Effects of dietary polyphenols on maternal and fetal outcomes in maternal diabetes.

The incidences of short-term or long-term adverse maternal and fetal outcomes caused by maternal diabetes are increasing. Due to toxicity or side effects, economic pressures, and other problems associated with injections or oral hypoglycemic drugs, many researchers have investigated natural treatment methods. Polyphenols can protect against chronic pathologies by regulating numerous physiological processes and provide many health benefits. Moreover, polyphenols have anti-diabetic properties and can be used to treat diabetic complications. Diets rich in polyphenols are beneficial to pregnant women with diabetes. Here, we review the epidemiological and experimental evidence on the impact of dietary polyphenols on maternal and fetal outcomes in pregnant women with diabetes, and the effects of polyphenols on biological changes and possible mechanisms. Previous data (mainly from in vitro and animal experiments) showed that polyphenols can alleviate gestational diabetes mellitus and diabetic embryopathy by reducing maternal hyperglycemia and insulin resistance, alleviating inflammation and oxidative stress, and regulating related signaling pathways. Although polyphenols have shown many health benefits, further research is needed to better understand the complex interactions between polyphenols and maternal diabetes.

The mediating role of general academic emotions in burnout and procrastination among Chinese medical undergraduates during the COVID-19 pandemic: A cross-sectional study.

Background: Academic procrastination has become more prevalent during the COVID-19 pandemic due to teaching/learning changes. This phenomenon induces academic burnout, which is already serious among medical students. However, the academic emotion, which is the factor most vulnerable to changes in the academic environment, is still unknown. Therefore, the current study aimed to investigate the mediating role of general academic emotions in procrastination and burnout among Chinese medical students during the COVID-19 pandemic. Methods: This cross-sectional study enrolled 995 medical students from China Medical University. We applied the Chinese version of the Maslach Burnout Inventory Student Survey (MBI-SS), the Aitken Procrastination Inventory (API) and the General Academic Emotion Questionnaire for College Students (GAEQ) to evaluate the variables of interest. We examined the mediation effects of GAEs by hierarchical linear regression analysis. Results: Correlation analyses showed a significant positive correlation between procrastination and burnout. Procrastination and burnout positively and negatively correlated with negative academic emotions, respectively. Hierarchical linear regression analyses showed that procrastination had positive associations with negative academic emotions, while it had negative associations with positive academic emotions. The contributions (as mediators) of GAEs to burnout and procrastination were 21.16% (NAEs), 29.75% (PAEs), 54.25% (NDEs) and 23.69% (PDEs). Conclusions: The results indicate that academic emotions had mediating effects on procrastination and burnout. Medical students' worries about the uncertainty of the learning environment may have exacerbated academic burnout. Targeted improvements in the teaching environment to communicate encouragement and reduce anxiety and helplessness among medical undergraduates for implementing medical education while preventing and controlling the infection.

Effects of perinatal di (2-ethylhexyl) phthalate exposure on thyroid function in rat offspring.

Di (2-ethylhexyl) phthalate (DEHP) is a commonly used plasticizer in industry and displays the characteristics of an endocrine disruptor. Disorders of the maternal thyroid hormone (TH) during pregnancy can cause adverse effects on the fetus. We investigated the effects and possible mechanism of perinatal DEHP exposure on the thyroid function of pups. Pregnant female Wistar rats were randomly divided into four groups and received doses of DEHP of 0, 30, 300, 750 mg/kg/day by gavage at from gestational day (GD) 0 to postnatal day (PN) 21. The concentration of serum THs and the ultrastructure of thyroid follicular cells in the offspring were examined. Related protein level and gene expression of thyroid proteins in pups were analyzed by western blotting and real-time PCR. We found that DEHP significantly reduced total thyroxine (TT4) and increased thyroid stimulating hormone (TSH) in pups, while total triiodothyronine (TT3) showed no change. Thyroid follicular cells ultrastructure was damaged in DEHP exposed pups as viewed by electron microscopy. Furthermore, exposure to DEHP significantly increased protein and mRNA levels of thyroid transcription factor 1 (TTF-1), paired box 8 (PAX8), sodium iodide symporter (NIS) and thyroid peroxidase (TPO) in pups. In addition, levels of deiodinases of pups were also affected. These findings indicated that DEHP can disrupt thyroid function by damaging thyroid follicles and affecting TTF-1, PAX8, NIS, TPO and the deiodinase protein family.

