-induced IκB phosphorylation/degradation and NF-κB DNA binding activity. The administration of oral WPE significantly reduced the severity of colitis in both acute and chronic colitis models, including the IL-10-/- mice. In immunohistochemical staining, WPE attenuated NF-κB signaling in the colons of both colitis models. Finally, WPE also significantly reduced tumor development in a murine model of colitis-associated colon cancer (CAC). CONCLUSIONS: WPE ameliorates acute and chronic colitis and CAC in mice, suggesting that WPE may have potentials for the treatment of inflammatory bowel disease.
Subject(s)
Colonic Diseases/drug therapy , Epithelial Cells/drug effects , Intestinal Mucosa/drug effects , Juglans , NF-kappa B/drug effects , Plant Extracts/pharmacology , Signal Transduction/drug effects , Animals , Colitis/drug therapy , Colitis/metabolism , Colonic Diseases/metabolism , Colonic Neoplasms/drug therapy , Colonic Neoplasms/metabolism , Disease Models, Animal , Epithelial Cells/metabolism , Intestinal Mucosa/metabolism , Mice , Mice, Inbred C57BL , NF-kappa B/metabolism , Plant Extracts/administration & dosageABSTRACT
BACKGROUND/OBJECTIVES: The objective of this study was to investigate the effects of vitamin C on inflammation, tumor development, and dysbiosis of intestinal microbiota in an azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced inflammation-associated early colon cancer mouse model. MATERIALS/METHODS: Male BALB/c mice were injected intraperitoneally with AOM [10 mg/kg body weight (b.w)] and given two 7-d cycles of 2% DSS drinking water with a 14 d inter-cycle interval. Vitamin C (60 mg/kg b.w. and 120 mg/kg b.w.) was supplemented by gavage for 5 weeks starting 2 d after the AOM injection. RESULTS: The vitamin C treatment suppressed inflammatory morbidity, as reflected by disease activity index (DAI) in recovery phase and inhibited shortening of the colon, and reduced histological damage. In addition, vitamin C supplementation suppressed mRNA levels of pro-inflammatory mediators and cytokines, including cyclooxygenase-2, microsomal prostaglandin E synthase-2, tumor necrosis factor-α, Interleukin (IL)-1ß, and IL-6, and reduced expression of the proliferation marker, proliferating cell nuclear antigen, compared to observations of AOM/DSS animals. Although the microbial composition did not differ significantly between the groups, administration of vitamin C improved the level of inflammation-related Lactococcus and JQ084893 to control levels. CONCLUSION: Vitamin C treatment provided moderate suppression of inflammation, proliferation, and certain inflammation-related dysbiosis in a murine model of colitis associated-early colon cancer. These findings support that vitamin C supplementation can benefit colonic health. Long-term clinical studies with various doses of vitamin C are warranted.
ABSTRACT
Obesity is a public concern and is responsible for various metabolic diseases. Xylobiose (XB), an alternative sweetener, is a major component of xylo-oligosaccharide. The purpose of this study was to investigate the effects of XB on obesity and its associated metabolic changes in related organs. For these studies, mice received a 60% high-fat diet supplemented with 15% d-xylose, 10% XB, or 15% XB as part of the total sucrose content of the diet for ten weeks. Body weight, fat and liver weights, fasting blood glucose, and blood lipids levels were significantly reduced with XB supplementation. Levels of leptin and adipokine were also improved and lipogenic and adipogenic genes in mesenteric fat and liver were down-regulated with XB supplementation. Furthermore, pro-inflammatory cytokines, fatty acid uptake, lipolysis, and ß-oxidation-related gene expression levels in mesenteric fat were down-regulated with XB supplementation. Thus, XB exhibited therapeutic potential for treating obesity which involved suppression of fat deposition and obesity-related metabolic disorders.
