Τόμος 17 (1999) – Τεύχος 2 – Άρθρο 5Σ – Επιθεώρηση Κλινικής Φαρμακολογίας και Φαρμακοκινητικής-Ελληνική Έκδοση – Volume 17 (1999) – Issue 2 – Article 5Σ – Epitheorese Klinikes Farmakologias και Farmakokinetikes-Greek Edition

Από | | Άρθρο - Article, Γεωργία Μαργαρίτη,Georgia Margariti, Ναυσικά Βιολάκη - Nausica Violaki, Πλήρες Κείμενο στα Ελληνικά - Full Text in Greek, Πλούταρχος Κούρτης - Ploutarchos Kourtis, Σταύρος Τ. Πλέσσας - Stavros T. Plessas, Υβόννη Δημουλά - Yvonne Dimoula

 

Τίτλος – Title

Παχυσαρκία και Ορμόνες

Obesity and Hormones
Συγγραφέας – Author

Υβόννη Δημουλά1,  Πλούταρχος Κούρτης1, Ναυσικά Βιολάκη2, Γεωργία Μαργαρίτη2, Σταύρος Τ.  Πλέσσας2

1 Εργαστήριο Φυσιολογίας του Ανθρώπου, Σχολή Επιστημών Υγείας ΤΕΙ Αθήνας 2 Τμήμα Νοσηλευτικής, Πανεπιστήμιο Αθηνών

Yvonne Dimoula1, Ploutarchos Kourtis1, Nausika Violaki2, Georgia Margariti2, Stavros T. Plessas2

1 Laboratory of Physiology, Department of Health and Caring Professions, Technological Educa­tional Institution of Athens, 2 Faculty of Nurs­ing, University of Athens, Athens Greece
Παραπομπή – Citation

Δημουλά,Χ.,  Κούρτης,Π., Βιολάκη,Ν., Μαργαρίτη,Γ., Πλέσσας,Σ.Τ. : Παχυσαρκία και Ορμόνες , Επιθεώρηση Κλιν. Φαρμακολ. Φαρμακοκινητ. 17 : 137-152 (1999)

Dimoula,Y., Kourtis,P., Violaki,N., Margariti,G., Plessas,S.T. : Obesity and Hormones, Epitheorese Klin. Farmakol. Farmakokinet. 17: 137-152 (1999)
Ημερομηνία Δημοσιευσης – Publication Date
18-09-1999
Γλώσσα Πλήρους Κειμένου –
Full Text Language

Ελληνικά – Greek
Παραγγελία – Αγορά –
Order – Buy
Ηλεκτρονική Μορφή: pdf (15 €) –
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Λέξεις κλειδιά – Keywords

Παχυσαρκία, ορμόνες, αδρεναλίνη, νοραδρεναλίνη, σεροτονίνη, νευροπεπτίδιο Υ, πεπτίδιο ΥΥ, γαλανίνη, γλυκαγονοειδές πεπτίδιο, ινσουλίνη, εκλυτικός παράγων κορτικοτροπίνης, θυροξίνη, τριιωδοθυρονίνη, λεπτίνη, ασύζευκτες πρωτεΐνες

Obesity, hormones, adrenalin, noradrenalin, serotonin, neuropeptide Y, peptide YY, galanin, glucagon-like peptide, insulin, corticotropin releasing hormone, thyroxin, leptin, uncoupling proteins
Λοιποί Όροι – Other Terms

