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...

Full description

Saved in:
Bibliographic Details
Published inGenetic testing and molecular biomarkers Vol. 23; no. 10; p. 737
Main Authors Sabbah, Norhan Abdalla, Rezk, Noha A, Saad, Mohamed S S
Format Journal Article
LanguageEnglish
Published United States 01.10.2019
Subjects
Online AccessGet more information

Cover

Loading…
More Information
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.
ISSN:1945-0257
DOI:10.1089/gtmb.2019.0062