Visceral obesity, skeletal muscle mass and resistin in metabolic syndrome development
Background: obesity implies an increase in the visceral adipose tissue (VAT), which is a risk factor for various metabolic diseases. VAT releases proinflammatory mediators, like resistin. In addition, it has been noted that the skeletal muscle mass (SMM) is involved in the development of metabolic s...
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Veröffentlicht in: | Nutrición hospitalaria : organo oficial de la Sociedad Española de Nutrición Parenteral y Enteral 2019-01, Vol.36 (1), p.43-50 |
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Sprache: | eng |
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Zusammenfassung: | Background: obesity implies an increase in the visceral adipose tissue (VAT), which is a risk factor for various metabolic diseases. VAT releases proinflammatory mediators, like resistin. In addition, it has been noted that the skeletal muscle mass (SMM) is involved in the development of metabolic syndrome (MS). Objective: this study was designed to determine the relationship of body components (VAT and SMM) with MS and resistin in patients with obesity. Methods: body composition and anthropometric and biochemical measurements to assess MS, and ELISA tests for resistin were carried out in 40 patients aged 18-40 years. Results: overweight and obesity were observed in 72% of patients; visceral obesity was found in 53% and 35% had MS. A positive correlation between VAT and SMM in patients with MS was detected. In the entire population, an increase of 1 kg of SMM was found to be associated with an increase of 3 cm2 of VAT, and an increase of 4 cm2 of VAT was observed in individuals with MS. According to resistin, people with increased VAT had higher concentration than persons with normal VAT. Furthermore, an increase of 1 cm2 of VAT accounted for a person entertaining a 3.3 fold greater risk of MS for different values of SMM and resistin. Conclusion: the transcendence and significance of VAT as a main factor in triggering the chronic inflammatory process and MS, the SMM and resistin were also related. |
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ISSN: | 1699-5198 1699-5198 |
DOI: | 10.20960/nh.1889 |