title: Forced catch-up growth after fetal protein restriction alters the adipose tissue gene expression program leading to obesity in adult mice.
abstract: A mismatch between fetal and postnatal environment can permanently alter the body structure and physiology and therefore contribute later to obesity and related disorders, as revealed by epidemiological studies. Early programming of adipose tissue might be central in this observation. Moreover, adipose tissue secretes adipokines that provide a molecular link between obesity and its related disorders. Therefore, our aim was to investigate whether a protein restriction during fetal life, followed by catch-up growth could lead to obesity in 9-mo-old male mice and could alter the adipose tissue gene expression profile. Dams were fed a low-protein (LP) or an isocaloric control (C) diet during gestation. Postnatal catch-up growth was induced in LP offspring by feeding dams with control diet and by culling LP litters to four pups instead of eight in the C group. At weaning, male mice were fed by lab chow alone (C) or supplemented with a hypercaloric diet (HC), to induce obesity (C-C, C-HC, LP-C, and LP-HC groups). At 9 mo, LP offspring featured increased relative fat mass, hyperglycemia, hypercholesterolemia, and hyperleptinemia. Using a microarray designed to study the expression of 89 genes involved in adipose tissue differentiation/function, we demonstrated that the expression profile of several genes were dependent upon the maternal diet. Among the diverse genes showing altered expression, we could identify genes encoding several enzymes involved in lipid metabolism. These results indicated that offspring submitted to early mismatched nutrition exhibited alterations in adipose tissue gene expression that probably increases their susceptibility to overweight when challenged after weaning with a HC diet.
authors.affiliation: Laboratory of Cell Biology Institute of Life Science, Université catholique de Louvain, Place Croix du Sud 5, 1348 Louvain-la-Neuve, Belgium.
authors.forename: V V
authors.initials: VV
authors.lastname: Bol
authors.forename: A-I
authors.initials: AI
authors.lastname: Delattre
authors.forename: B
authors.initials: B
authors.lastname: Reusens
authors.forename: M
authors.initials: M
authors.lastname: Raes
authors.forename: C
authors.initials: C
authors.lastname: Remacle
mesh_terms: D052438:Adipocytes, White / Q000473:pathology; D052436:Adipose Tissue, White / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D001786:Blood Glucose / Q000502:physiology; D001823:Body Composition / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D050260:Carbohydrate Metabolism / Q000235:genetics; D004032:Diet; D018753:Diet, Protein-Restricted / Q000009:adverse effects*; D015536:Down-Regulation / Q000235:genetics; D004435:Eating / Q000502:physiology; D005260:Female; D047109:Fetal Development / Q000502:physiology*; D005317:Fetal Growth Retardation / Q000473:pathology; D015870:Gene Expression / Q000502:physiology*; D020869:Gene Expression Profiling; D020738:Leptin / Q000235:genetics / Q000378:metabolism; D050356:Lipid Metabolism / Q000235:genetics; D008055:Lipids / Q000097:blood; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D009929:Organ Size / Q000502:physiology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000378:metabolism* / Q000473:pathology; D015854:Up-Regulation / Q000235:genetics
chemical_list: D001786:Blood Glucose; D020738:Leptin; D008055:Lipids