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Carbon monoxide-induced metabolic switch in adipocytes improves insulin resistance in obese mice

Identifikátory výsledku

  • Kód výsledku v IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F18%3A10383532" target="_blank" >RIV/00216208:11110/18:10383532 - isvavai.cz</a>

  • Výsledek na webu

    <a href="https://doi.org/10.1172/jci.insight.123485" target="_blank" >https://doi.org/10.1172/jci.insight.123485</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1172/jci.insight.123485" target="_blank" >10.1172/jci.insight.123485</a>

Alternativní jazyky

  • Jazyk výsledku

    angličtina

  • Název v původním jazyce

    Carbon monoxide-induced metabolic switch in adipocytes improves insulin resistance in obese mice

  • Popis výsledku v původním jazyce

    Obesity is characterized by accumulation of adipose tissue and is one the most important risk factors in the development of insulin resistance. Carbon monoxide-releasing (CO-releasing) molecules (CO-RMs) have been reported to improve the metabolic profile of obese mice, but the underlying mechanism remains poorly defined. Here, we show that oral administration of CORM-401 to obese mice fed a high-fat diet (HFD) resulted in a significant reduction in body weight gain, accompanied by a marked improvement in glucose homeostasis. We further unmasked an action we believe to be novel, by which CO accumulates in visceral adipose tissue and uncouples mitochondrial respiration in adipocytes, ultimately leading to a concomitant switch toward glycolysis. This was accompanied by enhanced systemic and adipose tissue insulin sensitivity, as indicated by a lower blood glucose and increased Akt phosphorylation. Our findings indicate that the transient uncoupling activity of CO elicited by repetitive administration of CORM-401 is associated with lower weight gain and increased insulin sensitivity during HFD. Thus, prototypic compounds that release CO could be investigated for developing promising insulin-sensitizing agents.

  • Název v anglickém jazyce

    Carbon monoxide-induced metabolic switch in adipocytes improves insulin resistance in obese mice

  • Popis výsledku anglicky

    Obesity is characterized by accumulation of adipose tissue and is one the most important risk factors in the development of insulin resistance. Carbon monoxide-releasing (CO-releasing) molecules (CO-RMs) have been reported to improve the metabolic profile of obese mice, but the underlying mechanism remains poorly defined. Here, we show that oral administration of CORM-401 to obese mice fed a high-fat diet (HFD) resulted in a significant reduction in body weight gain, accompanied by a marked improvement in glucose homeostasis. We further unmasked an action we believe to be novel, by which CO accumulates in visceral adipose tissue and uncouples mitochondrial respiration in adipocytes, ultimately leading to a concomitant switch toward glycolysis. This was accompanied by enhanced systemic and adipose tissue insulin sensitivity, as indicated by a lower blood glucose and increased Akt phosphorylation. Our findings indicate that the transient uncoupling activity of CO elicited by repetitive administration of CORM-401 is associated with lower weight gain and increased insulin sensitivity during HFD. Thus, prototypic compounds that release CO could be investigated for developing promising insulin-sensitizing agents.

Klasifikace

  • Druh

    J<sub>imp</sub> - Článek v periodiku v databázi Web of Science

  • CEP obor

  • OECD FORD obor

    30202 - Endocrinology and metabolism (including diabetes, hormones)

Návaznosti výsledku

  • Projekt

  • Návaznosti

    V - Vyzkumna aktivita podporovana z jinych verejnych zdroju

Ostatní

  • Rok uplatnění

    2018

  • Kód důvěrnosti údajů

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

Údaje specifické pro druh výsledku

  • Název periodika

    JCI Insight [online]

  • ISSN

    2379-3708

  • e-ISSN

  • Svazek periodika

    3

  • Číslo periodika v rámci svazku

    22

  • Stát vydavatele periodika

    US - Spojené státy americké

  • Počet stran výsledku

    14

  • Strana od-do

  • Kód UT WoS článku

    000450338900011

  • EID výsledku v databázi Scopus

    2-s2.0-85063243749