IntroductionThe study aimed to explore the association of serum 25(OH)D3 and hepatic steatosis in non-alcoholic fatty liver disease (NAFLD) patients and to determine whether the effect of vitamin D (VD) is mediated by activation of the peroxisome proliferator-activated receptor α (PPARα) pathway.MethodsThe study contained a case-control study, in vivo and in vitro experiments. A case-control study was conducted to compare serum parameters between NAFLD patients and controls and to evaluate the association of 25(OH)D3 and NAFLD. In vivo study, male Wistar rats were randomly divided into control and model groups, fed a standard chow diet and a high-fat diet (HFD), respectively, for 7 weeks to generate an NAFLD model. Then, the rats were treated with VD and a PPARα antagonist (MK886) for 7 weeks. Tissue and serum were collected and assessed by biochemical assays, morphological analysis, histological analysis, and western blot analysis. In vitro, HepG2 cells were incubated with oleic acid (OA) to induce steatosis, which was evaluated by staining. HepG2 cells were pretreated with MK886 followed by calcitriol treatment, and differences in lipid metabolism-related proteins were detected by western blot.ResultsNAFLD patients were characterized by impaired liver function, dyslipidemia, and insulin resistance. Serum 25(OH)D3 was negatively associated with alanine aminotransferase (ALT) in NAFLD. VD deficiency was a risk factor for patients with no advanced fibrosis. Adequate VD status (25(OH)D3 >20 ng/mL) had a protective effect in patients after adjustment for confounding variables. NAFLD rats showed hyperlipidemia with severe hepatic steatosis, systematic inflammation, and lower serum 25(OH)D3. VD treatment ameliorated hepatic steatosis both in NAFLD rats and OA-induced HepG2 cells. Further, MK886 inhibited the anti-steatosis effect of VD.ConclusionThe study revealed that an adequate VD level may act as a protective factor in NAFLD and that VD may alleviate hepatic steatosis via the PPARα signaling pathway.
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.
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