Project description:Assessment of diet currently relies on self-reporting, such as food logs, 24 hour recalls and food frequency questionnaires. Self-reporting of diet is inaccurate due to memory lapses, lying and biased language. A molecular-based approach to assess diet would allow accurate reporting of diet for researchers, medical professionals and patients. We performed metaproteomic analysis of 22 human stool samples collected from four individuals enrolled at the Duke Diet and Fitness Center. Samples were collected between 01Aug19 and 22Nov19. All meals at the Duke Diet and Fitness Center were recorded such that the approximate quantities of each food item consumed are known.
Project description:Purpose: The goals of this study were to identify preferential gene expression signatures that are unique to hepatic macrophages in high-fat diet -induced non-alcoholic fatty liver disease. Methods and results: Wild-type and Casp11-/- mice were treated with high fat and normal chow diet for a period of 12 weeks. Hepatic macrophages from liver were isolated to generate mRNA transcription. Conclusion: Our study represents detailed analysis of caspase-11 in regulating hepatic macrophages in high-fat diet -induced non-alcoholic fatty liver disease.
Project description:Assessment of diet currently relies on self-reporting, such as food logs, 24 hour recalls and food frequency questionnaires. Self-reporting of diet is inaccurate due to memory lapses, lying and biased language. A molecular-based approach to assess diet would allow accurate reporting of diet for researchers, medical professionals and patients. We performed metaproteomic analysis of five human stool samples collected from a free-eating individual over five consecutive days (25Jun18-29Jun18). The free-eating individual maintained a food log during the sample collection period. We used these samples to develop a molecular-based approach for assessing diet.
Project description:This study aimed to investigate the effect and underlying mechanism of Didymin on lipid metabolic disturbance in rats with non-alcoholic fatty liver disease (NAFLD). Rats were administrated with a high-fat diet (HFD) for 8 weeks to induce NAFLD, followed by different dose Didymin treatment for further 8 weeks.
Project description:Non-alcoholic fatty liver disease (NAFLD) is associated with obesity and lifestyle. Exercise is known to be beneficial for NAFLD treatment. Recent studies have shown the critical involvement of microRNA in NAFLD. However, it is unclear whether exercise could prevent NAFLD via miRNA targeting. We used microarrays to examine microRNA profiles in high-fat diet fed mice with and without exercise in comparison to normal diet fed mice.
Project description:This study aimed to investigate the effect and underlying mechanism of Smilax china L. Saponins (SCS) on lipid metabolic disturbance in rats with non-alcoholic fatty liver disease (NAFLD). Rats were administrated with a high-fat diet (HFD) for 8 weeks to induce NAFLD, followed by SCS treatment for further 8 weeks.
Project description:Non-alcoholic fatty liver disease (NAFLD) is most prevalent form of liver disease, affecting over 30% of Americans. Perfluoroalkyl substances (PFAS) represent a family of environmental toxicants that have infiltrated the living world. This study explores diet-PFAS interactions and their potential role in the increasing global incidence of NAFLD. Male C57BL/6 mice were fed with either a low-fat diet (11% kcal from fat) or a high fat (58% kcal from fat) high carbohydrate (42g/L) diet with or without PFOS or PFHxS in feed (0.0003% w/w) for 29 weeks. Proteomic, lipidomic, and gene expression measurement techniques were utilized to explore mechanistic pathways. With administration of a high fat high carbohydrate (HFHC) diet, PFOS and PFHxS augmented macrovesicular steatosis, indicative of fatty liver. There was a clear shift in the lipidome of the serum phosphatidylcholines, phosphatidylethanolamines, and triglycerides with PFAS exposure. Finally, chain length exerted significant influence on tissue partitioning and the resulting hepatic gene and protein signatures of PFHxS and PFOS in vivo.