J. Lipid Res.
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Originally published In Press as doi:10.1194/jlr.M800033-JLR200 on May 20, 2008

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Journal of Lipid Research, Vol. 49, 1936-1945, September 2008
Copyright © 2008 by American Society for Biochemistry and Molecular Biology

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

Donatella Gniuli1,*, Alessandra Calcagno{dagger}, Maria Emiliana Caristo§, Alessandra Mancuso§, Veronica Macchi**, Geltrude Mingrone* and Roberto Vettor**

* Department of Internal Medicine, Università Cattolica S. Cuore, Roma, Italy
{dagger} Department of Medical and Surgical Sciences, Internal Medicine, University of Padua, Padua, Italy
§ Department of Animal House, Università Cattolica S. Cuore, Roma, Italy
** Department of Human Anatomy and Physiology, Section of Anatomy, University of Padua, Padua, Italy

Published, JLR Papers in Press, May 20, 2008.

This work was supported by MIUR (Ministero Italiano dell'Istruzione e Ricerca scientifica, Italian Ministry of Education and scientific research) Grants RBNE01KCX4_008 MIUR-FIRB and 2003061834_006 MIUR-COFIN (R.V.).

1 To whom correspondence should be addressed. e-mail: dgniuli{at}gmail.com

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 β-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. β-cell mass, replication, and neogenesis were high in HF diet-exposed mice and decreased after diet suspension. β-cell mass and replication remained high in F1 mice and decreased in F2 mice whose mothers were exposed to a HF diet. β-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.

Supplementary key words beta cell • PDX-1 • KI67


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