Maternal di-(2-ethylhexyl) phthalate exposure inhibits cerebellar granule precursor cell proliferation via down-regulating the Shh signaling pathway in male offspring.

Di-(2-ethylhexyl) phthalate (DEHP) is an endocrine disrupting chemical (EDC) widely used as a plasticizer in many materials. Epidemiological investigations have shown that DEHP exposure during early development is related to cerebellar-related adverse neurodevelopmental outcomes. However, animal studies involving the effect of DEHP exposure on cerebellar development have rarely been reported and the potential mechanisms are unclear. The aim of this study was to investigate the effect of maternal DEHP exposure on the proliferation of cerebellar granule cell precursor cells (GCPs) and the mechanisms involved. Wistar rats were randomly assigned to four exposure groups and given 0, 30, 300, or 750 mg/kg/d DEHP by intragastric administration from gestational day (GD) 0 to postnatal day (PN) 21. Exposure to 300 and 750 mg/kg/d DEHP restrained GCPs proliferation and impaired neurodevelopment for males. Furthermore, exposure to 300 and 750 mg/kg/d DEHP decreased male pups protein expressions and mRNA levels of molecules related to proliferation, including Shh, Gli1, N-Myc, CyclinD1. In addition, the estrogen level and aromatase expression also reduced in male pups after maternal exposure to DEHP. However, effects on females were not obvious. These results suggested that 300 and 750 mg/kg/d DEHP exposure inhibit the proliferation of GCPs in male offspring and ultimately contribute to the impairment of neuromotor development. This, may be caused by the down-regulation of Shh signaling. And the susceptibility of male offspring to DEHP exposure may be attributed to the decreased estrogen level and aromatase expression in male pup's cerebellum.

Exposure to Di-(2-ethylhexyl) Phthalate During Perinatal Period Gender-Specifically Impairs the Dendritic Growth of Pyramidal Neurons in Rat Offspring.

Di-(2-ethylhexyl) phthalate (DEHP), as a prevalent xenoestrogen endocrine disrupter, is omnipresent in the environment and commonly used in polyethylene plastic products. Although DEHP has potential adverse effects on multisystem organs, damage to the central nervous system is more significant. However, the consequences and mechanisms of DEHP exposure remain to be explored. The aim of this study was to investigate the effects and related mechanisms of maternal DEHP exposure on dendritic development of hippocampal pyramidal neurons in a rat model. Pregnant Wistar rats were intragastrically administrated either vehicle or DEHP (30, 300, and 750 mg/kg/d) from gestation day 0 to postnatal day (PN) 21. The dendritic length and complexity of dendritic arbors' pattern in pyramidal neurons of the hippocampus were measured using Golgi-Cox staining and Sholl analysis. The expression of dendritic development-related proteins was detected using western blot and immunofluorescence staining. DEHP-treated male but not female pups showed an obvious decrease in the total length and branching numbers of basal dendrites on PN7, PN14, and PN21. The phosphorylation of MAP2c, stathmin, and JNK1 in the male pup hippocampus was significantly decreased in DEHP treatment groups compared to controls. However, protein expression alteration in the hippocampus of female offspring was not observed. In summary, our study indicated that DEHP has a gender-specific negative impact on the dendritic growth of CA1 pyramidal neurons in male offspring of a rat model of DEHP exposure. The adverse impact may be related to the dysregulation of phosphorylated and total MAP2c and stathmin mediated by JNK1.