Papers by Mauricio Morales
Obesity Surgery, 2010
Background The enzyme 11-β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) catalyzes intracellular... more Background The enzyme 11-β-hydroxysteroid dehydrogenase type 1 (11β-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 11β-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. Methods A prospective study was conducted over a 27-month period. Hepatic, VAT, and SAT samples were obtained at the time of surgery. 11β-HSD1 and 18S gene expression was measured using real-time quantitative reverse transcriptase-polymerase chain reaction. Results Forty nine patients met the inclusion criteria [mean age: 42.2 ± 10 years, body mass index (BMI): 42 ± 6 kg/m2, 71% women and 63% with metabolic syndrome (MS)]. 11β-HSD1 mRNA levels were higher in liver than fat tissue (p < 0.001), being higher in SAT than in VAT (p < 0.001) without gender-specific differences. Hepatic expression of 11β-HSD1 correlated positively with SAT and VAT, alanine aminotransferase (ALT), and serum glucose and was inversely associated with BMI. 11β-HSD1 mRNA in VAT correlated positively with insulinemia, ALT, and LDL cholesterol. There were no associations between 11β-HSD1 mRNA in SAT and the variables analyzed. Conclusions 11β-HSD1 expression is higher in liver in comparison to adipose tissue in obese patients. The observed correlations between hepatic and VAT 11β-HSD1 expression with dyslipidemia and insulin resistance suggest that this enzyme might have a pathogenic role in obesity and related metabolic disorders.
Obesity Surgery, 2010
Background The enzyme 11-β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) catalyzes intracellular... more Background The enzyme 11-β-hydroxysteroid dehydrogenase type 1 (11β-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 11β-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. Methods A prospective study was conducted over a 27-month period. Hepatic, VAT, and SAT samples were obtained at the time of surgery. 11β-HSD1 and 18S gene expression was measured using real-time quantitative reverse transcriptase-polymerase chain reaction. Results Forty nine patients met the inclusion criteria [mean age: 42.2 ± 10 years, body mass index (BMI): 42 ± 6 kg/m2, 71% women and 63% with metabolic syndrome (MS)]. 11β-HSD1 mRNA levels were higher in liver than fat tissue (p < 0.001), being higher in SAT than in VAT (p < 0.001) without gender-specific differences. Hepatic expression of 11β-HSD1 correlated positively with SAT and VAT, alanine aminotransferase (ALT), and serum glucose and was inversely associated with BMI. 11β-HSD1 mRNA in VAT correlated positively with insulinemia, ALT, and LDL cholesterol. There were no associations between 11β-HSD1 mRNA in SAT and the variables analyzed. Conclusions 11β-HSD1 expression is higher in liver in comparison to adipose tissue in obese patients. The observed correlations between hepatic and VAT 11β-HSD1 expression with dyslipidemia and insulin resistance suggest that this enzyme might have a pathogenic role in obesity and related metabolic disorders.
Metabolism-clinical and Experimental
11-β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts cortisone to cortisol, mainly in the... more 11-β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts cortisone to cortisol, mainly in the liver and visceral adipose tissue (VAT), and has been implicated in several metabolic disorders. The absence of systemic hypercortisolism in central obesity could be due to increased inactivation of cortisol to its tetrahydrometabolites by the hepatic enzymes 5αand 5β-reductases. Our aim was to assess the expression of the reductases in the liver and of 11β-HSD1 in the liver and VAT in morbidly obese patients and to analyze their association with clinical, anthropometric, and biochemical parameters. Hepatic and VAT samples were obtained during bariatric surgery. 