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This Article Full Text Full Text (PDF) All Versions of this Article: 292/4/E1095    most recent 00390.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Gallou-Kabani, C. Articles by Junien, C. Search for Related Content PubMed PubMed Citation Articles by Gallou-Kabani, C. Articles by Junien, C.

Resistance to high-fat diet in the female progeny of obese mice fed a control diet during the periconceptual, gestation, and lactation periods

¹Institut National de la Santé et de la Recherche Médicale, Assistance Publique-Hôpitaux de Paris, Université Paris-Descartes, Faculté de Médecine, Hôpital Necker-Enfants Malades, ⁴Service de Biostatistique et Informatique Médicale, Paris; ²Assistance Publique-Hopitaux de Paris, Faculté de Médecine Paris Ile-de-France-Ouest, Université Versailles-Saint-Quentin-en-Yvelines, Laboratoire de biochimie, Hôpital Ambroise Paré, Boulogne; and ³Institut National de la Santé et de la Recherche Médicale, Université de Lille 2, Département d'Athérosclérose, Loos, France

Submitted 3 August 2006 ; accepted in final form 5 December 2006

With the worldwide epidemic of metabolic syndrome (MetS), the proportion of women that are overweight/obese and overfed during pregnancy has increased. The resulting abnormal uterine environment may have deleterious effects on fetal metabolic programming and lead to MetS in adulthood. A balanced/restricted diet and/or physical exercise often improve metabolic abnormalities in individuals with obesity and type 2 diabetes mellitus (T2D). We investigated whether reducing fat intake during the periconceptual/gestation/lactation period in mothers with high-fat diet (HFD)-induced obesity could be used to modify fetal/neonatal MetS programming positively, thereby preventing MetS. First generation (F1) C57BL/6J female mice with HFD-induced obesity and T2D were crossed with F1 males on control diet (CD). These F1 females were switched to a CD during the periconceptual/gestation/lactation period. At weaning, both male and female second generation (F2) mice were fed a HFD. Weight, caloric intake, lipid parameters, glucose, and insulin sensitivity were assessed. Sensitivity/resistance to the HFD differed significantly between generations and sexes. A similar proportion of the F1 and F2 males (80%) developed hyperphagia, obesity, and T2D. In contrast, a significantly higher proportion of the F2 females (43%) than of the previous F1 generation (17%) were resistant (P < 0.01). Despite having free access to the HFD, these female mice were no longer hyperphagic and remained lean, with normal insulin sensitivity and glycemia but mild hypercholesterolemia and glucose intolerance, thus displaying a "satiety phenotype." This suggests that an appropriate dietary fatty acid profile and intake during the periconceptual/gestation/lactation period helps the female offspring to cope with deleterious intrauterine conditions.

epigenetics; nutrition; metabolic syndrome; fetal programming