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 m RNA levels.
Taken 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. It also represents a major risk factor for various health disorders including insulin resistance, diabetes, hypertension and cardiovascular diseases (CVD).
As physical inactivity, sedentary lifestyle and increased energy intake are key contributing factors to obesity, healthy diet and regular exercise are usually prescribed as a first line non-medical therapy to control obesity-related complications .
Each exercise session includes 10 minutes warming-up and cooling down steps at 50-60% of max HR, along with 40 minutes of the prescribed exercise program at 65-80% of max HR.
HSPs can also be released into the circulation and exert an immune-stimulatory effect by interacting with pattern recognition receptors, such as toll-like receptors, and thereby activate the host inflammatory response .
The best characterized heat shock protein is HSP-72, the inducible member of the HSP-70 family and its role in insulin resistance was recently a subject of intense investigations.
Strength training was performed 2 to 3 times a week according to the program plan.
Exercise intensity, duration and blood pressures were recorded for each session.
Obesity is characterized by a chronic low-grade inflammation and altered stress responses in key metabolic tissues.