Year-end Sale % OFF 
Abstract
BackgroundObesity is characterized by a chronic low-grade inflammation and altered stress responses in key metabolic tissues. Impairment of heat shock response (HSR) has been already linked to diabetes and insulin resistance as reflected by decrease in heat shock proteins (HSPs) expression. However, the status of HSR in non-diabetic human obese has not yet been elucidated. The aim of the current study was to investigate whether obesity triggers a change in the HSR pattern and the impact of physical exercise on this pattern at protein and mRNA levels.MethodsTwo groups of adult non-diabetic human subjects consisting of lean and obese (n = 47 for each group) were enrolled in this study. The expression pattern of HSP-27, DNAJB3/HSP-40, HSP-60, HSC-70, HSP72, HSP-90 and GRP-94 in the adipose tissue was primarily investigated by immunohistochemistry and then complemented by western blot and qRT-PCR in Peripheral blood mononuclear cells (PBMCs). HSPs expression levels were correlated with various physical, clinical and biochemical parameters. We have also explored the effect of a 3-month moderate physical exercise on the HSPs expression pattern in obese subjects.ResultsObese subjects displayed increased expression of HSP-60, HSC-70, HSP-72, HSP-90 and GRP-94 and lower expression of DNAJB3/HSP-40 (P < 0.05). No differential expression was observed for HSP-27 between the two groups. Higher levels of HSP-72 and GRP-94 proteins correlated positively with the indices of obesity (body mass index and percent body fat) and circulating levels of IFN-gamma-inducible protein 10 (IP-10) and RANTES chemokines. This expression pattern was concomitant with increased inflammatory response in the adipose tissue as monitored by increased levels of Interleukin-6 (IL-6), Tumor necrosis factor-α (TNF-α), and RANTES (P < 0.05). Physical exercise reduced the expression of various HSPs in obese to normal levels observed in lean subjects with a parallel decrease in the endogenous levels of IL-6, TNF-α, and RANTES.ConclusionTaken together, these data indicate that obesity triggers differential regulation of various components of the HSR in non-diabetic subjects and a 3-month physical moderate exercise was sufficient to restore the normal expression of HSPs in the adipose tissue with concomitant attenuation in the inflammatory response.
Highlights
Obesity has become a major medical, social and economic burden worldwide by reducing both life quality and expectancy [1,2]
Obese subjects had increased inflammatory response as monitored by the inflammatory chemokines inducible protein 10 (IP-10), MIP-1a and RANTES (P = 0.0002, P = 0.04 and P = 0.01; respectively) but there was no significant difference in the plasma levels of the classic inflammatory markers IL-6 and Tumor necrosis factor-α (TNF-α) between lean and obese groups
The endogenous expression of IL-6 and TNF-α protein and mRNA in the adipose tissue were significantly increased in obese subjects (Figure 1)
Summary
Obesity has become a major medical, social and economic burden worldwide by reducing both life quality and expectancy [1,2]. It represents a major risk factor for various health disorders including insulin resistance, diabetes, hypertension and cardiovascular diseases (CVD). HSR is one of the important cellular endogenous components that allow the body to cope with stressful conditions including metabolic stress [9,10] This response involves a set of highly conserved proteins called Heat shock proteins (HSPs) known as molecular chaperones, glucose regulated proteins (GRPs) and other proteins essential for protection and recovery from tissue damage [11,12,13]. The aim of the current study was to investigate whether obesity triggers a change in the HSR pattern and the impact of physical exercise on this pattern at protein and mRNA levels
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
