Journal
JOURNAL OF LIPID RESEARCH
Volume 49, Issue 9, Pages 1936-1945Publisher
ELSEVIER
DOI: 10.1194/jlr.M800033-JLR200
Keywords
beta cell; PDX; KI67
Categories
Funding
- MIUR (Ministero Italiano dell'Istruzione e Ricerca scientifica, Italian Ministry of Education and scientific research) [RBNE01KCX4_008 MIUR-FIRB, 2003061834_006 MIUR-COFIN]
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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.-Gniuli, D., A. Calcagno, M. E. Caristo, A. Mancuso, V. Macchi, G. Mingrone, and R. Vettor. Effects of high- fat diet exposure during fetal life on type 2 diabetes development in the progeny.
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