5α-and 5β-reductases, 11β-HSD1, and 18S expression was measured using real-time polymerase chain reaction. Anthropometric and biochemical variables were analyzed. Forty-one patients were recruited (age, 41.8 ± 10.6 years; body mass index, 42.1 ± 6.6 kg/m 2 ; 71% women). The expression of hepatic 5α-and 5β-reductases was positively correlated (r = +0.53, P = .004), and their expression levels were correlated with hepatic 11β-HSD1 expression (r = +0.61, P < .001 for 5α-reductase and r = +0.50, P < .001 for 5βreductase). Hepatic 5α-reductase was associated with insulin (r = +0.34, P = .015). Visceral adipose tissue 11β-HSD1 expression was associated with glucose (r = +0.37, P = .025) and M E T A B O L I S M C L I N I C A L A N D E X P E R I M E N T A L 6 0 ( 2 0 1 1 ) 1 7 7 5 -1 7 8 0 A v a i l a b l e a t w w w . s c i e n c e d i r e c t . c o m Metabolism w w w . m e t a b o l i s m j o u r n a l . c o m
Metabolism-clinical and Experimental
11-β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts cortisone to cortisol, mainly in the... more 11-β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts cortisone to cortisol, mainly in the liver and visceral adipose tissue (VAT), and has been implicated in several metabolic disorders. The absence of systemic hypercortisolism in central obesity could be due to increased inactivation of cortisol to its tetrahydrometabolites by the hepatic enzymes 5αand 5β-reductases. Our aim was to assess the expression of the reductases in the liver and of 11β-HSD1 in the liver and VAT in morbidly obese patients and to analyze their association with clinical, anthropometric, and biochemical parameters. Hepatic and VAT samples were obtained during bariatric surgery. 5α-and 5β-reductases, 11β-HSD1, and 18S expression was measured using real-time polymerase chain reaction. Anthropometric and biochemical variables were analyzed. Forty-one patients were recruited (age, 41.8 ± 10.6 years; body mass index, 42.1 ± 6.6 kg/m 2 ; 71% women). The expression of hepatic 5α-and 5β-reductases was positively correlated (r = +0.53, P = .004), and their expression levels were correlated with hepatic 11β-HSD1 expression (r = +0.61, P < .001 for 5α-reductase and r = +0.50, P < .001 for 5βreductase). Hepatic 5α-reductase was associated with insulin (r = +0.34, P = .015). Visceral adipose tissue 11β-HSD1 expression was associated with glucose (r = +0.37, P = .025) and M E T A B O L I S M C L I N I C A L A N D E X P E R I M E N T A L 6 0 ( 2 0 1 1 ) 1 7 7 5 -1 7 8 0 A v a i l a b l e a t w w w . s c i e n c e d i r e c t . c o m Metabolism w w w . m e t a b o l i s m j o u r n a l . c o m
Obesity Surgery, 2010
Background The enzyme 11-β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) catalyzes intracellular... more Background The enzyme 11-β-hydroxysteroid dehydrogenase type 1 (11β-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 11β-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. Methods A prospective study was conducted over a 27-month period. Hepatic, VAT, and SAT samples were obtained at the time of surgery. 11β-HSD1 and 18S gene expression was measured using real-time quantitative reverse transcriptase-polymerase chain reaction. Results Forty nine patients met the inclusion criteria [mean age: 42.2 ± 10 years, body mass index (BMI): 42 ± 6 kg/m2, 71% women and 63% with metabolic syndrome (MS)]. 11β-HSD1 mRNA levels were higher in liver than fat tissue (p < 0.001), being higher in SAT than in VAT (p < 0.001) without gender-specific differences. Hepatic expression of 11β-HSD1 correlated positively with SAT and VAT, alanine aminotransferase (ALT), and serum glucose and was inversely associated with BMI. 11β-HSD1 mRNA in VAT correlated positively with insulinemia, ALT, and LDL cholesterol. There were no associations between 11β-HSD1 mRNA in SAT and the variables analyzed. Conclusions 11β-HSD1 expression is higher in liver in comparison to adipose tissue in obese patients. The observed correlations between hepatic and VAT 11β-HSD1 expression with dyslipidemia and insulin resistance suggest that this enzyme might have a pathogenic role in obesity and related metabolic disorders.