Subject(s)
Adipose Tissue/metabolism , Adiposity/drug effects , Disaccharides/pharmacology , Disaccharides/therapeutic use , Obesity/drug therapy , Obesity/metabolism , Adipogenesis/drug effects , Adipogenesis/genetics , Adipose Tissue/drug effects , Animals , Blood Glucose/metabolism , Body Weight/drug effects , Cytokines/metabolism , Diet, High-Fat , Fatty Acids/metabolism , Gene Expression Regulation/drug effects , Inflammation Mediators/metabolism , Lipids/blood , Lipogenesis/drug effects , Lipogenesis/genetics , Lipolysis/drug effects , Liver/drug effects , Liver/metabolism , Mice, Inbred C57BL , Obesity/genetics , Obesity/prevention & control , Organ Size/drug effects , Oxidation-ReductionABSTRACT
Phyllodulcin is a natural sweetener found in Hydrangea macrophylla var. thunbergii. This study investigated whether phyllodulcin could improve metabolic abnormalities in high-fat diet (HFD)-induced obese mice. Animals were fed a 60% HFD for 6 weeks to induce obesity, followed by 7 weeks of supplementation with phyllodulcin (20 or 40 mg/kg body weight (b.w.)/day). Stevioside (40 mg/kg b.w./day) was used as a positive control. Phyllodulcin supplementation reduced subcutaneous fat mass, levels of plasma lipids, triglycerides, total cholesterol, and low-density lipoprotein cholesterol and improved the levels of leptin, adiponectin, and fasting blood glucose. In subcutaneous fat tissues, supplementation with stevioside or phyllodulcin significantly decreased mRNA expression of lipogenesis-related genes, including CCAAT/enhancer-binding protein α (C/EBPα), peroxisome proliferator activated receptor γ (PPARγ), and sterol regulatory element-binding protein-1C (SREBP-1c) compared to the high-fat group. Phyllodulcin supplementation significantly increased the expression of fat browning-related genes, including PR domain containing 16 (Prdm16), uncoupling protein 1 (UCP1), and peroxisome proliferator-activated receptor γ coactivator 1-α (PGC-1α), compared to the high-fat group. Hypothalamic brain-derived neurotrophic factor-tropomyosin receptor kinase B (BDNF-TrkB) signaling was upregulated by phyllodulcin supplementation. In conclusion, phyllodulcin is a potential sweetener that could be used to combat obesity by regulating levels of leptin, fat browning-related genes, and hypothalamic BDNF-TrkB signaling.
Subject(s)
Adipose Tissue, Brown/drug effects , Diet, High-Fat , Energy Metabolism/drug effects , Isocoumarins/pharmacology , Obesity/drug therapy , Subcutaneous Fat/drug effects , Sweetening Agents/pharmacology , Adiponectin/blood , Adipose Tissue, Brown/metabolism , Adipose Tissue, Brown/physiopathology , Adiposity/drug effects , Animals , Blood Glucose/drug effects , Blood Glucose/metabolism , Disease Models, Animal , Gene Expression Regulation , Hypothalamus/drug effects , Hypothalamus/metabolism , Leptin/blood , Lipids/blood , Male , Membrane Glycoproteins/metabolism , Mice, Inbred C57BL , Obesity/genetics , Obesity/metabolism , Obesity/physiopathology , Protein-Tyrosine Kinases/metabolism , RNA, Messenger/genetics , RNA, Messenger/metabolism , Signal Transduction/drug effects , Subcutaneous Fat/metabolism , Subcutaneous Fat/physiopathologyABSTRACT
BACKGROUND: Although coffee consumption is increasing rapidly, the results of previous studies regarding the association between coffee consumption and stroke risk have been conflicting. This was a multi-center cross-sectional study that aimed to evaluate the relationship between coffee consumption and stroke risk in Korean population. METHODS: Data were obtained from the Health Examinees (HEXA) Study, which involved 146,830 individuals aged 40-69 years. Coffee consumption was categorized as none, < 1 cup/day, 1 to < 3 cups/day, and ≥ 3 cups/day. We used logistic regression models to examine the association between coffee consumption and the risk of stroke while controlling for potential confounders and performed subgroup analyses. RESULTS: After adjusting for age and various possible confounders, high coffee consumption was associated with a 38% lower odds ratio for stroke in women (none vs. ≥ 3 cups/day: OR, 0.62; 95% CI 0.47-0.81; P for trend < 0.0001). No significant association was found in men (none vs. ≥ 3 cups/day: OR, 0.84; 95% CI, 0.66-1.07; P for trend = 0.1515). In analyses stratified by covariates, an inverse association between coffee consumption and stroke risk was most evident among healthy women who were younger, non-obese, non-hypertensive, non-diabetic, non-smokers, and non-alcohol drinkers. CONCLUSION: Our results suggest that higher coffee consumption may have protective benefits with regards to stroke risk in middle-aged Korean women.
