title: Long-term consequences of maternal high-fat feeding on hypothalamic leptin sensitivity and diet-induced obesity in the offspring.
abstract: Epidemiological and animal studies suggest that the alteration of hormonal and metabolic environment during fetal and neonatal development can contribute to development of metabolic syndrome in adulthood. In this paper, we investigated the impact of maternal high-fat (HF) diet on hypothalamic leptin sensitivity and body weight gain of offspring. Adult Wistar female rats received a HF or a control normal-fat (C) diet for 6 wk before gestation until the end of the suckling period. After weaning, pups received either C or HF diet during 6 wk. Body weight gain and metabolic and endocrine parameters were measured in the eight groups of rats formed according to a postweaning diet, maternal diet, and gender. To evaluate hypothalamic leptin sensitivity in each group, STAT-3 phosphorylation was measured in response to leptin or saline intraperitoneal bolus. Pups exhibited similar body weights at birth, but at weaning, those born to HF dams weighed significantly less (-12%) than those born to C dams. When given the HF diet, males and females born to HF dams exhibited smaller body weight and feed efficiency than those born to C dams, suggesting increased energy expenditure programmed by the maternal HF diet. Thus, maternal HF feeding could be protective against adverse effects of the HF diet as observed in male offspring of control dams: overweight (+17%) with hyperleptinemia and hyperinsulinemia. Furthermore, offspring of HF dams fed either C or HF diet exhibited an alteration in hypothalamic leptin-dependent STAT-3 phosphorylation. We conclude that maternal high-fat diet programs a hypothalamic leptin resistance in offspring, which, however, fails to increase the body weight gain until adulthood.
authors.affiliation: Neurobiologie de l'Olfaction et de la Prise Alimentaire, UMR 1197, Bâtiment 447, Université Paris-Sud, F-91 405-Orsay Cedex, France. jacqueline.ferezou@u-psud.fr
authors.forename: Jacqueline
authors.initials: J
authors.lastname: Férézou-Viala
authors.forename: Anne-France
authors.initials: AF
authors.lastname: Roy
authors.forename: Colette
authors.initials: C
authors.lastname: Sérougne
authors.forename: Daniel
authors.initials: D
authors.lastname: Gripois
authors.forename: Michel
authors.initials: M
authors.lastname: Parquet
authors.forename: Virginie
authors.initials: V
authors.lastname: Bailleux
authors.forename: Arieh
authors.initials: A
authors.lastname: Gertler
authors.forename: Bernadette
authors.initials: B
authors.lastname: Delplanque
authors.forename: Jean
authors.initials: J
authors.lastname: Djiane
authors.forename: Michel
authors.initials: M
authors.lastname: Riottot
authors.forename: Mohammed
authors.initials: M
authors.lastname: Taouis
mesh_terms: D000818:Animals; D000833:Animals, Suckling / Q000502:physiology; D015153:Blotting, Western; D001835:Body Weight / Q000502:physiology; D004032:Diet; D004041:Dietary Fats / Q000494:pharmacology*; D005260:Female; D007031:Hypothalamus / Q000502:physiology*; D020738:Leptin / Q000502:physiology*; D008297:Male; D009765:Obesity / Q000209:etiology*; D010766:Phosphorylation; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D017208:Rats, Wistar; D050796:STAT3 Transcription Factor / Q000502:physiology; D015430:Weight Gain / Q000187:drug effects / Q000502:physiology
chemical_list: D004041:Dietary Fats; D020738:Leptin; D050796:STAT3 Transcription Factor