GDF11 inhibits adipogenesis and improves mature adipocytes metabolic function via WNT/beta-catenin and ALK5/SMAD2/3 pathways

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F22%3A00077732" target="_blank" >RIV/00159816:_____/22:00077732 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216224:14310/22:00127398

Výsledek na webu

<a href="https://onlinelibrary.wiley.com/doi/10.1111/cpr.13310" target="_blank" >https://onlinelibrary.wiley.com/doi/10.1111/cpr.13310</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1111/cpr.13310" target="_blank" >10.1111/cpr.13310</a>

Jazyk výsledku

angličtina

Název v původním jazyce

GDF11 inhibits adipogenesis and improves mature adipocytes metabolic function via WNT/beta-catenin and ALK5/SMAD2/3 pathways

Popis výsledku v původním jazyce

Objective: GDF11 is a member of the TGF-beta superfamily that was recently implicated as potential &quot;rejuvenating&quot; factor, which can ameliorate metabolic disorders. The main objective of the presented study was to closely characterize the role of GDF11 signaling in the glucose homeostasis and in the differentiation of white adipose tissue. Methods: We performed microscopy imaging, biochemical and transcriptomic analyses of adipose tissues of 9 weeks old ob/ob mice and murine and human preadipocyte cell lines. Results: Our in vivo experiments employing GDF11 treatment in ob/ob mice showed improved glucose/insulin homeostasis, decreased weight gain and white adipocyte size. Furthermore, GDF11 treatment inhibited adipogenesis in pre-adipocytes by ALK5-SMAD2/3 activation in cooperation with the WNT/beta-catenin pathway, whose inhibition resulted in adipogenic differentiation. Lastly, we observed significantly elevated levels of the adipokine hormone adiponectin and increased glucose uptake by mature adipocytes upon GDF11 exposure. Conclusion: We show evidence that link GDF11 to adipogenic differentiation, glucose, and insulin homeostasis, which are pointing towards potential beneficial effects of GDF11-based &quot;anti-obesity&quot; therapy.

Název v anglickém jazyce

GDF11 inhibits adipogenesis and improves mature adipocytes metabolic function via WNT/beta-catenin and ALK5/SMAD2/3 pathways

Popis výsledku anglicky

Objective: GDF11 is a member of the TGF-beta superfamily that was recently implicated as potential &quot;rejuvenating&quot; factor, which can ameliorate metabolic disorders. The main objective of the presented study was to closely characterize the role of GDF11 signaling in the glucose homeostasis and in the differentiation of white adipose tissue. Methods: We performed microscopy imaging, biochemical and transcriptomic analyses of adipose tissues of 9 weeks old ob/ob mice and murine and human preadipocyte cell lines. Results: Our in vivo experiments employing GDF11 treatment in ob/ob mice showed improved glucose/insulin homeostasis, decreased weight gain and white adipocyte size. Furthermore, GDF11 treatment inhibited adipogenesis in pre-adipocytes by ALK5-SMAD2/3 activation in cooperation with the WNT/beta-catenin pathway, whose inhibition resulted in adipogenic differentiation. Lastly, we observed significantly elevated levels of the adipokine hormone adiponectin and increased glucose uptake by mature adipocytes upon GDF11 exposure. Conclusion: We show evidence that link GDF11 to adipogenic differentiation, glucose, and insulin homeostasis, which are pointing towards potential beneficial effects of GDF11-based &quot;anti-obesity&quot; therapy.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

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OECD FORD obor

10601 - Cell biology

Projekt

<a href="/cs/project/EF15_003%2F0000492" target="_blank" >EF15_003/0000492: Mapování molekulární podstaty procesů stárnutí pro vývoj nových léčebných metod</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2022

Kód důvěrnosti údajů

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

Název periodika

CELL PROLIFERATION

ISSN

0960-7722

e-ISSN

1365-2184

Svazek periodika

55

Číslo periodika v rámci svazku

10

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

15

Strana od-do

nestrankovano

Kód UT WoS článku

000835228000001

EID výsledku v databázi Scopus

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