Project description:To establish the consequences of whole-animal deletion of CYP2E1, we isolated RNA from bulk liver tissue of 16-week male and female WT and KO mice. Mice were maintained on a normal chow diet and were euthanized using CO2 and cervical dislocation prior to liver dissection.
Project description:To establish the consequences of whole-animal deletion of CYP2E1, we isolated RNA from bulk liver tissue of 12-13-week male and female WT and KO mice. Mice were maintained on a normal chow diet and were euthanized using CO2 and cervical dislocation prior to liver dissection.
Project description:To identify molecular mechanism underlying the protection from diet-induced hepatic steatosis in AHNAK deficiency mice, we examined microarray analysis with liver sample from HFD-fed AHNAK KO and WT mice. Two-condition experiment, regular chow (CD) -fed WT vs. CD-fed AHNAK KO and High fat diet(HFD)-fed WT vs. HFD-fed AHNAK KO mice. Biological replicates: 3 control, One replicate per array.
Project description:Liver samples of mice harboring liver-specific deletion of Lats2 (Lats2-CKO) were compared to WT mice. This effect was tested along with the effect of diet - high cholesterol diet (Paigen-PD) vs. normal chow (ND).
Project description:To establish the consequences of whole-animal deletion of CYP2E1, we isolated RNA from dissected brain tissue (cerebellum, medial prefrontal cortex, dorsal hippocampus, and ventral hippocampus) of 16-week male and female WT and KO mice. Mice were maintained on a normal chow diet and were euthanized using CO2 and decapitation prior to brain dissection.
Project description:Isolated glomeruli from mice were analyzed. The grouping was as follows: WT mice exposed to normal diet, podocyte specific Pdzd8 KO mice exposed to normal diet, WT mice exposed to 12w high fat diet, podocyte specific Pdzd8 KO mice exposed to 12w high fat diet.
Project description:The popularity of high fat foods in modern society has been associated with epidemic of various metabolic diseases characterized by insulin resistance, the pathology of which involves complex interactions between multiple tissues such as liver, skeletal muscle and white adipose tissue (WAT). To uncover the mechanism by which excessive fat impairs insulin sensitivity, we conducted a multi- tissue study by using TMT-based quantitative proteomics. 3-week-old ICR mice were fed with high fat diet (HFD) for 19 weeks to induce insulin resistance. Liver, skeletal muscle and epididymal fat were collected for proteomics screening. Additionally, PRM was used for validating adipose differential proteins. By comparing tissue-specific protein profiles of HFD mice, multi-tissue regulation of glucose and lipid homeostasis and corresponding underlying mechanisms was systematically investigated and characterized. NC: normal birth weight + chow diet; NH: normal birth weight + high fat diet; LC: low birth weight + chow diet; LH: low birth weight + high fat diet.
