title: Organ-specific alterations in fatty acid de novo synthesis and desaturation in a rat model of programmed obesity.
abstract: BACKGROUND
  Small for gestational age (SGA) leads to increased risk of adult obesity and metabolic syndrome. Offspring exposed to 50% maternal food restriction in utero are born smaller than Controls (FR), catch-up in growth by the end of the nursing period, and become obese adults. The objective of the study was to determine stearoyl-CoA desaturase activity (SCD1) and rates of de novo fatty acid synthesis in young FR and Control offspring tissues at the end of the nursing period, as possible contributors to catch-up growth.
  
  
  METHODS
  From gestational day 10 to term, dams fed ad libitum (Control) or were 50% food-restricted to produce small FR pups. Control dams nursed all pups. At postnatal day 1 (p1) and p21, offspring body tissues were analyzed by GC/MS, and desaturation indices of palmitoleate/palmitate and oleate/stearate were calculated. SCD1 gene expression was determined by real-time PCR on adipose and liver. Offspring were enriched with deuterium that was given to dams in drinking water during lactation and de novo synthesis of offspring body tissues was determined at p21. Primary adipocyte cell cultures were established at p21 and exposed to U(13)C-glucose.
  
  
  RESULTS
  FR offspring exhibited higher desaturation index in p1 and p21 adipose tissue, but decreased desaturation index in liver at p21. SCD1 gene expression at p21 was correspondingly increased in adipose and decreased in liver. FR subcutaneous fat demonstrated increased de novo synthesis at p21. Primary cell cultures exhibited increased de novo synthesis in FR.
  
  
  CONCLUSIONS
  Adipose tissue is the first site to exhibit increased de novo synthesis and desaturase activity in FR. Therefore, abnormal lipogenesis is already present prior to onset of obesity during the period of catch-up growth. These abnormalities may contribute to future obesity development.
authors.affiliation: Department of Pediatrics, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Bldg RB-1, Harbor Box 446, Torrance, CA 90502, USA. jyee@labiomed.org
authors.forename: Jennifer K
authors.initials: JK
authors.lastname: Yee
authors.forename: Wai-Nang P
authors.initials: WN
authors.lastname: Lee
authors.forename: Guang
authors.initials: G
authors.lastname: Han
authors.forename: Michael G
authors.initials: MG
authors.lastname: Ross
authors.forename: Mina
authors.initials: M
authors.lastname: Desai
mesh_terms: D000105:Acetyl Coenzyme A / Q000378:metabolism; D017667:Adipocytes / Q000378:metabolism; D000273:Adipose Tissue / Q000201:enzymology; D000818:Animals; D001835:Body Weight; D002478:Cells, Cultured; D004195:Disease Models, Animal; D005227:Fatty Acids / Q000096:biosynthesis* / Q000097:blood; D005260:Female; D015971:Gene Expression Regulation, Enzymologic; D008099:Liver / Q000201:enzymology; D009765:Obesity / Q000097:blood / Q000378:metabolism*; D009928:Organ Specificity; D010641:Phenotype; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013230:Stearoyl-CoA Desaturase / Q000235:genetics / Q000378:metabolism
chemical_list: D005227:Fatty Acids; D012333:RNA, Messenger; D000105:Acetyl Coenzyme A; D013230:Stearoyl-CoA Desaturase