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      • KCI등재

        Cyanidin 3-O-β-D-Glucoside Improves Bone Indices

        Lydia Kaume,William Gilbert,Breda J. Smith,Latha Devareddy 한국식품영양과학회 2015 Journal of medicinal food Vol.18 No.6

        Oxidative stress (OS) promotes bone loss after menopause, and there is evidence that dietary antioxidants may reduce the level of OS in vivo. This study examined dose-dependent effects of blackberries (BBs) containing mainly cyanidin 3-O-β-D-glucoside (C3G) in preventing bone loss in an ovariectomized (Ovx) rat model. Nine-month-old female (N = 38) Sprague-Dawley rats were scanned using dual-energy X-ray absorptiometry for baseline whole body, bone mineral content (BMC), and bone mineral density (BMD). One group was sham operated (Sham) and three groups were ovariectomized (Ovx). The groups and corresponding diets were Sham + control diet (n = 12), Ovx + control diet (n = 12), Ovx + 5% BB (n = 7), and Ovx + 10% BB (n = 7). Control diet was AIN-93M rodent diet, and the Ovx +5% BB and Ovx + 10% BB were a diet modified to contain powdered, freeze-dried BB at levels of 5% and 10% (w/w). Following 100 days of treatment, whole body BMC and BMD were reassessed and bone specimens, blood, and 24-h urine samples were collected for analyses. Findings indicate that ovariectomy (Ovx) compromised whole body BMC and trabecular microarchitecture of the proximal tibia and fourth lumbar vertebra. C3G-rich BB at the level of 5% modestly protected BMDs, loss of the tibia, lumbar vertebra, and femur by 2.4%, 2.7%, and 4.3% (P < .0013; .0437; .0004), respectively. BB 5% treatment significantly prevented loss of tibial trabecular bone volume and trabecular number by 37% and 21%, respectively (P < .05), and also significantly prevented tibial trabecular separation by 22%. We conclude that C3G-rich BB treatment at the level of 5% (w/w) but not at 10% (w/w) may modestly reduce Ovx-induced bone loss evident by improved tibial, vertebral, and femoral BMD values, and tibial bone microstructural parameters. Bone protective effects may be as a result of the synergistic effects of phenolic compounds; however, further work is required to determine BBs’ specific mechanisms of action.

      • KCI등재

        Dietary Bitter Melon Seed Increases Peroxisome Proliferator-Activated Receptor-γ Gene Expression in Adipose Tissue, Down-Regulates the Nuclear Factor-κB Expression, and Alleviates the Symptoms Associated with Metabolic Syndrome

        Vidya Gadang,William Gilbert,Navam Hettiararchchy,Ronny Horax,Laxmansa Katwa,Latha Devareddy 한국식품영양과학회 2011 Journal of medicinal food Vol.14 No.1

        The objective of this study was to examine the extent to which bitter melon seed (BMS) alleviates the symptoms associated with metabolic syndrome and elucidate the mechanism by which BMS exerts beneficial effects. Three-month-old female Zucker rats were assigned to following groups: lean control (L-Ctrl), obese control (O-Ctrl), and obese + BMS (O-BMS). The control groups were fed AIN-93M purified rodent diet, and the O-BMS group was fed AIN-93M diet modified to contain 3.0% (wt/wt) ground BMS for 100 days. After 100 days of treatment, BMS supplementation in the obese rats lowered the total serum cholesterol by 38% and low-density lipoprotein-cholesterol levels by about 52% and increased the ratio of serum high-density lipoprotein-cholesterol to total cholesterol compared to the O-Ctrl group. The percentage of total liver lipids was about 32% lower and serum triglyceride levels were 71% higher in the O-BMS group compared to the O-Ctrl group. Serum glucose levels were significantly lowered partly because of the increase in the serum insulin levels in the BMS-based diet groups. BMS supplementation increased the expression of peroxisome proliferator-activated receptor-γ (PPAR-γ) in the white adipose tissue of the obese rats significantly (P<.05) and down-regulated the expression of PPAR-γ, nuclear factor-κB (NF-κB), and interferon-γ mRNA in heart tissue of the obese rats. The findings of this study suggest that BMS improves the serum and liver lipid profiles and serum glucose levels by modulating PPAR-γ gene expression. To our knowledge, this study for the first time shows that BMS exerts cardioprotective effects by down-regulating the NF-κB inflammatory pathway.

      • KCI등재후보

        Effect of Vitamin E on Lipid Parameters in Ovariectomized Rats

        Bahram H. Arjmandi,Edralin A. Lucas,Tai-Yuan Chen,Sheau C. Chai,Latha Devareddy,Shanil Juma,Cheng-I Wei,Yamini B. Tripathi,Bruce P. Daggy,Deng-Fwu Hwang 한국식품영양과학회 2006 Journal of medicinal food Vol.9 No.1

        The risk of cardiovascular disease drastically increases at the onset of menopause, in part, because of rise inblood cholesterol and unfavorable changes in lipid profile. This study was designed to investigate the dose-dependent effectsof vitamin E supplementation on lipid parameters in ovariectomized (ovx) rats. Sixty 12-month-old female Sprague-Dawleyrats were either sham-operated (sham; one group) or ovx (four groups). All rats were maintained on a semipurified casein-based diet (AIN-93M; 75 IU vitamin E/kg of diet) for a period of 120 days. Thereafter, ovx rats were placed on one of fourdoses of vitamin E treatment (75, 300, 525, or 750 IU vitamin E/kg of diet), while the sham group was continued on 75 IUvitamin E/kg of diet for 100 days. Ovariectomy tended to increase (by 24%, P. 0.1) serum nonhigh-density lipoprotein(HDL) cholesterol and decrease (by 14%, P. 0.1) HDL cholesterol. Vitamin E did not have any significant effects on serumlipid parameters. Liver total lipids were notably increased (P. .001) in ovx animals, and supplementation with vitamin E at525 IU/kg of diet was able to significantly reduce liver total lipids by 13%. Additionally, ovariectomy caused an increase inserum glucose and liver C18:1fatty acid concentrations along with decreases in C18:0, C20:4, and C22:6fatty acid concentra-tions. These alterations on liver fatty acid profiles were unaffected by vitamin E. The findings of this study suggest that vit-amin E supplementation moderately improves lipid parameters in ovarian hormone-deficient rats.

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