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1.
J Exp Child Psychol ; 244: 105956, 2024 Aug.
Article in English | MEDLINE | ID: mdl-38735222

ABSTRACT

Screen-based sedentary behavior (SSB) is a significant risk factor for the health of school-aged children, and guidelines recommend limiting SSB to 2 hr per day. This study aimed to examine association and potential mechanisms between SSB and executive function (EF) by comparing Stroop performance and frontal hemodynamic responses between children with and without excessive SSB. A total of 70 children aged 10 to 15 years were recruited and divided into two groups: excessive screen time (≥2 hr/day; n = 35; ES group) and normal screen time (<2 hr/day; n = 35; NS group). The Chinese version of the Adolescent Sedentary Activities Questionnaire was used to assess SSB, whereas EF was evaluated using the Stroop task. The frontal hemodynamic responses during the Stroop task were measured using functional near-infrared spectroscopy. The results indicated that the ES group had lower accuracy, longer reaction times, and greater activation in the bilateral dorsolateral prefrontal cortex (DLPFC) and left pre-supplementary motor area (Pre-SMA) compared with the NS group. Furthermore, significant correlations were observed between Stroop performance and cortical activation in the left DLPFC and Pre-SMA. These findings demonstrate that excessive SSB is associated with poor EF, which may be explained by a decrease in neural efficiency of the left DLPFC and Pre-SMA.


Subject(s)
Executive Function , Screen Time , Sedentary Behavior , Spectroscopy, Near-Infrared , Stroop Test , Humans , Child , Male , Female , Spectroscopy, Near-Infrared/methods , Executive Function/physiology , Adolescent , Reaction Time , Dorsolateral Prefrontal Cortex
2.
Anim Nutr ; 16: 34-44, 2024 Mar.
Article in English | MEDLINE | ID: mdl-38131029

ABSTRACT

Skatole, a strong fecal odor substance, is generated through microbial degradation of tryptophan in the animal hindgut. It easily accumulates in adipose tissue and affects meat quality. In this study, the effect of mulberry leaf supplementation on skatole in finishing pigs was studied. In a 35-day trial, 20 finishing pigs (barrows and gilts) were fed with a basal diet or basal diet with 6% mulberry leaves. Growth performance of the pigs (n = 10) was automatically recorded by a performance-testing feeder system and 8 pigs in each treatment were slaughtered and sampled for the remaining tests. Skatole and short-chain fatty acids were detected using HPLC and gas chromatography, respectively. Fecal microbiota were analyzed using 16S rRNA gene sequencing. The metabolomics analysis of feces and serum was performed with UHPLC-MS/MS. The major cytochrome P450 (CYP) enzymes that catalyze skatole degradation in the liver were tested by using RT-PCR and Western blot. Effects of major bioactive compounds in mulberry leaves on the CYP genes were verified in the hepatic cell line HepG2 in an in vitro test (n = 3). In finishing pigs, mulberry leaf supplementation had no significant effect on the average daily gain, average daily feed intake, and feed conversion ratio (P > 0.05), but reduced skatole levels in feces, serum, and backfat (P < 0.05), and increased acetic acid levels in feces (P = 0.027). Mulberry leaf supplementation decreased the relative abundance of the skatole-producing bacteria Megasphaera and Olsenella (P < 0.05). Indole-3-acetic acid, the intermediate that is essential for skatole production, was significantly reduced in feces by mulberry leaf supplementation (P < 0.05) and was positively correlated with skatole content in feces (P = 0.004). In pigs treated with mulberry leaves, liver CYP1A1 expression was increased (P < 0.05) and was negatively correlated with skatole content in backfat (P = 0.045). The in vitro test demonstrated that mulberry leaf polyphenols and polysaccharides could directly stimulate CYP1A1 expression in hepatic cells. These findings suggest that mulberry leaf supplementation reduces skatole production and deposition in finishing pigs by regulating the gut microbiota and promoting skatole degradation in liver.

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