Relationship Between Heat Shock Protein Expression and Obesity With and Without Metabolic Syndrome
Obesity is considered a chronic inflammatory disease in which the physiological mechanism responsible for reducing inflammation is weakened, prompting low-grade inflammation throughout the body. One of the key stress response systems that is dysregulated in obesity is the heat shock response, which...
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Published in | Genetic testing and molecular biomarkers Vol. 23; no. 10; p. 737 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
United States
01.10.2019
|
Subjects | |
Online Access | Get more information |
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Summary: | Obesity is considered a chronic inflammatory disease in which the physiological mechanism responsible for reducing inflammation is weakened, prompting low-grade inflammation throughout the body. One of the key stress response systems that is dysregulated in obesity is the heat shock response, which is a critical defense mechanism that is activated in stressful conditions. Obesity is primary to metabolic syndrome (MetS) as it appears to lead to the increase in other MetS risk factors.
We aimed to investigate the different expression levels of intracellular heat shock protein (
) 70 and
in obese patients with and without MetS and compare these levels to those of a lean control group.
One hundred ten lean subjects were compared with 44 obese subjects without MetS and 56 obese subjects with MetS.
and
mRNA expression levels were measured by quantitative real-time polymerase chain reaction.
mRNA expression was significantly higher in obese subjects without MetS than in lean subjects (
= 0.04), whereas
mRNA expression was significantly lower in obese subjects with MetS than in those without MetS (
= 0.02) as well as in those in the lean group (
= 0.03).
mRNA expression was significantly lower in obese subjects with MetS than in those without MetS and in lean subjects (
= 0.037 and 0.031, respectively).
We conclude that the intracellular expression levels of
and
may play an important role in the pathogenesis of MetS. |
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ISSN: | 1945-0257 |
DOI: | 10.1089/gtmb.2019.0062 |