Project description:Ramulus Mori (Sangzhi) alkaloids (SZ-A) improves lipid metabolism and adipose tissue inflammation in HFD-induced obese mice.This study compares transcriptome profiling (RNA-seq) in the epididymal adipose tissue of normal chow, high-fat diet (HFD) control and SZ-A-treated HFD mice to verify the regulatory mechanisms of SZ-A. These results demonstrated that SZ-A regulates lipid metabolism and inflammation.
Project description:CNE-2Z cells transfected with an empty vector or a TIPE1 lentiviral vector were collected for gene expression detection. Some of them, for instance, the expression of the downstream mTOR signaling pathway was dramatically upregulated. We used microarrays to detail the gene expression after transfection with TIPE1 and identified distinct classes of changed genes during this process. We used microarrays to detail the gene expression after transfected with TIPE1 and identified distinct classes of changed genes during this process.
Project description:HeLa cells transfected with an empty vector or a TIPE1 lentiviral vector were collected for gene expression detection. Some of them, for instance, the expression of genes induced by p53 was dramatically decreased. We used microarrays to detail the gene expression after transfection with TIPE1 and identified distinct classes of changed genes during this process.
Project description:C57BL/6 mice received methionine/choline deficient (MCD) diet to establish the model of non-alcoholic fatty liver disease (NAFLD) with or without Diethyldithiocarbamate (DDC) treatment. DDC improves hepatic steatosis, ballooning, inflammation and fibrosis in rodent models of NAFLD through modulating lipid metabolism and oxidative stress.
Project description:Macrophages perform key and distinct functions in maintaining tissue homeostasis through finely tuning their polarization state.Here, we found that tumor necrosis factor-α-induced protein 8-like 1 (TIPE1) was highly expressed in macrophages and Tipe1 depletion impeded M2 polarization of macrophages. The goals of this study are to compare BMDMs from LyzM-Cre; Tipe1f/f or Tipe1f/f mice to have a further view of the potential difference.
Project description:Background and aims: Trichosanthis Pericarpium injection (TPI) produces a significant effect on regulating lipid metabolism and antioxidation, whose effects on non-alcoholic fatty liver disease (NAFLD) still remain unclear. In this study, we delved into the pharmacological functions of TPI on NAFLD and its underlying mechanisms. Methods: NAFLD mice model was induced by administering a high-fat diet (HFD) for 12 weeks, followed by intraperitoneal injection of TPI for 4 weeks. Concurrently, to explore the potential mechanisms, we utilized AML12 cells exposed to oleic acid (OA) as an in vitro model. Non target metabolomics and transcriptomics were used to explore the mechanism by which TPI improves lipid metabolism in mouse liver. Results: Our findings indicate that TPI significantly improved metabolic abnormalities and hepatic fat deposition in HFD mice. TPI treatment also yielded analogous results in AML12 cells treated with OA. Metabolomic analysis revealed alterations in metabolites in NAFLD mice, with ABC transporters exhibiting the most prominent changes. Further screening of gene changes related to this pathway showed a significant increase in ABCC5 expression in the NAFLD mice, while TPI treatment effectively reduced the expression level of ABCC5. Transcriptomic analysis demonstrated a marked increase in the expression of the transcription factor KLF6 in the NAFLD group, which positively correlated with ABCC5 expression. Further luciferase reporter gene experiments confirmed that KLF6 can directly regulate the expression of ABCC5, thereby affecting lipid metabolism and participating in the development of NAFLD. Notably, TPI treatment was able to reverse this process. Conclusions: In conclusion, TPI improves NAFLD by alleviating hepatic lipid metabolism dysregulation through the KLF6/ABCC5 pathway.
Project description:Intestinal surface changes in size and function, but what propels these alterations and what are their metabolic consequences is unknown. Here we show that the food amount is a major positive determinant of the gut surface area contributing to an increased absorptive function, reversible by reducing daily food. While several upregulated intestinal energetic pathways are dispensable, the intestinal lipid metabolism is instead necessary for the genetic and environment overeating–induced increase of the gut absorptive capacity. In presence of dietary lipids, intestinal PPARα knock-out or its pharmacological antagonism suppress intestinal crypt expansion and shorten villi in mice and in human intestinal biopsies, diminishing the post-prandial triglyceride transport and nutrient uptake. Intestinal PPARα ablation limits systemic lipid absorption and restricts lipid droplet expansion and PLIN2 levels, critical for droplet formation. This improves the lipid metabolism, and reduces body adiposity and liver steatosis, suggesting an alternative target for treating obesity.