Abstract Background The aim of this study was to examine the characteristics of diurnal cortisol rhythm in childhood obesity and its relationships with anthropometry, pubertal stage and physical activity. Methods Thirty-five children with obesity (median age: 11.80[interquartile range 10.30, 13.30] and median BMI z-score: 3.21[interquartile range 2.69, 3.71]) and 22 children with normal weight (median age: 10.85[interquartile range 8.98, 12.13] and median BMI z-score: − 0.27[interquartile range − 0.88, 0.35]) were recruited. Saliva samples were collected at 08:00, 16:00 and 23:00 h. Cortisol concentrations at 3 time points, corresponding areas under the curve (AUCs) and diurnal cortisol slope (DCS) were compared between the two groups. Anthropometric measures and pubertal stage were evaluated, and behavioural information was obtained via questionnaires. Results Children with obesity displayed significantly lower cortisol 08:00 (median [interquartile range]: 5.79[3.42,7.73] vs. 8.44[5.56,9.59] nmol/L, P = 0.030) and higher cortisol 23:00 (median [interquartile range]: 1.10[0.48,1.46] vs. 0.40[0.21,0.61] nmol/L, P < 0.001) with a flatter DCS (median [interquartile range]: − 0.29[− 0.49, 0.14] vs. -0.52[− 0.63, 0.34] nmol/L/h, P = 0.006) than their normal weight counterparts. The AUC increased with pubertal development (AUC 08:00–16:00 : P = 0.008; AUC 08:00–23:00 : P = 0.005). Furthermore, cortisol 08:00 was inversely associated with BMI z-score (β = − 0.247, P = 0.036) and waist-to-height ratio (WHtR) (β = − 0.295, P = 0.027). Cortisol 23:00 was positively associated with BMI z-score (β = 0.490, P <0.001), WHtR (β = 0.485, P <0.001) and fat mass percentage (FM%) (β = 0.464, P <0.001). Absolute values of DCS were inversely associated with BMI z-score (β = − 0.350, P = 0.009), WHtR (β = − 0.384, P = 0.004) and FM% (β = − 0.322, P = 0.019). In multivariate analyses adjusted for pubertal stage and BMI z-score, Cortisol 08:00 , AUC 08:00–16:00 and absolute values of DCS were inversely associated with the relative time spent in moderate to vigorous intensity physical activity ( P < 0.05). AUC 16:00–23:00 was positively associated with relative non-screen sedentary time and negatively associated with sleep ( P < 0.05). Conclusions The disorder of diurnal salivary cortisol rhythm is associated with childhood obesity, which is also influenced by puberty development and physical activity. Thus, stabilizing circadian cortisol rhythms may be an important approach for childhood obesity.
Objective
The effects of cigarette smoke exposure on airway ciliary structure in COPD rats were evaluated by the comprehensive evaluation of airway cilia ultrastructure.
Methods
Wister rats were randomly divided into two experimental groups (CON: control group, n=5; CS: cigarette smoke group, n=5). Rats in CS group were exposed to passive smoking for 45 days.The abnormalities of ciliary ultra-structures and the fluorescence intensity of ciliated microtubules were measured by electron microscopy (EM) and confocal microscopy.
Results
The ciliary ultrastructure abnormalities were found in CS group with typical cilia membrane vesiculation and dynein arm deficiency under EM.The vesiculation in CS group significantly increased (7.36±2.38) compared with CON group (0.66±1.21). Meanwhile, the microtubule of cilia in CS group decreased, with immune fluorescence intensity was (53.46±13.28), compared to CON group (120.00±26.86)(P<0.05).
Conclusions
Cigarette smoking could affect the ciliated epithelium in smoking induced airway rats model, with ciliary ultrastructural abnormalities and absence of cilia microtubules.