Subject(s)
Coffee , Stroke/epidemiology , Aged , Asian People , Cross-Sectional Studies , Female , Humans , Life Style , Logistic Models , Male , Middle Aged , Prevalence , Republic of Korea , Risk Factors , Socioeconomic Factors , Surveys and QuestionnairesABSTRACT
Type 2 diabetes is a major public health concern worldwide. Xylobiose (XB) consists of two molecules of d-xylose and is a major disaccharide in xylooligosaccharides that are used as prebiotics. We hypothesized that XB could regulate diabetes-related metabolic and genetic changes via microRNA expression in db/db mice. For six weeks, C57BL/KsJ-db/db mice received 5% XB as part of the total sucrose content of their diet. XB supplementation improved glucose tolerance with reduced levels of OGTT AUC, fasting blood glucose, HbA1c, insulin, and HOMA-IR. Furthermore, XB supplementation decreased the levels of total triglycerides, total cholesterol, and LDL-C. The expression levels of miR-122a and miR-33a were higher and lower in the XB group, respectively. In the liver, expressions of the lipogenic genes, including, fatty acid synthase (FAS), peroxisome proliferator activated receptor γ (PPARγ), sterol regulatory element-binding protein-1C (SREBP-1C), sterol regulatory element-binding protein-2 (SREBP-2), acetyl-CoA carboxylase (ACC), HMG-CoA reductase (HMGCR), ATP-binding cassette transporter G5/G8 (ABCG5/8), cholesterol 7 alpha-hydroxylase (CYP7A1), and sterol 12-alpha-hydroxylase (CYP8B1), as well as oxidative stress markers, including superoxide dismutase 1 (SOD1), superoxide dismutase 2 (SOD2), glutathione peroxidase (GPX), and catalase, were also regulated by XB supplementation. XB supplementation inhibited the mRNA expressions levels of the pro-inflammatory cytokines, tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, interleukin (IL)-6, and monocyte chemoattractant protein (MCP)-1, as well as phosphorylation of c-Jun N-terminal kinase/stress activated protein kinase (JNK/SAPK), p38 mitogen-activated protein kinases (MAPK), and extracellular signal-regulated kinases 1/2 (ERK1/2). These data demonstrate that XB exhibits anti-diabetic, hypolipogenic, and anti-inflammatory effects via regulation of the miR-122a/33a axis in db/db mice.
Subject(s)
Diabetes Mellitus, Experimental/therapy , Disaccharides/administration & dosage , Lipogenesis/physiology , MicroRNAs/metabolism , Sweetening Agents/administration & dosage , Animals , Diabetes Mellitus, Experimental/metabolism , Dietary Supplements , Lipogenesis/genetics , Liver/metabolism , Mice , Mice, Inbred C57BL , Prebiotics/administration & dosageABSTRACT
BACKGROUND: Inflammatory bowel diseases (IBD) are related to a dysfunction of the mucosal immune system and they result from complex interactions between genetics and environmental factors, including lifestyle, diet, and the gut microbiome. Therefore, the effect of Sasa quelpaertensis leaf extract (SQE) on gut microbiota in a dextran sulfate sodium (DSS)-induced colitis mouse model was investigated with pyrosequencing of fecal samples. METHODS: Three groups of animals were examined: i) a control group, ii) a group that was received 2.5% DSS in their drinking water for 7 days, followed by 7 days of untreated water, and then another 7 days of 2.5% DSS in their drinking water, and iii) a group that was presupplemented with SQE (300 mg/kg body weight) by gavage for two weeks prior to the same DSS treatment schedule described in ii. RESULTS: SQE supplementation alleviated disease activity scores and shortened colon length compared to the other two groups. In the DSS group, the proportion of Bacteroidetes increased, whereas that the proportion of Firmicutes was decreased compared to the control group. SQE supplementation recovered the proportions of Firmicutes and Bacteroidetes back to control levels. Moreover, the diversity of microbiota in the SQE supplementation group higher than that of the DSS group. CONCLUSION: SQE was found to protect mice from microbial dysbiosis associated with colitis by modulating the microbial composition and diversity of the microbiota present. These results provide valuable insight into microbiota-food component interactions in IBD.