title: Continuous intake of a high-fat diet beyond one generation promotes lipid accumulation in liver and white adipose tissue of female mice.
abstract: Lipid metabolism in a child may be altered when the mother has a high-fat diet (HFD), but it is unclear whether the lipid metabolism of future offspring (grandchildren) is also changed under these circumstances. In this study, we examined the influence of intake of an HFD beyond one generation on offspring in normal mice. Parent mice fed an HFD were bred and the resultant second and third generations were also fed an HFD. The diets used in the study had approximately 20% more energy than a standard chow diet. Changes in lipid metabolism were examined in each generation. Intake of an HFD from generation to generation promoted lipid accumulation in the white adipose tissue of female mice, increased lipid, glucose and insulin levels in the serum, increased the activities of enzymes associated with fatty acid metabolism in the liver, promoted lipid accumulation in hepatocytes and adipocytes and increased the mRNA levels of Cdkn1a in the liver and white adipose tissue. These results suggest that activation of Cdkn1a promoted lipid accumulation in the liver and white adipose tissue of third-generation female mice that were offspring from earlier generations fed HFDs. Moreover, intake of a high-energy diet beyond one generation led to offspring with obesity, fatty liver and hyperinsulinemia.
authors.affiliation: Laboratory of Food and Biomolecular Science, Graduate School of Agricultural Science, Tohoku University, Sendai, Japan.
authors.forename: Mariko
authors.initials: M
authors.lastname: Takasaki
authors.forename: Taro
authors.initials: T
authors.lastname: Honma
authors.forename: Miyuki
authors.initials: M
authors.lastname: Yanaka
authors.forename: Kenta
authors.initials: K
authors.lastname: Sato
authors.forename: Nahoko
authors.initials: N
authors.lastname: Shinohara
authors.forename: Junya
authors.initials: J
authors.lastname: Ito
authors.forename: Yurie
authors.initials: Y
authors.lastname: Tanaka
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Tsuduki
authors.forename: Ikuo
authors.initials: I
authors.lastname: Ikeda
mesh_terms: D052436:Adipose Tissue, White / Q000378:metabolism*; D000818:Animals; D001786:Blood Glucose; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000235:genetics / Q000378:metabolism; D059305:Diet, High-Fat / Q000009:adverse effects*; D004041:Dietary Fats / Q000008:administration & dosage / Q000009:adverse effects; D005234:Fatty Liver / Q000209:etiology / Q000503:physiopathology; D005260:Female; D006946:Hyperinsulinism / Q000209:etiology / Q000503:physiopathology; D007328:Insulin / Q000097:blood; D050356:Lipid Metabolism; D008099:Liver / Q000378:metabolism*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009765:Obesity / Q000209:etiology / Q000503:physiopathology
chemical_list: D001786:Blood Glucose; C493957:Cdkn1a protein, mouse; D050759:Cyclin-Dependent Kinase Inhibitor p21; D004041:Dietary Fats; D007328:Insulin