Key words:
Chronic obstructive pulmonary disease; Cilia; Microtubule; Ciliary ultrastructure; Cigarette smoke
Benzodione-3, triclosan, and parabens are well-known environmental endocrine-disrupting substances that may contribute to weight changes. Our aim was to determine whether urinary levels of benzodone-3, triclosan and parabens were associated with obesity and abdominal obesity. We used data from the National Health and Nutrition Examination Survey (NHANES) in 2007–2012 of 1894 adults aged >20 years. Online solidphase extraction in conjunction with high-performance liquid chromatography-tandem mass spectrometry was used to evaluate urinary levels of benzodione-3, triclosan, and parabens. We first used a logistic regression model to assess the association, and then built a mediator model using blood lipids as a mediator. Overall, there were 706 (37.3%) cases of obesity and 1083 (57.2%) cases of abdominal obesity. Binary logistic regression showed that urinary BP-3 and benzoate were negatively associated with general obesity (p<0.001). Compared with the lowest quartile, the odds ratios with 95% confidence intervals (CIs) across increasing quartiles were 1.173 (0.88, 1.56), 0.911 (0.68, 1.22), and 0.658 (0.48, 0.90) for urinary benzodione-3; 0.611 (0.46, 0.82), 0.627 (0.46, 0.85), and 0.618 (0.45, 0.85) for MP and 0.693 (0.52, 0.93), 0.627 (0.46, 0.86), and 0.544 (0.39, 0.75) for PP. Urinary triclosan was not correlated with general obesity. There was also a similar association between exposure to these chemicals and abdominal obesity. Based on our mediation analysis, HDL mediates the effects of BP3, triclosan, and parabens on obesity levels, while LDL only mediates the effects of BP3. Triglycerides are not a mediator. These results highlight the importance of longitudinally assessing the effects of environmental exposures to benzodone-3, triclosan and parabens on human obesity.
Exposure to the antibacterial agent triclosan (TCS) is associated with abnormal placenta growth and fetal development during pregnancy. Peroxisome proliferator-activated receptor γ (PPARγ) is crucial in placenta development. However, the mechanism of PPARγ in placenta injury induced by TCS remains unknown. Herein, we demonstrated that PPARγ worked as a protector against TCS-induced toxicity. TCS inhibited cell viability, migration, and angiogenesis dose-dependently in HTR-8/SVneo and JEG-3 cells. Furthermore, TCS downregulated expression of PPARγ and its downstream viability, migration, angiogenesis-related genes HMOX1, ANGPTL4, VEGFA, MMP-2, MMP-9, and upregulated inflammatory genes p65, IL-6, IL-1β, and TNF-α in vitro and in vivo. Further investigation showed that overexpression or activation (rosiglitazone) alleviated cell viability, migration, angiogenesis inhibition, and inflammatory response caused by TCS, while knockdown or inhibition (GW9662) of PPARγ had the opposite effect. Moreover, TCS caused placenta dysfunction characterized by the significant decrease in weight and size of the placenta and fetus, while PPARγ agonist rosiglitazone alleviated this damage in mice. Taken together, our results illustrated that TCS-induced placenta dysfunction, which was mediated by the PPARγ pathway. Our findings reveal that activation of PPARγ might be a promising strategy against the adverse effects of TCS exposure on the placenta and fetus.
Iodide accumulates in milk at a concentration that is more than an order of magnitude higher than the iodide concentration in maternal plasma. In earlier studies from our laboratory, we have shown that prolactin (PRL) enhances iodide accumulation by two- to threefold in cultured mammary tissues taken from pregnant mice. In the present studies, we demonstrate via Western blotting techniques that prolactin elevates the quantity of the sodium iodide symporter (NIS) in cultured mouse mammary tissues. In time-course studies, the onset of the PRL effect of NIS accumulation was found to be between 4 and 16 h after addition of PRL to the explants. The lowest PRL concentration that elicited a significant response was 1 ng/ml, and a maximum effect was elicited with PRL concentrations >100 ng/ml. Actinomycin D, cycloheximide, and thiocyanate abolished the PRL effect on NIS accumulation, whereas perchlorate was without effect. These studies suggest that the PRL stimulation of iodide accumulation in milk is mediated, at least in part, by the PRL stimulation of NIS accumulation in mammary gland tissues. These studies further demonstrate that the PRL effect on NIS accumulation occurs via an RNA protein synthesis-dependent mechanism.
'/%3e%3cuse xlink:href='%23a' transform='rotate(23.036 .093 25.536)'/%3e%3cuse xlink:href='%23a' transform='rotate(45.87 1.273 16.18)'/%3e%3cuse xlink:href='%23a' transform='rotate(69.945 .996 12.078)'/%3e%3cuse xlink:href='%23a' transform='rotate(20.66 -19.689 31.932)'/%3e%3c/svg%3e)
