title: [Developmental programming of metabolic diseases--a review of studies on experimental animal models].
abstract: Growth and development in utero is a complex and dynamic process that requires interaction between the mother organism and the fetus. The delivery of macro--and micronutrients, oxygen and endocrine signals has crucial importance for providing a high level of proliferation, growth and differentiation of cells, and a disruption in food intake not only has an influence on the growth of the fetus, but also has negative consequences for the offspring’s health in the future. Diseases that traditionally are linked to inappropriate life style of adults, such as type 2 diabetes, obesity, and arterial hypertension, can be "programmed" in the early stage of life and the disturbed growth of the fetus leads to the symptoms of the metabolic syndrome. The structural changes of some organs, such as the brain, pancreas and kidney, modifications of the signaling and metabolic pathways in skeletal muscles and in fatty tissue, epigenetic mechanisms and mitochondrial dysfunction are the basis of the metabolic disruptions. The programming of the metabolic disturbances is connected with the disruption in the intrauterine environment experienced in the early and late gestation period. It causes the changes in deposition of triglycerides, activation of the hormonal "stress axis" and disturbances in the offspring’s glucose tolerance. The present review summarizes experimental results that led to the identification of the above-mentioned links and it underlines the role of animal models in the studies of this important concept.
authors.forename: Iwona
authors.initials: I
authors.lastname: Piotrowska
authors.forename: Paulina
authors.initials: P
authors.lastname: Zgódka
authors.forename: Marta
authors.initials: M
authors.lastname: Milewska
authors.forename: Maciej
authors.initials: M
authors.lastname: Błaszczyk
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Grzelkowska-Kowalczyk
mesh_terms: D000740:Anemia / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000196:embryology; D003924:Diabetes Mellitus, Type 2 / Q000196:embryology / Q000378:metabolism; D016640:Diabetes, Gestational / Q000378:metabolism; D004195:Disease Models, Animal; D044127:Epigenesis, Genetic; D005260:Female; D005315:Fetal Diseases / Q000235:genetics* / Q000378:metabolism*; D006973:Hypertension / Q000196:embryology / Q000378:metabolism; D007668:Kidney / Q000196:embryology; D008659:Metabolic Diseases / Q000196:embryology* / Q000235:genetics / Q000378:metabolism*; D024821:Metabolic Syndrome / Q000196:embryology / Q000378:metabolism; D009765:Obesity / Q000196:embryology / Q000378:metabolism; D010179:Pancreas / Q000196:embryology; D011247:Pregnancy; D011248:Pregnancy Complications / Q000378:metabolism*; D011297:Prenatal Exposure Delayed Effects / Q000378:metabolism*