Project description:Obesity is a complex disease with many causes, including a possible role of environmental chemicals. Perfluorohexane sulfonate (PFHxS) is one of many per- and polyfluoroalkyl substances (PFASs) frequently detected in humans and it is a suspected obesogenic compound. We examined the potential long-term effects of PFHxS on metabolic parameters in rats after developmental exposure to 0.05, 5 or 25 mg/kg bw/day, with or without co-exposure to a background mixture of 12 endocrine disrupting chemicals (EDmix). Both male and female offspring showed signs of lower birth weight following intrauterine exposure. Female offspring exposed to both PFHxS and EDmix showed increased body weight in adulthood. Furthermore, the retroperitoneal fat pad was larger in these female offspring when compared to those exposed to EDmix alone. An attempt to detect putative molecular markers in the fat tissue by performing whole transcriptome profiling resulted in no significant changes between groups and there were no significant effects on plasma leptin levels in exposed females. These results show that early life exposure to endocrine disrupting chemicals can influence body weight later in life, but the effect is not necessarily reflected in changed gene expression in the fat tissue.
Project description:The purpose of this study was to investigate whether paternal high-fat diet (HFD) transgenerationally remodels the epigenome of spermatozoa to alter metabolism in the F1 and F2 generation offspring White adipose tissue mRNA expression profiling of F2-female offspring from F0-founders fed either a chow or a chronic HFD challenged. Adult females were challenged or not a high-fat diet for 12 weeks. White adipose tissue was dissected at an endpoint experiment. Rats were subjected to 4 hours fasting prior to anesthesia with pentobarbital and tissue collection.
Project description:Analysis of gene expression in adipose tissue of female mice after continuous high fat diet (HFD) feeding for three generations. The hypothesis in this study is that continuous HFD feeding has transgenerational amplification effects to the offspring. Results provide important information on the impacts of over-nutrition over one generation on the offspring, such as transgenerational up-regulated or down-regulated genes.
Project description:Oxidative stress in adipose tissue and liver has been linked to the development of obesity. NADPH oxidases (NOX) enzymes are a major source of reactive oxygen species (ROS). The current study was designed to determine if NOX2-generated ROS play a role in development of obesity and metabolic syndrome after high fat feeding. Wild type (WT) mice and mice lacking the cytosolic NOX2 activated protein p47phox (P47KO) were fed AIN-93G diets or high fat diets (HFD) containing 45% fat and 0.5% cholesterol for 13 weeks from weaning. Affymetrix array analysis revealed dramatically less expression of mRNA of genes linked to energy metabolism, adipocyte differentiation (PPARM-NM-3, Runx2) and fatty acid uptake (CD36, lipoprotein lipase) in fat pads from female HFD-P47KO mice compared to HFD-WT females. These data suggest that NOX2 is an important regulator of metabolic homeostasis and that NOX2-associated ROS plays an important role in development of diet-induced obesity particularly in the female fat pads from p47phox and wild type fed a high fat or control diet
Project description:Oxidative stress in adipose tissue and liver has been linked to the development of obesity. NADPH oxidases (NOX) enzymes are a major source of reactive oxygen species (ROS). The current study was designed to determine if NOX2-generated ROS play a role in development of obesity and metabolic syndrome after high fat feeding. Wild type (WT) mice and mice lacking the cytosolic NOX2 activated protein p47phox (P47KO) were fed AIN-93G diets or high fat diets (HFD) containing 45% fat and 0.5% cholesterol for 13 weeks from weaning. Affymetrix array analysis revealed dramatically less expression of mRNA of genes linked to energy metabolism, adipocyte differentiation (PPARγ, Runx2) and fatty acid uptake (CD36, lipoprotein lipase) in fat pads from female HFD-P47KO mice compared to HFD-WT females. These data suggest that NOX2 is an important regulator of metabolic homeostasis and that NOX2-associated ROS plays an important role in development of diet-induced obesity particularly in the female
Project description:Analysis of gene expression in adipose tissue of female mice after continuous high fat diet (HFD) feeding for three generations. The hypothesis in this study is that continuous HFD feeding has transgenerational amplification effects to the offspring. Results provide important information on the impacts of over-nutrition over one generation on the offspring, such as transgenerational up-regulated or down-regulated genes. Total RNA was obtained from adipose tissue of the HFD fed mice, including F0, F1 and F2 generations. Normal chow fed mice were used as controls.
Project description:Nonalcoholic fatty liver disease (NAFLD) is a common disorder characterized by excessive hepatic fat accumulation, and potentially resulting in non-alcoholic steatohepatitis (NASH), liver cirrhosis (LC) and end-stage liver disease We used Rat Genome 230 2.0 microarray to further highlight the rat liver tissues after high-fat emulsion feeding.
Project description:The purpose of this study was to investigate whether paternal high-fat diet (HFD) transgenerationally remodeled the hepatic transcriptome of F2 female rats Liver mRNA expression profiling of F2-female from F0-founders fed either a chow or a chronic HFD challenged. Adult females were challenge or not a high-fat diet for 12 weeks. Liver was dissected at an endpoint experiment. Rats were subjected to 4 hours fasting prior to anesthesia with pentobarbital and tissue collection.
Project description:Reduced representation bisulfite sequencing was used to explore differentially methylated regions and sites within the amygdala of female rat offspring during earlylife and adulthood, in response to maternal high fat diet exposure. DMRs shared across early life and adulthood included pathways involved in neurodevelopment and genes regulating the DNMT machinery and protein function. To our knowledge, this is the first study to identify persistent genome-wide DNA methylation modifications associated with mHFD exposure in offspring from early life to adulthood.