Browsing by Author "Perez, Gustavo"

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    Laparoscopic Roux-en-Y gastric bypass versus laparoscopic adjustable gastric banding: five years of follow-up
    (ELSEVIER SCIENCE INC, 2010) Boza, Camilo; Gamboa, Cristian; Awruch, Diego; Perez, Gustavo; Escalona, Alex; Ibanez, Luis
    Background: Bariatric surgery is an effective treatment for morbid obesity Laparoscopic Rouxen-Y gastric bypass (LRYGB) and laparoscopic adjustable gastric banding (LAGB) are commonly performed procedures The aim of the present study was to evaluate and compare the lone-term outcomes after LRYGB and LAGB
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    Laparoscopic sleeve gastrectomy in obese adolescents: results in 51 patients
    (ELSEVIER SCIENCE INC, 2012) Boza, Camilo; Viscido, German; Salinas, Jose; Crovari, Fernando; Funke, Ricardo; Perez, Gustavo
    Background: Adolescent obesity has become an important health problem. Bariatric surgery in this population continues to be a matter of debate. The aim of our study was to present our experience and results with laparoscopic sleeve gastrectomy (LSG) in obese adolescents at the digestive surgery department of the Hospital Clinico Pontificia Universidad Catolica de Chile.
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    Overexpression of 11 beta-Hydroxysteroid Dehydrogenase Type 1 in Hepatic and Visceral Adipose Tissue is Associated with Metabolic Disorders in Morbidly Obese Patients
    (SPRINGER, 2010) Baudrand, Rene; Carvajal, Cristian A.; Riquelme, Arnoldo; Morales, Mauricio; Solis, Nancy; Pizarro, Margarita; Escalona, Alex; Boza, Camilo; Perez, Gustavo; Dominguez, Angelica; Arrese, Marco; Fardella, Carlos E.
    The enzyme 11-beta-hydroxysteroid dehydrogenase type 1 (11 beta-HSD1) catalyzes intracellular glucocorticoid reactivation by conversion of cortisone to cortisol in different tissues and have been implicated in several metabolic disorders associated with obesity. The aim of this study was to evaluate the 11 beta-HSD1 expression in liver, visceral adipose tissue (VAT), and subcutaneous adipose tissue (SAT) in morbidly obese patients undergoing bariatric surgery and its correlations with clinical, anthropometric, and biochemical variables.
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    Overexpression of 11 beta-hydroxysteroid dehydrogenase type 1 in visceral adipose tissue and portal hypercortisolism in non-alcoholic fatty liver disease
    (WILEY, 2012) Candia, Roberto; Riquelme, Arnoldo; Baudrand, Rene; Carvajal, Cristian A.; Morales, Mauricio; Solis, Nancy; Pizarro, Margarita; Escalona, Alex; Carrasco, Gonzalo; Boza, Camilo; Perez, Gustavo; Padilla, Oslando; Cerda, Jaime; Fardella, Carlos E.; Arrese, Marco
    Background: The enzyme 11 beta-hydroxysteroid-dehydrogenase type 1 (11 beta HSD1) catalyses the reactivation of intracellular cortisol. We explored the potential role of 11 beta-HSD1 overexpression in visceral adipose tissue (VAT) in non-alcoholic fatty liver disease (NAFLD) assessing sequential changes of enzyme expression, in hepatic and adipose tissue, and the occurrence of portal hypercortisolism in obese mice. 11 beta-HSD1 expression was also assessed in tissues from obese patients undergoing bariatric surgery. Methods: Peripheral and portal corticosterone levels and liver histology were assessed in ob/ob mice at two time points (8-12 weeks of age). 11 beta-HSD1 tissue expression was assessed in by RT-pcr in ob/ob mice and in 49 morbidly obese patients. Results: Portal corticosterone serum levels were higher in obese mice with a 26% decrease between 8 and 12 weeks of age (controls: 78.3 +/- 19.7 ng/ml, 8-week-old ob/ob: 167.5 +/- 14.5 ng/ml and 12-week-old ob/ob: 124.3 +/- 28 ng/ml, P < 0.05). No significant differences were found in peripheral corticosterone serum levels. Expression of 11b-HSD1 was lower in the liver [-45% at 8 weeks and -35% at 12-weeks (P = 0.0001)] and highly overexpressed in VAT in obese mice, compared to controls (128-fold higher in 8-week-old ob/ob and 41-fold higher in 12-week-old ob/ob, P < 0.01). No significant differences were seen in the expression of 11 beta-HSD1 in subcutaneous adipose tissue. In multivariate analysis, human 11 beta-HSD1 expression in VAT (OR: 1.385 +/- 1.010-1.910) was associated with NAFLD. Conclusion: Murine NAFLD is associated with portal hypercortisolism and 11 beta-HSD1 overexpression in VAT. In humans, 11 beta-HSD1 VAT expression was associated with the presence of NAFLD. Thus, local corticosteroid production in VAT may contribute to NAFLD pathogenesis.
