Title
Doprinos povećanog kalorijskog unosa u ranom postnatalnom periodu razvoju metaboličkih poremećaja u animalnom modelu policističnih jajnika
Creator
Mićić, Bojana, 1991-
CONOR:
62282505
Copyright date
2023
Object Links
Select license
Autorstvo-Nekomercijalno-Bez prerade 3.0 Srbija (CC BY-NC-ND 3.0)
License description
Dozvoljavate samo preuzimanje i distribuciju dela, ako/dok se pravilno naznačava ime autora, bez ikakvih promena dela i bez prava komercijalnog korišćenja dela. Ova licenca je najstroža CC licenca. Osnovni opis Licence: http://creativecommons.org/licenses/by-nc-nd/3.0/rs/deed.sr_LATN. Sadržaj ugovora u celini: http://creativecommons.org/licenses/by-nc-nd/3.0/rs/legalcode.sr-Latn
Language
Serbian
Cobiss-ID
Theses Type
Doktorska disertacija
description
Datum odbrane: 22.12.2023.
Other responsibilities
Academic Expertise
Prirodno-matematičke nauke
Academic Title
-
University
Univerzitet u Beogradu
Faculty
Biološki fakultet
Alternative title
Contribution of early postnatal overfeeding to metabolic disorders in animal model of polycystic ovary syndrome
Publisher
[B. B. Mićić]
Format
88 str.
description
Biologija - Animalna i humana fiziologija / Biology
- Animal and human physiology
Abstract (en)
Sindrom policističnih jajnika (PCOS) je reproduktivni poremećaj u čijoj osnovi je
hiperandrogenemija, ali ga prate i metaboličke komplikacije. PCOS se može javiti u
prepubertetskom uzrastu , a povećanj e telesne mase tokom ovog uzrasta predisponira za
kasniji razvoj sindroma. Kalorijski suficit u perinatalnom periodu, koji se kod glodara
postiže manipulacijom veličine legla, utiče na neuroendokrino programiranje, dovodeći do
gojenja i ranijeg nastupanja puberteta. Cilj ove disertacije je bio da se na animalnom
modelu PCOS ispita doprinos povećanog kalorijskog unosa u ranom postnatalnom
periodu razvoju metaboličkih poremećaja udruženih sa sindromom. M odel PCOS je
kreiran tretmanom ženki paco va 5α dihidrotestosteronom ( DHT), a prepubertetska
gojaznost posti gnuta kalorijsk i m suficit om kroz smanjenje veličine legla Analizirani su
parametri sistemske insulinske osetljivosti i lipidni status, kao i markeri insulin s ke
signalizacije i energetskog meta bolizma na nivou visceralnog (VAT) i subkutanog (SAT)
masnog tkiva i skeletnih mišića. DHT tretman u kombinaciji sa povećanim kal orijskim
unosom je uslovi o sistemsku hiperinsulinemiju i smanjenje insulinske osetljivosti. Uprkos
hipertrofiji adipocita, insu linska osetljivost na nivou VAT je očuvana, verovatno usled
aktivacije AMPK. Izostanak proliferacije SAT i istovremeno aktivirani lipolitički i lipogeni
putevi ukazuju na njegovu d i sfunkcionalnost. Skeletni mišići u uslovima smanjene
osetljivosti na insuli n koriste masne kiseline kao energetski supstrat, a aktivacija AMPK
doprinosi funkcionalnosti tkiva kroz povećanje stope β oksidacije. Dobijeni rezultati
sugerišu da povećanje telesne mase pre puberteta predisponira razvoj insulinske
rezi s tencije u PCOS, dok je za njeno puno ispoljavanje ključna interakcija sa
hiperandrogenemijom.
Abstract ()
Polycystic ovary syndrome (PCOS) is a reproductive disorder based on
hyperandrogenemia but also associated with metabolic complications. PCOS can occur in
girls before puberty, and the increase in body weight at this age predisposes them to later
developme nt of the syndrome. Increased caloric intake in the perinatal period, easily
mimicked in rodents by manipulating litter size, affects neuroendocrine programming and
leads to hyperphagia and weight gain, as well as earlier onset of puberty. The aim of this
doctoral dissertation was to examine the contribution of increased caloric intake in early
postnatal period to the development of metabolic disorders associated with the syndrome
using an animal model of PCOS. An animal model of PCOS induced by 5α
dihydrot estosterone was additionally challenged with caloric excess by litter size
reduction to induce prepubertal obesity. Parameters of systemic insulin sensitivity and
lipid status were analyzed, as were markers of insulin signaling and energy metabolism at
the level of visceral (VAT) and subcutaneous (SAT) adipose tissue and skeletal muscle.
The combination of treatments resulted in systemic hyperinsulinemia and decreased
insulin sensitivity. Despite adipocyte hypertrophy, insulin sensitivity is maintained at t he
VAT level, likely due to activation of AMPK. The absence of SAT proliferation and the
concomitantly activated lipolytic and lipogenic metabolic pathways suggest its
dysfunction. Skeletal muscles in conditions of reduced sensitivity to insulin use fatty acids
as an energy substrate, and activation of AMPK contributes to the functionality of this
tissue by increasing the rate of β oxidation. Our results suggest that weight gain before
puberty predisposes to the development of insulin resistance in PCOS, wh ile interaction
with hyperandrogenemia is critical for its full manifestation.
Authors Key words
sindrom policističnih jajnika, prepubertetska gojaznost, 5α
dihidrotestosteron, hiperandrogenemija, rani postnatalni povećani kalorijski unos,
visceralno masno tkivo, subkutano masno tkivo, skeletni mišići, insulinska rezistencija,
hiperinsulinemija
Authors Key words
PCOS, prepubertal weight gain, 5α dihydrotestosterone, hyperandrogenemia,
early postnatal overfeeding, visceral adipose tissue, subcutaneous adipose tissue, skeletal
muscle, insulin resistance, hyperinsulinemia.
Classification
577.175.72:612.621(043.3)
Type
Tekst
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