title: High dietary cholesterol intake during lactation promotes development of fatty liver in offspring of mice.
abstract: We have previously demonstrated in mice that a maternal high fat diet during lactation enhances the susceptibility of offspring to obesity and fatty liver. A causative molecule, however, is yet to be identified. Therefore, we examined the role of cholesterol, the dietary intake of which increases with consumption of a high fat diet. Excessive cholesterol intake is involved in the development of fatty liver, which in turn becomes a risk factor for metabolic syndrome, which includes obesity, insulin resistance, and dyslipidemia. However, our knowledge of the influences on offspring of excessive maternal cholesterol intake alone during pregnancy and lactation is limited. We examined how excessive maternal cholesterol intake during lactation influences susceptibility of the offspring to metabolic syndrome in mice.
  
  
  
  High cholesterol intake promoted triacylglycerol accumulation in the liver of offspring (p < 0.05), and elevated expression of molecules involved in hepatic lipoprotein influx was identified as the underlying mechanism.
  
  
  
  These findings demonstrate that excessive maternal cholesterol intake during lactation enhances the susceptibility of the offspring to development of fatty liver.
authors: Laboratory of Food and Biomolecular Science, Graduate School of Agriculture, Tohoku University, Sendai, Japan.
authors: Tsuyoshi
authors: T
authors: Tsuduki
authors: Laboratory of Food and Biomolecular Science, Graduate School of Agriculture, Tohoku University, Sendai, Japan.
authors: Kazushi
authors: K
authors: Yamamoto
authors: Laboratory of Food and Biomolecular Science, Graduate School of Agriculture, Tohoku University, Sendai, Japan.
authors: Yu
authors: Y
authors: Hatakeyama
authors: Laboratory of Food and Biomolecular Science, Graduate School of Agriculture, Tohoku University, Sendai, Japan.
authors: Yu
authors: Y
authors: Sakamoto
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D002784:Cholesterol / Q000097:blood; D002791:Cholesterol, Dietary / Q000008:administration & dosage* / Q000009:adverse effects*; D059305:Diet, High-Fat / Q000009:adverse effects*; D050171:Dyslipidemias / Q000503:physiopathology; D005234:Fatty Liver / Q000209:etiology / Q000503:physiopathology*; D005260:Female; D007333:Insulin Resistance; D007774:Lactation; D008099:Liver / Q000378:metabolism; D026503:Low Density Lipoprotein Receptor-Related Protein-1; D039382:Maternal Nutritional Physiological Phenomena; D024821:Metabolic Syndrome / Q000503:physiopathology; D051379:Mice; D009765:Obesity / Q000503:physiopathology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011973:Receptors, LDL / Q000235:genetics / Q000378:metabolism; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood; D025521:Tumor Suppressor Proteins / Q000235:genetics / Q000378:metabolism
chemical_list: D002791:Cholesterol, Dietary; D026503:Low Density Lipoprotein Receptor-Related Protein-1; C486645:Lrp1 protein, mouse; D011973:Receptors, LDL; D014280:Triglycerides; D025521:Tumor Suppressor Proteins; D002784:Cholesterol; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase
keywords: Cholesterol; Fatty liver; Lactation; Maternal nutrition; Offspring