|Title||The effect of dietary fat intake on hepatic gene expression in LG/J AND SM/J mice.|
|Publication Type||Journal Article|
|Year of Publication||2014|
|Authors||Partridge, CG, Fawcett, GL, Wang, B, Semenkovich, CF, Cheverud, JM|
|Keywords||Animals, Diabetes Mellitus, Diet, High-Fat, Down-Regulation, Female, Liver, Male, Mice, Mice, Inbred Strains, Non-alcoholic Fatty Liver Disease, Obesity, Quantitative Trait Loci, Up-Regulation|
BACKGROUND: The liver plays a major role in regulating metabolic homeostasis and is vital for nutrient metabolism. Identifying the genetic factors regulating these processes could lead to a greater understanding of how liver function responds to a high-fat diet and how that response may influence susceptibilities to obesity and metabolic syndrome. In this study we examine differences in hepatic gene expression between the LG/J and SM/J inbred mouse strains and how gene expression in these strains is affected by high-fat diet. LG/J and SM/J are known to differ in their responses to a high-fat diet for a variety of obesity- and diabetes-related traits, with the SM/J strain exhibiting a stronger phenotypic response to diet.
RESULTS: Dietary intake had a significant effect on gene expression in both inbred lines. Genes up-regulated by a high-fat diet were involved in biological processes such as lipid and carbohydrate metabolism; protein and amino acid metabolic processes were down regulated on a high-fat diet. A total of 259 unique transcripts exhibited a significant diet-by-strain interaction. These genes tended to be associated with immune function. In addition, genes involved in biochemical processes related to non-alcoholic fatty liver disease (NAFLD) manifested different responses to diet between the two strains. For most of these genes, SM/J had a stronger response to the high-fat diet than LG/J.
CONCLUSIONS: These data show that dietary fat impacts gene expression levels in SM/J relative to LG/J, with SM/J exhibiting a stronger response. This supports previous data showing that SM/J has a stronger phenotypic response to high-fat diet. Based upon these findings, we suggest that SM/J and its cross with the LG/J strain provide a good model for examining non-alcoholic fatty liver disease and its role in metabolic syndrome.
|Alternate Journal||BMC Genomics|
|PubMed Central ID||PMC4028868|
|Grant List||DK-055736 / DK / NIDDK NIH HHS / United States |
P30 DK020579 / DK / NIDDK NIH HHS / United States
P30 DK056341 / DK / NIDDK NIH HHS / United States
R01 DK076729 / DK / NIDDK NIH HHS / United States
RR015116 / RR / NCRR NIH HHS / United States