Effects of high-fat diet exposure during fetal life on type 2 diabetes development in the progeny

Geltrude Mingrone, Alessandra Mancuso, D Gniuli, A Calcagno, Me Caristo, V Macchi, R. Vettor

Risultato della ricerca: Contributo in rivistaArticolo in rivista

75 Citazioni (Scopus)

Abstract

Nutrition during fetal life is a critical factor contributing to diabetes development in adulthood. The aim of our study was to verify: 1) whether a high-fat (HF) diet in young adult mice induces alterations in beta-cell mass, proliferation, neogenesis, and apoptosis, as well as insulin sensitivity and secretion; 2) whether these alterations may be reversible after HF diet suspension; 3) the effects in a first (F1) and second generation (F2) of mice without direct exposure to a HF diet after birth. Type 2 diabetes developed in adult mice on a HF diet, in F1 mice that were HF diet-exposed during fetal or neonatal life, and in F2 mice whose mothers were HF diet-exposed during their fetal life. beta-cell mass, replication, and neogenesis were high in HF diet-exposed mice and decreased after diet suspension. beta-cell mass and replication remained high in F1 mice and decreased in F2 mice whose mothers were exposed to a HF diet. beta-cell neogenesis was present in adult mice on a HF diet and in F1 mice that were HF diet-exposed during fetal and/or neonatal life. We conclude that a HF diet during fetal life, particularly if combined with the same insult during the suckling period, can induce the type 2 diabetes phenotype, which can be directly transmitted to the progeny even in the absence of additional dietary insults.
Lingua originaleEnglish
pagine (da-a)1936-1945
Numero di pagine10
RivistaJournal of Lipid Research
Volume49
DOI
Stato di pubblicazionePubblicato - 2008

Keywords

  • Animals
  • Diabetes Mellitus, Type 2
  • Dietary Fats
  • Female
  • Insulin Resistance
  • Insulin-Secreting Cells
  • Mice
  • Pancreas
  • Pregnancy
  • Prenatal Exposure Delayed Effects

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