Άρθρο

Article
Περίληψη – Summary

Η παχυσαρκία, η αύξηση δηλαδή του βάρους του σώματος, τουλάχιστον κατά 15%, από αποθηκευμένο λίπος, είναι νόσος πολυπαραγοντικής αιτιολογίας, αποτελούσα παράγοντα κινδύνου για πολλές παθήσεις με σημαντικό κοινωνικοοικονομικό κόστος. Η ειδική δίαιτα απίσχνασης δεν επιτυγχάνει συνήθως μακροχρόνια διατήρηση του κανονικού σωματικού βάρους και οι περισσότεροι παχύσαρκοι ανακτούν το απολεσθέν βάρος. Αυτή η σχετική σταθερότητα στο σωματικό βάρος δείχνει πως το ισοζύγιο ενεργείας πιθανόν να ελέγχεται από καμπύλη παλίνδρομης αλληλορύθμισης που διατηρεί σταθερές τις συνολικές αποθήκες ενεργείας του σώματος. Πολλές ουσίες έχει ευρεθεί να επηρεάζουν τη διατροφική συμπεριορά. Στις ουσίες που αυξάνουν την πρόσληψη τροφής συμπεριλαμβάνονται η νοραδρεναλίνη, το GABA, η εκλυτική ορμόνη της αυξητικής ορμόνης, τα οπιοειδή β-ενδορφίνη, εγκεφαλίνη και δυνορφίνη, η γαλανίνη, το πεπτίδιο ΥΥ και τέλος το νευροπεπτίδιο Υ, που αποτελεί ένα από τους ισχυρότερους, μέχρι σήμερα γνωστούς, διεγέρτες της πρόσληψης τροφής. Στις ουσίες που αναστέλλουν την πρόσληψη τροφής συμπεριλαμβάνονται η σεροτονίνη, η ντοπαμίνη, υπό ορισμένες συνθήκες η αδρεναλίνη και η νοραδρεναλίνη, η νευροτασίνη, η εκλυτική ορμόνη της κορτικοτροπίνης, η χoλoκυστοκυνίνη, η καλσιτονίνη, η ινσουλίνη, όταν χορηγείται κεντρικά και το γλυκαγονοειδές πεπτίδιο-1. H ανακάλυψη της λεπτίνης το 1994, της κυριότερης από τις ορμόνες που παράγει ο λιπώδης ιστός, προσέθεσε ένα σημαντικό νέο δεδομένο στο πρόβλημα της παχυσαρκίας. Η λεπτίνη είναι παράγωγο του ob γονιδίου και συντίθεται από το λευκό λιπώδη ιστό σε συνθήκες ενεργειακής επαρκείας. Οι συγκεντρώσεις της λεπτίνης στο πλάσμα συσχετίζονται με τη μάζα του λιπώδους ιστού, μειώνονται μετά από απώλεια βάρους και γίνονται αισθητές από ομάδες νευρώνων στον υποθάλαμο. Κατά τη διάρκεια της νηστείας οι συγκεντρώσεις της λεπτίνης πίπτουν με αποτέλεσμα να ενεργοποιείται αντιρροπιστική ορμονική και μεταβολική απόκριση καθώς και κατάλληλη διατροφική συμπεριφορά, όταν υπάρχει διαθέσιμη τροφή. Η αύξηση του βάρους αυξάνει τις συγκεντρώσεις λεπτίνης και προκαλεί διαφορετική απόκριση που οδηγεί σε κατάσταση αρνητικού ισοζυγίου ενεργείας. Τέλος, η πρόσφατη ανακάλυψη των ασύζευκτων πρωτεϊνών των μιτοχονδρίων έδωσε νέα ώθηση στην έρευνα της παχυσαρκίας. Ασύζευκτη πρωτεΐνη περιεγράφη αρχικά στην έσω μεμβράνη των μιτοχονδρίων των κυττάρων του φαιού λιπώδους ιστού, επιτρέπουσα την οξείδωση θρεπτικών ουσιών. Αντίστοιχες πρωτεΐνες ευρέθησαν σε πολλούς ιστούς και ρυθμίζονται από ορμόνες και διαιτητικούς παράγοντες. Το επίπεδο της έκφρασης και/ή της δραστηριότητας αυτών των πρωτεϊνών είναι πιθανό να παίζει ρόλο στις διαφορές στο μεταβολισμό και στη μάζα του σωματικού λίπους που υπάρχουν στα διάφορα άτομα με ενδεχόμενη συμμετοχή στην ανάπτυξη παχυσαρκίας στον άνθρωπο.

The ability to store sufficient quantities of energy-dense triglyceride in adi­pose tissue allows survival during the frequent periods of food deprivation encountered during evolution. However, obesity which means the presence of excess adipose tissue, can be maladaptive. Obesity is an independent risk factor for a number of medical conditions, including diabetes mellitus, hypertension, coro­nary heart disease, depression, musculoskeletal disorders and several cancers. The economic costs associated with specific obesity-related diseases in USA represent 5.5% to 7.8% of total healthcare expenditures. A complex physiologi­cal system has evolved to regulate fuel stores and energy balance to an optimum level, and body weight appears to be homeostatically regulated at a certain set point. To be able to regulate body weight the brain must be able to sense the size of adipose mass and to adjust hunger, satiety and energy expenditure accord­ingly so as to maintain and defend body fat   mass at a certain level. Many monoamines and peptides (substances) have been found to have effects in eating behavior. The feeding stimula­tory transmitters include the catecholamine norepinephrine, the aminoacid GABA, the re­leas­ing factor of growth hormone, the opioids β-endorphin, enkefalin and dynorphin, the pan­creatic polypeptides neuropeptide Y (which is one of the most potent inducers of food intake known in central administration) and peptide YY and finally the peptide galanin. The feeding-inhibitory neurotransmitters include the monoamines 5-HT, DA, and under certain conditions NE and EPI, neurotensin, corticotro­phin releas­ing hormone, cholo-cystokinin, calci­tonin, cen­trally administered insulin, glucagon like peptide-1 and glucagon. The discovery of leptin in 1994 has provided a major new piece in the puzzle of obesity. Leptin, product of the ob gene, controls appetite through the hypo­thalamus and may affect many other tissues because of the widespread distribution of its receptors. Leptin is synthesised by white adi­pose tissue under conditions of high energy availability and the plasma leptin levels are highly correlated with adipose tissue mass and fall in both humans and mice after weight loss. Leptin concentrations are sensed by groups of neurons in the hypo-thala­mus. During starvation, leptin levels fall, thus activating a behavioural, hormonal and metabolic response that is adap­tive when food is available. Weight gain in­creases plasma leptin concentra­tion and elicits a different response, leading to a state of negative energy balance. Finally the recent discovery of uncoupling proteins brings new hope to obesity re-search. Uncoupling protein, originally de­scribed in the inner mito­chondrial membrane of brown adipose tissue, permits the oxidation of fuels without the gen­eration of ATP. Closely related proteins have now been found in many other tissues and shown to be regulated by thyroid hormones and dietary factors. The expression level and/or the activity of these proteins may play a role in the differences in metabolic rates and body fat mass observed between individuals with implications for the development of human obesity.

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