Intermittent Hypoxia Stimulates Lipolysis, But Inhibits Differentiation and De Novo Lipogenesis in 3T3-L1 Cells

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11120%2F20%3A43919629" target="_blank" >RIV/00216208:11120/20:43919629 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11310/20:10403740 RIV/75010330:_____/20:00012984

Výsledek na webu

<a href="https://doi.org/10.1089/met.2019.0112" target="_blank" >https://doi.org/10.1089/met.2019.0112</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1089/met.2019.0112" target="_blank" >10.1089/met.2019.0112</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Intermittent Hypoxia Stimulates Lipolysis, But Inhibits Differentiation and De Novo Lipogenesis in 3T3-L1 Cells

Popis výsledku v původním jazyce

Exposure to intermittent hypoxia (IH) may play a role in the development of metabolic impairments in the context of obstructive sleep apnea syndrome, probably by elevated plasma levels of free fatty acids. Employing gas-permeable cultureware to grow differentiated human and mouse adipocytes , we directly studied the effects of pericellular oxygen fluctuations on key adipocyte metabolic functions-spontaneous lipolytic rates, triglyceride accumulation, lipogenesis, and expression of adipocyte-specific marker genes. 3T3-L1 fibroblasts and human subcutaneous preadipocytes were differentiated under conditions that induced repetitive pericellular-oxygen cycles IH between 1% O (5 min) and 16% O (5 min), continuously for 14 days or under control conditions. Chemicals were used to inhibit the flux of acetyl-CoA from glycolysis (alfa-cyano-4-hydroxy cinnamate) or the tricarboxylic acid cycle (SB204990), or to stimulate the flux of acetyl-CoA from pyruvate to the lipogenic pool. Lipolytic rate, intracellular lipids, and expression of adipocyte differentiation markers were assessed and -test or ANOVA were used to find significant differences. The rate of lipolysis increased by 211% in 3T3-L1 cells and by 39% in obese human adipocytes. Exposure to IH reduced intracellular lipid stores by 37% and reduced the expression of adipocyte differentiation markers. Pharmacological stimulation or inhibition of lipogenesis did not modify the intracellular lipid content under IH. Pericellular oxygen fluctuations directly stimulated lipolysis, but did not increase lipogenesis from endogenous substrates. Similarly, IH hampered adipocyte differentiation from precursors.

Název v anglickém jazyce

Intermittent Hypoxia Stimulates Lipolysis, But Inhibits Differentiation and De Novo Lipogenesis in 3T3-L1 Cells

Popis výsledku anglicky

Exposure to intermittent hypoxia (IH) may play a role in the development of metabolic impairments in the context of obstructive sleep apnea syndrome, probably by elevated plasma levels of free fatty acids. Employing gas-permeable cultureware to grow differentiated human and mouse adipocytes , we directly studied the effects of pericellular oxygen fluctuations on key adipocyte metabolic functions-spontaneous lipolytic rates, triglyceride accumulation, lipogenesis, and expression of adipocyte-specific marker genes. 3T3-L1 fibroblasts and human subcutaneous preadipocytes were differentiated under conditions that induced repetitive pericellular-oxygen cycles IH between 1% O (5 min) and 16% O (5 min), continuously for 14 days or under control conditions. Chemicals were used to inhibit the flux of acetyl-CoA from glycolysis (alfa-cyano-4-hydroxy cinnamate) or the tricarboxylic acid cycle (SB204990), or to stimulate the flux of acetyl-CoA from pyruvate to the lipogenic pool. Lipolytic rate, intracellular lipids, and expression of adipocyte differentiation markers were assessed and -test or ANOVA were used to find significant differences. The rate of lipolysis increased by 211% in 3T3-L1 cells and by 39% in obese human adipocytes. Exposure to IH reduced intracellular lipid stores by 37% and reduced the expression of adipocyte differentiation markers. Pharmacological stimulation or inhibition of lipogenesis did not modify the intracellular lipid content under IH. Pericellular oxygen fluctuations directly stimulated lipolysis, but did not increase lipogenesis from endogenous substrates. Similarly, IH hampered adipocyte differentiation from precursors.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30202 - Endocrinology and metabolism (including diabetes, hormones)

Projekt

<a href="/cs/project/GA18-10144S" target="_blank" >GA18-10144S: Hypoxií-indukované adaptace mitochondrií jako sjednocující faktor rozvoje diabetes mellitus 2. typu při syndromu spánkové apnoe</a><br>

Návaznosti

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

Rok uplatnění

2020

Kód důvěrnosti údajů

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

Název periodika

Metabolic Syndrome and Related Disorders

ISSN

1540-4196

e-ISSN

—

Svazek periodika

18

Číslo periodika v rámci svazku

3

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

8

Strana od-do

146-153

Kód UT WoS článku

000507270000001

EID výsledku v databázi Scopus

2-s2.0-85083041201