Metformin attenuates myocardium dicarbonyl stress induced by chronic hypertriglyceridemia

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60461373%3A22330%2F18%3A43913828" target="_blank" >RIV/60461373:22330/18:43913828 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00023761:_____/18:N0000042 RIV/00023001:_____/18:00076902

Výsledek na webu

<a href="http://www.biomed.cas.cz/physiolres/pdf/67/67_181.pdf" target="_blank" >http://www.biomed.cas.cz/physiolres/pdf/67/67_181.pdf</a>

DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Metformin attenuates myocardium dicarbonyl stress induced by chronic hypertriglyceridemia

Popis výsledku v původním jazyce

Reactive dicarbonyls stimulate production of advanced glycation endproducts, increase oxidative stress and inflammation and contribute to the development of vascular complications. We measured concentrations of dicarbonyls - methylglyoxal (MG), glyoxal (GL) and 3-deoxyglucosone (3-DG) - in the heart and kidney of a model of metabolic syndrome - hereditary hypertriglyceridemic rats (HHTg) and explored its modulation by metformin. Adult HHTg rats were fed a standard diet with or without metformin (300 mg/kg b.wt.) and dicarbonyl levels and metabolic parameters were measured. HHTg rats had markedly elevated serum levels of triacylglycerols (p&lt;0.001), FFA (p&lt;0.01) and hepatic triacylglycerols (p&lt;0.001) along with increased concentrations of reactive dicarbonyls in myocardium (MG: p&lt;0.001; GL: p&lt;0.01; 3-DG: p&lt;0.01) and kidney cortex (MG: p&lt;0.01). Metformin treatment significantly reduced reactive dicarbonyls in the myocardium (MG: p&lt;0.05, GL: p&lt;0.05, 3-DG: p&lt;0.01) along with increase of myocardial concentrations of reduced glutathione (p&lt;0.01) and glyoxalase 1 mRNA expression (p&lt;0.05). Metformin did not have any significant effect on dicarbonyls, glutathione or on glyoxalase 1 expression in kidney cortex. Chronically elevated hypertriglyceridemia was associated with increased levels of dicarbonyls in heart and kidney. Beneficial effects of metformin on reactive dicarbonyls and glyoxalase in the heart could contribute to its cardioprotective effects.

Název v anglickém jazyce

Metformin attenuates myocardium dicarbonyl stress induced by chronic hypertriglyceridemia

Popis výsledku anglicky

Reactive dicarbonyls stimulate production of advanced glycation endproducts, increase oxidative stress and inflammation and contribute to the development of vascular complications. We measured concentrations of dicarbonyls - methylglyoxal (MG), glyoxal (GL) and 3-deoxyglucosone (3-DG) - in the heart and kidney of a model of metabolic syndrome - hereditary hypertriglyceridemic rats (HHTg) and explored its modulation by metformin. Adult HHTg rats were fed a standard diet with or without metformin (300 mg/kg b.wt.) and dicarbonyl levels and metabolic parameters were measured. HHTg rats had markedly elevated serum levels of triacylglycerols (p&lt;0.001), FFA (p&lt;0.01) and hepatic triacylglycerols (p&lt;0.001) along with increased concentrations of reactive dicarbonyls in myocardium (MG: p&lt;0.001; GL: p&lt;0.01; 3-DG: p&lt;0.01) and kidney cortex (MG: p&lt;0.01). Metformin treatment significantly reduced reactive dicarbonyls in the myocardium (MG: p&lt;0.05, GL: p&lt;0.05, 3-DG: p&lt;0.01) along with increase of myocardial concentrations of reduced glutathione (p&lt;0.01) and glyoxalase 1 mRNA expression (p&lt;0.05). Metformin did not have any significant effect on dicarbonyls, glutathione or on glyoxalase 1 expression in kidney cortex. Chronically elevated hypertriglyceridemia was associated with increased levels of dicarbonyls in heart and kidney. Beneficial effects of metformin on reactive dicarbonyls and glyoxalase in the heart could contribute to its cardioprotective effects.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

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OECD FORD obor

10613 - Zoology

Projekt

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Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2018

Kód důvěrnosti údajů

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

Název periodika

Physiological Research

ISSN

0862-8408

e-ISSN

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Svazek periodika

67

Číslo periodika v rámci svazku

2

Stát vydavatele periodika

CZ - Česká republika

Počet stran výsledku

9

Strana od-do

181-189

Kód UT WoS článku

000431452400004

EID výsledku v databázi Scopus

2-s2.0-85046754419