Home quarantine due to the global coronavirus disease 2019 (COVID-19) pandemic has had a significant impact on children. Lifestyle changes have led to an increase in precocious puberty (PP) among girls, and the underlying risk factors for this remain unclear. Thus, we aimed to assess the influence of environmental, genetic, nutritional, and other lifestyle factors on the risk of PP in girls. We evaluated the incidence of new-onset PP in girls during home quarantine for COVID-19 and analyzed the potential risk factors. This was a retrospective questionnaire and medical record-based study involving 22 representative medical units from 13 cities in Henan Province, China. Girls with new-onset PP (central precocious puberty, 58; premature thelarche, 58; age, 5–9 years) between February 2020 and May 2020 were included, along with 124 healthy, age-matched controls. The number of new-onset PP cases reported during the study period was compared with that reported between February and May in 2018 and 2019. Patients’ families completed a questionnaire to assess potential risk factors. There was a 5.01- and 3.14-fold increase in the number of new-onset PP cases from 2018 to 2020 and from 2019 to 2020, respectively; the differences were statistically significant ( p < 0.01 ). High-risk factors for PP included longer time spent using electronic devices, decreased exercise time, higher body mass index, vitamin D deficiency, young age (<12 years) of mother during menarche, consumption of fried food and processed meat, residence in rural areas, and consumption of off-season fruits. Thus, we found that lifestyle changes caused due to the COVID-19 pandemic led to a significant increase in PP in girls. Management of the risk factors identified in this study may help in PP prevention.

Background/Aims: Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease. This study aims to investigate whether chloride channel 2 (ClC-2) is involved in high fat diet (HFD)-induced NAFLD and possible molecular mechanisms. Methods: ClC-2 expression was liver-specifically downregulated using adeno-associated virus in C57BL/6 mice treated with a chow diet or HFD for 12 weeks. Peripheral blood and liver tissues were collected for biochemical and pathological estimation respectively. Western blotting was applied to detect the protein expressions of lipid synthesis-related enzymes and the phosphorylated level of IRS-1, Akt and mTOR. Results: ClC-2 mRNA level was significantly increased in patients with non-alcoholic steatohepatitis, which positively correlated with the plasma levels of alanine transaminase (ALT), aspartate transaminase (AST) and insulin. Knockdown of ClC-2 in liver attenuated HFD-induced weight gain, obesity, hepatocellular ballooning, and liver lipid accumulation and fibrosis, accompanied by reduced plasma free fatty acid (FFA), triglyceride (TG), total cholesterol (TC), ALT, AST, glucose and insulin levels and homeostasis model of insulin resistance (HOMA-IR) value. Moreover, HFD-treated mice lacking ClC-2 showed inhibited hepatic lipid accumulation via regulating lipid metabolism through decreasing sterol regulatory element binding protein (SREBP)-1c expression and its downstream targeting enzymes such as fatty acid synthase (FAS), HMG-CoA reductase (HMGCR) and acetyl-Coenzyme A carboxylase (ACCα). In addition, in vivo and in vitro results demonstrated that ClC-2 downregulation in HFD-treated mice or HepG2 cells increased the sensitivity to insulin via activation of IRS-1/Akt/mTOR signaling pathway. Conclusion: Our present study reveals a critical role of ClC-2 in regulating metabolic diseases. Mice lacking ClC-2 are associated with a remarkably beneficial metabolic phenotype, suggesting that decreasing ClC-2 may be an attractive therapeutic strategy for the treatment of NAFLD.

No abstract

No abstract