Autocrine effects of transgenic resistin reduce palmitate and glucose oxidation in brown adipose tissue

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F16%3A00460150" target="_blank" >RIV/68378050:_____/16:00460150 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/67985823:_____/16:00460150 RIV/61389005:_____/16:00460150 RIV/00216208:11160/16:10338232 RIV/00023001:_____/16:00059987

Výsledek na webu

<a href="http://dx.doi.org/10.1152/physiolgenomics.00122.2015" target="_blank" >http://dx.doi.org/10.1152/physiolgenomics.00122.2015</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1152/physiolgenomics.00122.2015" target="_blank" >10.1152/physiolgenomics.00122.2015</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Autocrine effects of transgenic resistin reduce palmitate and glucose oxidation in brown adipose tissue

Popis výsledku v původním jazyce

Resistin has been originally identified as an adipokine that links obesity to insulin resistance in mice. In our previous studies in spontaneously hypertensive rats (SHR) expressing a nonsecreted form of mouse resistin (Retn) transgene specifically in adipose tissue (SHR-Retn), we have observed an increased lipolysis and serum free fatty acids, ectopic fat accumulation in muscles and insulin resistance. Recently, brown adipose tissue (BAT) has been suggested to play an important role in the pathogenesis of metabolic disturbances. In the current study, we have analyzed autocrine effects of transgenic resistin on BAT glucose and lipid metabolism and mitochondrial function in the SHR-Retn versus nontransgenic SHR controls. We observed that interscapular BAT isolated from SHR-Retn transgenic rats when compared to SHR controls showed a lower relative weight, significantly reduced both basal and insulin stimulated incorporation of palmitate into BAT lipids, and significantly decreased palmitate oxidation and glucose oxidation. Gene expression profiles in BAT identified differentially expressed genes involved in skeletal muscle and connective tissue development, inflammation and MAPK and insulin signaling. These results provide evidence that autocrine effects of resistin attenuate differentiation and activity of BAT and thus may play a role in the pathogenesis of insulin resistance in the rat.

Název v anglickém jazyce

Autocrine effects of transgenic resistin reduce palmitate and glucose oxidation in brown adipose tissue

Popis výsledku anglicky

Resistin has been originally identified as an adipokine that links obesity to insulin resistance in mice. In our previous studies in spontaneously hypertensive rats (SHR) expressing a nonsecreted form of mouse resistin (Retn) transgene specifically in adipose tissue (SHR-Retn), we have observed an increased lipolysis and serum free fatty acids, ectopic fat accumulation in muscles and insulin resistance. Recently, brown adipose tissue (BAT) has been suggested to play an important role in the pathogenesis of metabolic disturbances. In the current study, we have analyzed autocrine effects of transgenic resistin on BAT glucose and lipid metabolism and mitochondrial function in the SHR-Retn versus nontransgenic SHR controls. We observed that interscapular BAT isolated from SHR-Retn transgenic rats when compared to SHR controls showed a lower relative weight, significantly reduced both basal and insulin stimulated incorporation of palmitate into BAT lipids, and significantly decreased palmitate oxidation and glucose oxidation. Gene expression profiles in BAT identified differentially expressed genes involved in skeletal muscle and connective tissue development, inflammation and MAPK and insulin signaling. These results provide evidence that autocrine effects of resistin attenuate differentiation and activity of BAT and thus may play a role in the pathogenesis of insulin resistance in the rat.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

FB - Endokrinologie, diabetologie, metabolismus, výživa

OECD FORD obor

—

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2016

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Physiological Genomics

ISSN

1094-8341

e-ISSN

—

Svazek periodika

48

Číslo periodika v rámci svazku

6

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

8

Strana od-do

420-427

Kód UT WoS článku

000378338300005

EID výsledku v databázi Scopus

2-s2.0-84983770971