|
Advertisement | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Papers In Press, published online ahead of print May 20, 2008 J. Lipid Res., doi:10.1194/jlr.M800033-JLR200
Istituto di Medicina Interna, Universita' Cattolica del Sacro Cuore, Rome, Italy 00168
Corresponding Author: dgniuli{at}gmail.com
Nutrition during fetal life is a critical factor contributing to diabetes development in the adulthood. Aim of our study was to verify: 1) whether a high fat diet (HFD) in young adult mice induces alterations of ß-cell mass, proliferation, neogenesis and apoptosis; as well as of insulin sensitivity and secretion; 2) whether these alterations may be reversible after HFD suspension; 3) the effects in a first (F1) and second generation (F2) of mice without direct exposure to HFD after the birth. Type 2 diabetes developed in adult mice on HFD, in F1 mice, HFD-exposed during the fetal or neonatal life, and in F2 mice, whose mothers were HFD-exposed during their fetal life. -cell mass, replication and neogenesis were high in HFD-exposed mice and decreased after diet suspension. -cell mass and replication remained high in F1 mice and decreased in F2 mice whose mothers were exposed to HFD. -cell neogenesis was present in adult mice on HFD and in F1 mice HFD-exposed during fetal and/or neonatal life. We conclude that HFD during fetal life, particularly if combined with the same insult during the suckling period, can induce the type 2 diabetes phenotype, that can be directly transmitted to the progeny even in absence of additional dietary insults.
This article has been cited by other articles:
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
Advertisement | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||