In the present study, we investigated the effects of eight weeks of aerobic exercise training in male smokers 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 to the CS group after the eight-week exercise intervention. Our results are in line with those of previous observations and reinforce the beneficial effect of exercise training on these important metabolic factors in confronting many diseases such as metabolic syndrome, type2 diabetes, and cardiovascular diseases [6, 16–17].
Many studies have found lower levels of omentin-1 in obesity, impaired glucose tolerance and type 2diabetes [18–20]. Also, lower levels of omentin in response to smoking may contribute to increased susceptibility to infections in smokers . In order to investigate the changes of omentin-1 in smokers, we explored the effect of eight weeks of aerobic exercise training on circulating omentin-1 in smokers and examined the omentin-1 response in relation to insulin resistance. The findings showed that the eight-week of aerobic exercise training at 55–70% of MHR led to a marked increase in omentin-1 concentration in the E and ES groups. Unfortunately, to the best of our knowledge, no study to date has examined the effect of exercise on circulating omentin-1 level in smokers. Nevertheless, some studies have been carried out on the effect of exercise training on omentin-1 . Our result was consistent with that of Wilms et al. , Ouerghi et al. , and Saremi et al. , who also found an increase in omentin level following exercise, and is inconsistent with the results of Faramarzi et al. . It seems that an intensity threshold is essential to improve plasma omentin-1 level, which can be the cause of the inconsistency with the findings of some studies .
We found that an increase in concentrations of serum omentin-1 was along with reduced blood glucose, fasting insulin level, HOMA-IR and some lipid profiles after the eight-week exercise training program . In the present study, eight weeks of aerobic exercise training effectively lowered insulin resistance in both trained smoker and non-smoker groups, which is in line with the findings of previous studies .
The role of omentin-1 in type 2 diabetes is also unclear. Omentin induces anti-inflammatory, anti-atherogenic and anti-diabetic effects [19, 25]. But, recently two studies have found a relationship between omentin-1 and increased risk of type 2 diabetes and cardiovascular diseases [26, 27]. In the study by Ouerghi et al. , omentin-1 was inversely correlated with cardio-metabolic risk factors, while the relationship disappeared after adjusting on potential confounders. They reported that omentin-1 was inversely correlated with insulin resistance and this adipokine could improve glucose metabolism and insulin sensitivity .
In line with our findings, previous studies have reported that omintin-1 has a negative correlation with fasting insulin, and HOMA-IR [18, 29]. Therefore, the mechanism for increased omentin is directly related to weight loss and a decrease in BMI after exercise training. In this regard, Moreno-Navarrete et al.  reported that the concentration of circulating omentin-1 rises after weight reduction, which is consistent with our observation.
The results of the present study showed that the levels of insulin, glucose and insulin resistance were reduced in the two training groups. Not much research has been done on the mechanism of omentin-1 and its association with glucose and insulin levels, but the few studies in this regard have confirmed the role of omentin-1 in transmitting insulin signaling via kinase B protein/Akt activation and increasing the insulin-stimulated glucose uptake into the adipose tissue . Also, omentin-1 can improve glucose metabolism and insulin sensitivity by increasing glucose transport into the muscles following exercise training. According to the results of Castro et al. , there is an association between skeletal muscle and adipose tissue in relation to omentin-1. In fact, exercise training causes an increase in omentin gene expression in adipocytes tissue and improves insulin sensitivity . Nonetheless, there is an inconsistency in terms of the relationship between omentin level and insulin resistance between the results of the present study and those of Hossein-Nezhad et al. , which might be due to various subject populations or other undefined components that may influence omentin-1 level.
In the current study, we discovered inverse correlations between serum omentin-1 level and TG, LDL-C, and TC. A direct correlation was also identified between omentin-1 and HDL-C levels. Contrary to our results, Hossein-Nezhad et al.  and Elsaid et al.  did not observe any significant relationship between serum omentin-1 and lipid levels. Moreno-Navarrete et al.  reported that omentin level was correlated with some lipid metabolic parameters such as TC, LDL-C, and TG. Abd-Elbaky et al.  also found an inverse relationship between omentin-1 and TC levels in adults, which is concurrent with our findings. It is proposed that the differences in body fat distribution in the subjects studied may impact on the production or secretion of adipokines and the results of investigations . Omentin seems to play an important role in lipid metabolism regulation and so against diabetic dyslipidemia as a compensatory mechanism  since it has been shown that omentin-1 promotes 5-AMP-activated protein kinase phosphorylation, which acts as an inhibitor of endogenous cholesterol synthesis .
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 affect HDL-C level through modulating insulin action [25, 36]. The potential mechanism involved in the increased HDL-C level following aerobic exercise training in the smokers may be linked to modifications in the activities of some enzymes such as lipoprotein lipase and lecithin-cholesterol acyltransferase and hepatic triglyceride lipase .