This study has been registered at Clinicaltrial.gov with registration number NCT02708589.

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Background. The aims of this study were to evaluate the short-term effects of laparoscopic restrictive bariatric surgery (LRBS) on plasma levels of vaspin and the potential associations of changes in vaspin levels with changes in anthropometric indices, insulin-resistance and dietary intake. Methods. Thirty, severely obese subjects (21 female; mean age, 32.5 years) with a mean body mass index (BMI) of 44.1 ± 4.9 kg/m 2 underwent LRBS. Measurements of anthropometric indices, dietary intakes, physical activity and plasma vaspin concentrations were performed prior to, and six weeks after LRBS. Insulin-sensitivity was estimated using the homeostasis model assessment of insulin-resistance (HOMA-IR). Results. Six weeks after LRBS, BMI decreased to a mean of 38.4 ± 4.9 kg/m 2. Significant reductions were also observed in waist circumference (WC), daily intakes of calorie, fat and protein, and plasma concentrations of triglyceride. No significant change was observed in fasting levels of insulin, blood sugar or HOMA-IR. Vaspin decreased significantly (0.26 ± 0.17 vs 0.36 ± 0.20, p=0.048) following surgery. While the percentage change of vaspin was not correlated with percent changes in anthropometric indices and HOMA-IR, it correlated positively with the percentage change in intake of calories, fat and protein: this correlation remained significant even after adjustment for sex and changes in WC and HOMA-IR. Conclusion. Our study suggests that LRBS decreases the serum vaspin concentrations in parallel with the restriction of dietary intake. Furthermore, decreased levels of vaspin early after LRBS seem more likely to result from decreased dietary intake rather than weight-loss-induced insulin sensitivity improvement.

The aim of the present study was to compare the levels of visfatin in portal and systemic circulations and to assess the possible relationship of visfatin with systemic inflammation and insulin resistance in morbidly obese patients undergoing bariatric surgery. A total of 46 morbidly obese patients (BMI = 45.3 ± 5.3 kg/m(2)) undergoing bariatric surgery were included in this study. Blood samplings were performed simultaneously from portal and systemic veins during surgery. Visfatin was measured in both portal and systemic venous samples. Besides, fasting serum levels of insulin, glucose, lipid profile, visfatin, and hs-CRP were determined in systemic venous blood samples. Insulin sensitivity was estimated using the homeostasis model assessment of insulin resistance (HOMA-IR). Visfatin concentrations were significantly higher in portal vein than systemic veins (11.9 ± 12.1 vs. 5.1 ± 3.3 ng/ml, p < 0.0001). While systemic levels of visfatin were significantly correlated with circulating levels of hs-CRP (r = 0.527, p < 0.0001), there were no significant correlations between portal levels of visfatin with systemic levels of hs-CRP concentrations. Substantially higher levels of visfatin in portal vein than systemic veins provide evidence that visceral adipose tissue is the major secretory source of visfatin in humans. Our findings underscore that visceral adipose tissue is an active endocrine organ that is involved in the complex interrelationship between obesity and pathologic conditions.

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Our findings shows that laparoscopic total gastric vertical plication results significant body weight reduction in morbidly obese subjects and it is associated with an improvement of the lipid and glucose metabolism, but it seems that we need further and longer time researches to clarify other metabolic changes after LTGVP. Our results may be useful for treatment of these high risk groups in practice.