ABSTRACT
BACKGROUND/OBJECTIVES@#A cross-sectional study was undertaken to evaluate fluid intake and hydration status in association with cognitive function among 230 adolescents (10–14 years of age) in Petaling Perdana, Selangor, Malaysia. @*SUBJECTS/METHODS@#Urine color was used to measure hydration status, while fluid intake was assessed using the 15-item beverage intake questionnaire. Cognitive function was assessed using the Wechsler Intelligence Scale for Children, Fourth Edition. @*RESULTS@#More than half of the adolescents were mildly or moderately dehydrated (59.6%) and only one-third (33.0%) were well hydrated. Among the daily fluid types, intakes of soft drinks (r = −0.180; P = 0.006), sweetened tea (r = −0.184; P= 0.005) and total sugarsweetened beverages (SSBs) (r = −0.199; P= 0.002) were negatively correlated with cognitive function. In terms of hydration status, cognitive function score was significantly higher (F-ratio = 4.102; P= 0.018) among hydrated adolescents (100.38 ± 12.01) than in dehydrated (92.00 ± 13.63) counterparts. Hierarchical multiple linear regression analysis, after adjusting for socio-demographic factors, showed that soft drinks (β = −0.009; P< 0.05) and sweetened tea (β = −0.019; P< 0.05) negatively predicted cognitive function (ΔR 2 = 0.044). When further control for sources of fluid, hydration status (β = −2.839; P< 0.05) was shown to negatively predict cognitive function (ΔR2 = 0.021). The above variables contributed 20.1% of the variance in cognitive function. @*CONCLUSIONS@#The results highlight the links between fluid intake (soft drinks, sweetened tea, total SSBs) and hydration status with cognitive function in adolescents. Interventions aimed at decreasing the consumption of SSBs and increasing hydration status through healthy fluid choices, such as water, could improve cognitive performance in adolescents.
ABSTRACT
This study aimed to investigate the absorption mechanism of three curcumin constituents in rat small intestines. Self-emulsification was used to solubilize the three curcumin constituents, and the rat in situ intestinal perfusion method was used to study factors on drug absorption, including drug mass concentration, absorption site, and the different types and concentrations of absorption inhibitors. Within the scope of experimental concentrations, three curcumin constituents were absorbed in rat small intestines through the active transport mechanism.
Subject(s)
Animals , Male , Female , Adjuvants, Pharmaceutic/pharmacology , Curcumin/analogs & derivatives , Curcumin/pharmacokinetics , Enzyme Inhibitors/pharmacokinetics , Intestinal Absorption , Intestine, Small/metabolism , Reference Values , Time Factors , Uncoupling Agents/pharmacology , Verapamil/pharmacology , Probenecid/pharmacology , Reproducibility of Results , Chromatography, High Pressure Liquid/methods , Rats, Sprague-Dawley , ATP-Binding Cassette Transporters/antagonists & inhibitors , 2,4-Dinitrophenol/pharmacokinetics , Curcumin/chemistry , Multidrug Resistance-Associated Proteins/analysis , Multidrug Resistance-Associated Proteins/antagonists & inhibitors , Emulsions , Perfusion Imaging/methods , Intestinal Absorption/drug effects , Intestine, Small/drug effectsABSTRACT
The intestinal lymph pathway plays an important role in the pathogenesis of organ injury following superior mesenteric artery occlusion (SMAO) shock. We hypothesized that mesenteric lymph reperfusion (MLR) is a major cause of spleen injury after SMAO shock. To test this hypothesis, SMAO shock was induced in Wistar rats by clamping the superior mesenteric artery (SMA) for 1 h, followed by reperfusion for 2 h. Similarly, MLR was performed by clamping the mesenteric lymph duct (MLD) for 1 h, followed by reperfusion for 2 h. In the MLR+SMAO group rats, both the SMA and MLD were clamped and then released for reperfusion for 2 h. SMAO shock alone elicited: 1) splenic structure injury, 2) increased levels of malondialdehyde, nitric oxide (NO), intercellular adhesion molecule-1, endotoxin, lipopolysaccharide receptor (CD14), lipopolysaccharide-binding protein, and tumor necrosis factor-α, 3) enhanced activities of NO synthase and myeloperoxidase, and 4) decreased activities of superoxide dismutase and ATPase. MLR following SMAO shock further aggravated these deleterious effects. We conclude that MLR exacerbates spleen injury caused by SMAO shock, which itself is associated with oxidative stress, excessive release of NO, recruitment of polymorphonuclear neutrophils, endotoxin translocation, and enhanced inflammatory responses.