FIND ARTICLE

Volume: 
Issue: 
1
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The aim of the presented paper is the description of disturbances in the central nervous system (OUN) functions of fa/fa Zucker rats, in which the development of morbid obesity is observed as a result of a defect in leptin functioning. Zucker fa/fa rats possess a defect in a gene, which codes leptin receptor. A single exchange of adenine to cytosine in the 806th position of extracellular domain of the receptor results in coding proline instead of glutamine (Gln269Pro). Due to point mutation, the regulation of food intake in fa/fa rats is drastically changed, probably caused by the lack of the leptin receptor and/or leptin protein in the OUN. As a consequence, the deregulation of energetic homeostasis and a dramatic increase of body mass are observed. In spite of the high level of leptin in the blood, these animals are resistant to the circulating hormone, which under regular conditions reaches the brain decreasing food intake and enhancing the energy metabolism. The involvement of leptin in the regulation of food intake comprises interactions with several hormonal systems in the OUN. In the presented review we have shown that the lack of the functional leptin receptors has an impact on synthesis of several mediators in the brain. Abnormalities in gene expression and/or protein levels of neuropeptide Y, orexin, CART peptide, or AgRP were observed in the brain of the rats. Additionally, lower concentration of insulin and its receptors have been also noted in the brain of fa/fa rats. Disrupted leptin function may also lead to an impairment of the system reacting to glucose in the brain. It has been shown that the brain of obese Zucker rat contains significantly reduced number of glucose-sensitive neurons and glucose ultilization was markedly dimini- shed in distinct hypothalamic regions. However, the presented data are only a part of a complicated and partially explained mechanisms regulating feeding behavior in fa/fa rats.

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The Editorial Board
Andrzej Łukaszyk - przewodniczący, Zofia Bielańska-Osuchowska, Szczepan Biliński, Mieczysław Chorąży, Aleksander Koj, Włodzimierz Korochoda, Leszek Kuźnicki, Aleksandra Stojałowska, Lech Wojtczak

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Katedra i Zakład Histologii i Embriologii Uniwersytetu Medycznego w Poznaniu, ul. Święcickiego 6, 60-781 Poznań, tel. +48 61 8546453, fax. +48 61 8546440, email: mnowicki@ump.edu.pl

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