..:: Rola oreksyn w regulacji łaknienia 95 ::..
| Rola oreksyn w regulacji łaknienia 95 |
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Małgorzata Janas-Kozik, Irena Krupka-Matuszczyk
Rola oreksyn w regulacji łaknienia 95
Summary Anorexia nervosa (AN) belongs to the group of eating disorders. Many different factors are taken into consideration as far as the origin of this disorder is concerned, among them: individual factors (genetic, biological), personality factors, sociocultural factors, family factors. Among the biological factors, the role of neuropeptides is considered. Last few years (1998) have resulted in the discovery of two neuropeptides - orexines OXA and OXB which - apart from being regarded as appetite stimulants - are also supposed to be responsible for the energy metabolism of an organism. Orexines, a.k.a. hypocretins, arise from the disintegration of their common precursor - the polypeptide: preorexine. Their name derives from the Greek word for appetite: orexis. The orexine A (OXA) is a 33 amino acid peptide consisting of 2 chains connected by the Cys 6 - Cys 12 and Cys 7 - Cys 14 bridges. It is a potential food intake and gastric juice secretion stimulant. The connecting bridges in OXA play a crucial role in the receptor OXA-1 activation. The orexine B (OXB) is a 28 amino acid peptide with no connecting bridges between the chains. It mainly plays a role in the energy metabolism of an organism and does not influence the secretion of gastric juice. The OXR-1 receptor is a selective receptor for OXA, while the OXR-2 receptor is not privileged for any of the two orexines - both of them can connect to it. Orexines are produced by a small number of hypothalamus neurons, mainly in the lateral hypothalamus (LHA), but also the posterior hypothalamus - the so-called "eating center". Orexines control: the wakefulness-sleep state, food intake (OXA over 100 times stronger than OXB) and the neuroendocrine system. Their discovery may help in understanding the mechanism of anorexia nervosa. |
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| Numer: |
1 |
| Tytuł: |
PSYCHIATRIA POLSKA 1/2004 |
| Wydany: |
2004-02-01 |
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