Metabolism-clinical and Experimental
11-β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts cortisone to cortisol, mainly in the... more 11-β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts cortisone to cortisol, mainly in the liver and visceral adipose tissue (VAT), and has been implicated in several metabolic disorders. The absence of systemic hypercortisolism in central obesity could be due to increased inactivation of cortisol to its tetrahydrometabolites by the hepatic enzymes 5αand 5β-reductases. Our aim was to assess the expression of the reductases in the liver and of 11β-HSD1 in the liver and VAT in morbidly obese patients and to analyze their association with clinical, anthropometric, and biochemical parameters. Hepatic and VAT samples were obtained during bariatric surgery. 5α-and 5β-reductases, 11β-HSD1, and 18S expression was measured using real-time polymerase chain reaction. Anthropometric and biochemical variables were analyzed. Forty-one patients were recruited (age, 41.8 ± 10.6 years; body mass index, 42.1 ± 6.6 kg/m 2 ; 71% women). The expression of hepatic 5α-and 5β-reductases was positively correlated (r = +0.53, P = .004), and their expression levels were correlated with hepatic 11β-HSD1 expression (r = +0.61, P < .001 for 5α-reductase and r = +0.50, P < .001 for 5βreductase). Hepatic 5α-reductase was associated with insulin (r = +0.34, P = .015). Visceral adipose tissue 11β-HSD1 expression was associated with glucose (r = +0.37, P = .025) and M E T A B O L I S M C L I N I C A L A N D E X P E R I M E N T A L 6 0 ( 2 0 1 1 ) 1 7 7 5 -1 7 8 0 A v a i l a b l e a t w w w . s c i e n c e d i r e c t . c o m Metabolism w w w . m e t a b o l i s m j o u r n a l . c o m
Obesity Surgery, 2010
Background The enzyme 11-β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) catalyzes intracellular... more Background The enzyme 11-β-hydroxysteroid dehydrogenase type 1 (11β-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 11β-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. Methods A prospective study was conducted over a 27-month period. Hepatic, VAT, and SAT samples were obtained at the time of surgery. 11β-HSD1 and 18S gene expression was measured using real-time quantitative reverse transcriptase-polymerase chain reaction. Results Forty nine patients met the inclusion criteria [mean age: 42.2 ± 10 years, body mass index (BMI): 42 ± 6 kg/m2, 71% women and 63% with metabolic syndrome (MS)]. 11β-HSD1 mRNA levels were higher in liver than fat tissue (p < 0.001), being higher in SAT than in VAT (p < 0.001) without gender-specific differences. Hepatic expression of 11β-HSD1 correlated positively with SAT and VAT, alanine aminotransferase (ALT), and serum glucose and was inversely associated with BMI. 11β-HSD1 mRNA in VAT correlated positively with insulinemia, ALT, and LDL cholesterol. There were no associations between 11β-HSD1 mRNA in SAT and the variables analyzed. Conclusions 11β-HSD1 expression is higher in liver in comparison to adipose tissue in obese patients. The observed correlations between hepatic and VAT 11β-HSD1 expression with dyslipidemia and insulin resistance suggest that this enzyme might have a pathogenic role in obesity and related metabolic disorders.
Obesity Surgery, 2010
Background The enzyme 11-β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) catalyzes intracellular... more Background The enzyme 11-β-hydroxysteroid dehydrogenase type 1 (11β-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 11β-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. Methods A prospective study was conducted over a 27-month period. Hepatic, VAT, and SAT samples were obtained at the time of surgery. 11β-HSD1 and 18S gene expression was measured using real-time quantitative reverse transcriptase-polymerase chain reaction. Results Forty nine patients met the inclusion criteria [mean age: 42.2 ± 10 years, body mass index (BMI): 42 ± 6 kg/m2, 71% women and 63% with metabolic syndrome (MS)]. 11β-HSD1 mRNA levels were higher in liver than fat tissue (p < 0.001), being higher in SAT than in VAT (p < 0.001) without gender-specific differences. Hepatic expression of 11β-HSD1 correlated positively with SAT and VAT, alanine aminotransferase (ALT), and serum glucose and was inversely associated with BMI. 11β-HSD1 mRNA in VAT correlated positively with insulinemia, ALT, and LDL cholesterol. There were no associations between 11β-HSD1 mRNA in SAT and the variables analyzed. Conclusions 11β-HSD1 expression is higher in liver in comparison to adipose tissue in obese patients. The observed correlations between hepatic and VAT 11β-HSD1 expression with dyslipidemia and insulin resistance suggest that this enzyme might have a pathogenic role in obesity and related metabolic disorders.
