Background Dietary culture affects people's cognition and attitudes toward nutrition, and it even dictates people's dietary behavior. This study aimed to assess the dietary-culture-related KAP of Chinese netizens during the corona virus disease 2019(COVID-19) pandemic. Methods A cross-sectional survey was conducted using an online KAP questionnaire in China. Volunteers were recruited at Southwest Medical University and were first trained to unify standards of distributing questionnaires. Participants were recruited by convenient- and snowball-sampling methods. Multiple regression analysis was used to analyze the influential factors. Results After 50 days of investigation, 3514 participants (40.6% men) were valid. The mean score of netizens’ nutrition knowledge was 3.9 ± 2.2 and the mean awareness rate was 31.7%. Women participants in the age group of 30–39 with higher education level had higher nutrition knowledge qualification rate. During the COVID-19 pandemic, the positive rate of attitude toward dietary-culture-related nutrition was 93.7%, and women netizens who had higher level of education and immigrated from other places had better attitudes. Moreover, the positive rate of dietary habits was 90.7%, and older women netizens had better dietary behavior. Conclusions Netizens’ knowledge of nutrition was poor, but their dietary habits and attitudes toward dietary-culture-related nutrition were generally positive, which was also a great progress for Chinese people.

Background Non-alcoholic fatty liver disease (NAFLD) is a common hepatic metabolic disorder that is characterized by the dyshomeostasis of lipid metabolism. It is usually accompanied by insulin resistance and hyperlipidemia. Regulating lipid metabolism via the peroxisome proliferator-activated receptor alpha (PPARα) pathway in the liver could potentially constitute a new target for elucidating the pathology of NAFLD. Therefore, we aimed to explore the PPARα pathway in a high-fat diet (HFD)-induced NAFLD rat model by non-competitive inhibitor MK886. Method Male Wistar rats were randomly divided into control (CON), HFD, HFD + MK 886 groups. After 14 weeks of intervention, body weight, energy intake, liver weight, serum biochemical markers, histology, morphology, and protein expression of PPARα, CPT1A, CD36, FABP1 in the liver were detected. Results Inhibiting PPARα by MK886 significantly reduced body weight; it improved hepatic function and serum lipid parameters. Furthermore, MK886 ameliorated hepatic steatosis by reducing the levels of CD36, PPARα and CPT1A. Conclusion The study indicates that inhibiting PPARα pathway could improve hepatic homeostasis by improving liver function and alleviating hepatic steatosis; this validated the role of PPARα and its downstream protein in hepatic fatty acid metabolism in NAFLD.

Backgound Non-alcoholic fatty liver disease (NAFLD) is a common hepatic metabolic disorder that is characterized by the dyshomeostasis of lipid metabolism. It is usually accompanied by insulin resistance and hyperlipidemia. Regulating lipid metabolism via the peroxisome proliferator-activated receptor alpha (PPARα) pathway in the liver could potentially constitute a new target for elucidating the pathology of NAFLD. Therefore, we aimed to explore the inhibitory role of MK886 through PPARα pathway in a high-fat diet (HFD)-induced NAFLD model. Method Male Wistar rats were randomly divided into control (CON), HFD, HFD + MK 886 groups. After 14 weeks of intervention, we evaluated body weight, energy intake, liver weight, serum inflammatory parameters, serum biochemical markers, histology, morphology, and lipid metabolism-associated proteins in the liver. Results MK886 significantly reduced body weight; it improved hepatic function, inflammatory cytokine levels, and serum lipid parameters. Furthermore, MK886 ameliorated hepatic steatosis by reducing the levels of lipid uptake-related proteins and β-oxidation-related proteins. Conclusion Our study indicates that MK886 could improve hepatic homeostasis by improving liver function and alleviating systemic inflammation and hepatic steatosis; this provides a basis for future drug development and future clinical trials.