In this study, we investigated the effects of 8 weeks aerobic exercise training in male smoker with normal weight. Body variables (i.e. body weight and BMI), insulin resistance (i.e. fasting glucose, insulin, and HOMA-IR), and blood lipid profile (i.e. TG, TC, LDL-C) decreased in the ES group compared with the CS group after the 8-week exercise intervention. Our result are in line with previous observations and reinforce the beneficial effect of exercise training on these important metabolic factor in confronting many diseases such as metabolic syndrome, type 2diabetes, and cardiovascular disease [6, 16–17].
Many studies have indicated lower concentration levels of omentin-1 in obesity, impaired glucose tolerance and type 2diabetes [18–20]. Also, lower levels of omentin in response to cigarette smoking may contribute to increased susceptibility to infections in smokers [11]. In order to investigating the changes of omentin-1 in smoker, we explored the effect of 8-weeks aerobic exercise training on circulating omentin-1 in smoker and examined the omentin-1 response in relation to insulin resistance [21]. The findings showed that 8-weeks of aerobic exercise training at 55–70% of MHR led to marked rise of omentin-1 concentration in the participants of E and ES groups. Unfortunately, to the best of our knowledge, no report to date has examined the effect of exercise on circulating omentin-1 level in smoker. Nevertheless, some studies have been done about the effect of exercise training on omentin-1 [21]. Our result was consistent with that of the studies by Wilms et al. [22], Ouerghi et al. [23], and Saremi et al. [6] which illustrated an increase in omentin level following exercise, and is inconsistent with Faramarzi et al. study [13]. It seems that an intensity threshold is essential to improve plasma omentin-1 level, and so it can be the cause of the contradictions with some reports [24]. We found that increase in concentrations of serum omentin-1 was in along with decreasing of blood glucose, fasting insulin level, HOMA-IR and some lipid profiles after 8-week exercise training program [21]. In the present study, 8-weeks of aerobic exercise training effectively lowered insulin resistance in both trained smokers and non-smokers groups, which is in line with previous investigation [17].
In accordance with our results, prior studies have reported that omintin has a negative correlation with fasting insulin, and HOMA-IR [18, 25]. Therefore, mechanism for increase of omentin is directly related to weight loss and a decrease in BMI after exercise training. In this regard, Moreno-Navarrete et al. [26] reported that the concentration of circulating omentin-1 rises after weight reduction, which is consistent with our observation.
The results of current study showed that the levels of insulin, glucose and insulin resistance were reduced in two training groups. Not much research has been done on the mechanism of omentin-1 and its association with glucose and insulin levels, but few studies has shown the role of omentin-1 in transmitting insulin signaling via kinase B protein/Akt activation and increasing the insulin-stimulated glucose uptake into adipose tissue [18]. Also, omentin-1 can improve glucose metabolism and insulin sensitivity by increase glucose transport into the muscles following exercise training. According to the results of Castro et al. [27], there is an association between skeletal muscle and adipose tissue in relation to omentin-1. In fact, exercise training cause an increase in omentin gene expression in adipocytes tissue and improve insulin sensitivity [28]. Nonetheless, there is inconsistency in relationship between omentin level and insulin resistance with the results of Hossein-nezhad study [8] which might be due to various subject populations or other undefined components that may influence on omentin-1 level.
In this study, we obtained inverse correlations between serum omentin-1 level and TG, LDL-C, TC, and also a direct correlation was identified between omentin-1 and HDL-C levels. Contrary to our results Hossein-Nezhad et al. [8] and Elsaid et al. [29] didn’t observe any significant relation between serum omentin-1 and lipid levels. Moreno-Navarrete et al. [26] reported that omentin level was correlated with some lipid metabolic parameters such as TC, LDL-C, and TG. Also Abd-Elbaky et al. [30] found an inverse relationship between omentin-1 and TC levels in adults' population that concurs with our findings. It is proposed that the differences in body fat distribution in the subjects studied may impact on production or secretion of adipokines and the results of investigations [31]. It seems that omentin play an important role in lipid metabolism regulation and so against diabetic dyslipidemia as a compensatory mechanism [26]. Since, it has been shown that omentin-1 promotes 5-AMP-activated protein kinase phosphorylation which acts as an inhibitor of endogenous cholesterol synthesis [21].
Moreover, in agreement with earlier findings [7, 19], we found out serum level of omentin-1 was positively associated with HDL-C level. It was suggested that omentin has anti-atherogenic behavior, thus it can effect on HDL-C level through modulating insulin action [32, 33]. A potential mechanism of increase in HDL-C level following aerobic exercise training in the smoker may be linked to modifications in the activities of some enzymes such as lipoprotein lipase and lecithin-cholesterol acyltransferase and hepatic triglyceride lipase [34].