Metabolism-clinical and Experimental
11-β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts cortisone to cortisol, mainly in the... more 11-β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts cortisone to cortisol, mainly in the liver and visceral adipose tissue (VAT), and has been implicated in several metabolic disorders. The absence of systemic hypercortisolism in central obesity could be due to increased inactivation of cortisol to its tetrahydrometabolites by the hepatic enzymes 5αand 5β-reductases. Our aim was to assess the expression of the reductases in the liver and of 11β-HSD1 in the liver and VAT in morbidly obese patients and to analyze their association with clinical, anthropometric, and biochemical parameters. Hepatic and VAT samples were obtained during bariatric surgery. 5α-and 5β-reductases, 11β-HSD1, and 18S expression was measured using real-time polymerase chain reaction. Anthropometric and biochemical variables were analyzed. Forty-one patients were recruited (age, 41.8 ± 10.6 years; body mass index, 42.1 ± 6.6 kg/m 2 ; 71% women). The expression of hepatic 5α-and 5β-reductases was positively correlated (r = +0.53, P = .004), and their expression levels were correlated with hepatic 11β-HSD1 expression (r = +0.61, P < .001 for 5α-reductase and r = +0.50, P < .001 for 5βreductase). Hepatic 5α-reductase was associated with insulin (r = +0.34, P = .015). Visceral adipose tissue 11β-HSD1 expression was associated with glucose (r = +0.37, P = .025) and M E T A B O L I S M C L I N I C A L A N D E X P E R I M E N T A L 6 0 ( 2 0 1 1 ) 1 7 7 5 -1 7 8 0 A v a i l a b l e a t w w w . s c i e n c e d i r e c t . c o m Metabolism w w w . m e t a b o l i s m j o u r n a l . c o m
Obesity Surgery, 2010
Background The enzyme 11-β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) catalyzes intracellular... more Background The enzyme 11-β-hydroxysteroid dehydrogenase type 1 (11β-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 11β-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. Methods A prospective study was conducted over a 27-month period. Hepatic, VAT, and SAT samples were obtained at the time of surgery. 11β-HSD1 and 18S gene expression was measured using real-time quantitative reverse transcriptase-polymerase chain reaction. Results Forty nine patients met the inclusion criteria [mean age: 42.2 ± 10 years, body mass index (BMI): 42 ± 6 kg/m2, 71% women and 63% with metabolic syndrome (MS)]. 11β-HSD1 mRNA levels were higher in liver than fat tissue (p < 0.001), being higher in SAT than in VAT (p < 0.001) without gender-specific differences. Hepatic expression of 11β-HSD1 correlated positively with SAT and VAT, alanine aminotransferase (ALT), and serum glucose and was inversely associated with BMI. 11β-HSD1 mRNA in VAT correlated positively with insulinemia, ALT, and LDL cholesterol. There were no associations between 11β-HSD1 mRNA in SAT and the variables analyzed. Conclusions 11β-HSD1 expression is higher in liver in comparison to adipose tissue in obese patients. The observed correlations between hepatic and VAT 11β-HSD1 expression with dyslipidemia and insulin resistance suggest that this enzyme might have a pathogenic role in obesity and related metabolic disorders.