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    Plasminogen activator inhibitor type 1 serum levels and 4G/5G gene polymorphism in morbidly obese Hispanic patients with non-alcoholic fatty liver disease
    (Elsevier España, 2011) Espino Espino, Alberto Antonio; Villagran Torres, Andrea Alejandra; Vollrath Reyes, Valeska Yolanda; Hanckes Mayo, Maria Paulina; Salas Ocaranza, Roberto Ignacio; Farah Samaan, Andrea Catherina; Solis, Nancy; Pizarro Rojas, Margarita Alicia; Escalona Perez, Alex Gamaliel; Boza Wilson, Camilo; Perez, Gustavo; Carrasco, Gonzalo; Padilla, Orlando; Francisco Miguel, Juan; Nervi Oddone, Flavio; Chavez Tapia, Norberto C.; Arab Verdugo, Juan Pablo; Alvarez Lobos, Manuel Marcelo; Arrese Jimenez, Marco Antonio; Riquelme Perez, Arnoldo Javier
    Background. The plasminogen activator inhibitor type-1 (PAI-1) has been implicated in the regulation of fibrinolysis and extracellular matrix components. The single base pair guanine insertion/deletion polymorphism (4G/5G) within the promoter region of the PAI-1 gene influences PAI-1 synthesis and may modulate hepatic fibrogenesis. Aim. To evaluate the influence of PAI-1 serum levels and 4G/5G polymorphism on the risk of liver fibrosis associated to non-alcoholic fatty liver disease (NAFLD) in morbidly obese patients. Material and methods. Case-control study of 50 obese patients undergoing bariatric surgery and 71 non-obese subjects matched by age and sex. Anthropometric and biochemical measurements were performed, including PAI-1 serum levels. Genomic DNA was obtained to assess the presence of 4G/5G polymorphism. Results. BMI, insulinemia, triglycerides, HOMA-IR, hypertension and diabetes were significantly higher in obese patients compared to control subjects. PAI-1 serum levels observed in obese patients were significantly lower (10.63 +/- 4.82) compared to controls (14.26 +/- 11.4; p < 0.05). No differences were observed in the PAI-1 4G/5G promoter genotypes frequencies (p = 0.12). No differences were observed in PAI-1 plasma levels among obese patients with liver fibrosis (10.64 +/- 4.35) compared to patients without liver fibrosis (10.61 +/- 5.2; p = 0.985). PAI-1 4G/5G promoter genotypes frequencies were similar in patients with or without liver fibrosis associated to NASH (p = 0.6). Conclusions. Morbidly obese patients had significantly Lower PAI-1 serum levels with similar PAI-1 4G/5G genotypes frequencies compared to non-obese subjects. The frequency of 4G/5G genotypes in Chilean Hispanic healthy subjects was similar to that described in other populations. No association was found between PAI-1 serum levels or 4G/5G genotype with liver fibrosis in obese patients.