It has been reported that abnormalities in the circulating levels of vaspin and omentin and the gene expression of both factors are related to BMI and markers of insulin sensitivity in metabolic syndrome patients, although to date, the findings of various authors are confusing. Our objective in this study was to measure vaspin and omentin circulating levels and mRNA expression in subcutaneous and visceral adipose tissue in morbidly obese women and to compare them to age-matched controls. We also assessed the relationship between these two adipokines and biochemical markers of metabolic syndrome and other adipo/cytokines.
In the current study, we demonstrate that serum vaspin levels are not increased in morbidly obese women and that vaspin levels do not correlate with BMI, markers of glucose or lipid metabolism.
In studies involving humans, and as has been mentioned in the introduction, how vaspin serum levels correlate with BMI, markers of insulin sensitivity and glucose metabolism is unclear. Youn et al. have reported that elevated vaspin serum concentrations correlated with obesity and impaired insulin sensitivity, although not in patients with type 2 diabetes . In obese children, Lee et al. have observed a negative correlation between vaspin concentration and HOMA-IR . However, in agreement with our results, von Loeffelholz et al. have shown that there is no association between serum vaspin and HOMA-IR in nondiabetic humans . Seeger et al. have also reported that circulating vaspin is not independently associated with markers of glucose metabolism , and Briana et al. have shown that vaspin concentrations do not correlate with insulin levels in maternal, fetal and neonatal samples , as occurs in our population.
To our knowledge, this is the first time that the relation between vaspin levels and other adipo/cytokines in the circulation has been studied.
In our study, serum vaspin levels correlate inversely with levels of LCN2 and IL 6. It has been reported that LCN2 is an adipokine that seems to be an independent risk factor for hyperglycemia and insulin resistance in humans. It has also been related to inflammation . IL 6 is a known proinflammatory cytokine that also increased in obesity . Taken together, these findings might suggest that vaspin has an anti-inflammatory profile.
On the other hand, vaspin mRNA expression is significantly higher in our morbidly obese cohort in SAT and VAT. Kloting et al. have reported that vaspin expression was not detectable in lean subjects but that it was present in both the SAT and VAT of obese patients. Its levels were significantly correlated with parameters of obesity, insulin resistance and impaired glucose tolerance . However, we have not been able to support their findings.
In untreated OLETF rats, vaspin expression and its serum levels decreased as diabetes worsened and body weight fell. The expression and serum levels were normalized by treatment with insulin or pioglitazone, suggesting that vaspin exerts a defensive action against insulin resistance. On the other hand, the administration of recombinant human vaspin improved insulin sensitivity and glucose tolerance, and reverses the expression of those genes that can promote insulin resistance such as leptin, resistin and TNF-α, in diet-induced obese mice .
To sum up, in our study serum vaspin levels are inversely related to IL 6. SAT and VAT vaspin expression is significantly higher in morbidly obese women. In addition, as mentioned above, the literature confirms that vaspin has an insulin-sensitizing effect. In conjunction with our results, then, this suggests that vaspin has a compensatory role in the inflammatory complications of obesity.
The second important finding of our study is that plasma omentin levels are significantly lower in the morbidly obese and that these levels inversely correlate with glucidic metabolism parameters, in accordance with the findings of de Souza et al.  and Yang et al. . In the same context, we found a negative correlation with systolic blood pressure.
We also demonstrate that patients with omentin levels in the lowest tertile were 90 times more likely to have the MS than those in the highest tertile, after adjustment for age and BMI. Moreover, women with omentin levels in the second tertile were 25 times more likely to have the MS.
Omentin expression in visceral adipose tissue is significantly lower in the morbidly obese women in our study in agreement with the results of Souza et al . Also, Cai et al. demonstrate that omentin mRNA expression decreases in overweight/obese individuals and decreases further when overweight/obesity is combined with type 2 diabetes. Thus, omentin expression is negatively correlated with fasting insulin, HOMA-IR and BMI .
The major limitation of the present study is the relatively small number of subjects in the sample. Although our specific cohort of non-diabetic morbidly obese women showed a clear relationship between the MS and omentin levels without the interference of confounding factors, these results are not extrapolable to other obesity groups or men. Secondly, due to the difficulty of obtaining tissue samples, the expression results need to be confirmed in larger study populations. Another limitation of the study is that it is cross-sectional. We could not prove a causal link between the levels of omentin and the development of MS or the levels of vaspin and anti-inflammatory action. Further prospective studies are required to explain these phenomena.