Metabolism-clinical and Experimental
11-β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts cortisone to cortisol, mainly in the... more 11-β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts cortisone to cortisol, mainly in the liver and visceral adipose tissue (VAT), and has been implicated in several metabolic disorders. The absence of systemic hypercortisolism in central obesity could be due to increased inactivation of cortisol to its tetrahydrometabolites by the hepatic enzymes 5αand 5β-reductases. Our aim was to assess the expression of the reductases in the liver and of 11β-HSD1 in the liver and VAT in morbidly obese patients and to analyze their association with clinical, anthropometric, and biochemical parameters. Hepatic and VAT samples were obtained during bariatric surgery. 5α-and 5β-reductases, 11β-HSD1, and 18S expression was measured using real-time polymerase chain reaction. Anthropometric and biochemical variables were analyzed. Forty-one patients were recruited (age, 41.8 ± 10.6 years; body mass index, 42.1 ± 6.6 kg/m 2 ; 71% women). The expression of hepatic 5α-and 5β-reductases was positively correlated (r = +0.53, P = .004), and their expression levels were correlated with hepatic 11β-HSD1 expression (r = +0.61, P < .001 for 5α-reductase and r = +0.50, P < .001 for 5βreductase). Hepatic 5α-reductase was associated with insulin (r = +0.34, P = .015). Visceral adipose tissue 11β-HSD1 expression was associated with glucose (r = +0.37, P = .025) and M E T A B O L I S M C L I N I C A L A N D E X P E R I M E N T A L 6 0 ( 2 0 1 1 ) 1 7 7 5 -1 7 8 0 A v a i l a b l e a t w w w . s c i e n c e d i r e c t . c o m Metabolism w w w . m e t a b o l i s m j o u r n a l . c o m
Obesity Surgery, 2010
Background The enzyme 11-β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) catalyzes intracellular... more Background The enzyme 11-β-hydroxysteroid dehydrogenase type 1 (11β-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 11β-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. Methods A prospective study was conducted over a 27-month period. Hepatic, VAT, and SAT samples were obtained at the time of surgery. 11β-HSD1 and 18S gene expression was measured using real-time quantitative reverse transcriptase-polymerase chain reaction. Results Forty nine patients met the inclusion criteria [mean age: 42.2 ± 10 years, body mass index (BMI): 42 ± 6 kg/m2, 71% women and 63% with metabolic syndrome (MS)]. 11β-HSD1 mRNA levels were higher in liver than fat tissue (p < 0.001), being higher in SAT than in VAT (p < 0.001) without gender-specific differences. Hepatic expression of 11β-HSD1 correlated positively with SAT and VAT, alanine aminotransferase (ALT), and serum glucose and was inversely associated with BMI. 11β-HSD1 mRNA in VAT correlated positively with insulinemia, ALT, and LDL cholesterol. There were no associations between 11β-HSD1 mRNA in SAT and the variables analyzed. Conclusions 11β-HSD1 expression is higher in liver in comparison to adipose tissue in obese patients. The observed correlations between hepatic and VAT 11β-HSD1 expression with dyslipidemia and insulin resistance suggest that this enzyme might have a pathogenic role in obesity and related metabolic disorders.
Metabolism-clinical and Experimental
11-β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts cortisone to cortisol, mainly in the... more 11-β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts cortisone to cortisol, mainly in the liver and visceral adipose tissue (VAT), and has been implicated in several metabolic disorders. The absence of systemic hypercortisolism in central obesity could be due to increased inactivation of cortisol to its tetrahydrometabolites by the hepatic enzymes 5αand 5β-reductases. Our aim was to assess the expression of the reductases in the liver and of 11β-HSD1 in the liver and VAT in morbidly obese patients and to analyze their association with clinical, anthropometric, and biochemical parameters. Hepatic and VAT samples were obtained during bariatric surgery. 5α-and 5β-reductases, 11β-HSD1, and 18S expression was measured using real-time polymerase chain reaction. Anthropometric and biochemical variables were analyzed. Forty-one patients were recruited (age, 41.8 ± 10.6 years; body mass index, 42.1 ± 6.6 kg/m 2 ; 71% women). The expression of hepatic 5α-and 5β-reductases was positively correlated (r = +0.53, P = .004), and their expression levels were correlated with hepatic 11β-HSD1 expression (r = +0.61, P < .001 for 5α-reductase and r = +0.50, P < .001 for 5βreductase). Hepatic 5α-reductase was associated with insulin (r = +0.34, P = .015). Visceral adipose tissue 11β-HSD1 expression was associated with glucose (r = +0.37, P = .025) and M E T A B O L I S M C L I N I C A L A N D E X P E R I M E N T A L 6 0 ( 2 0 1 1 ) 1 7 7 5 -1 7 8 0 A v a i l a b l e a t w w w . s c i e n c e d i r e c t . c o m Metabolism w w w . m e t a b o l i s m j o u r n a l . c o m
Metabolism-clinical and Experimental
11-β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts cortisone to cortisol, mainly in the... more 11-β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts cortisone to cortisol, mainly in the liver and visceral adipose tissue (VAT), and has been implicated in several metabolic disorders. The absence of systemic hypercortisolism in central obesity could be due to increased inactivation of cortisol to its tetrahydrometabolites by the hepatic enzymes 5αand 5β-reductases. Our aim was to assess the expression of the reductases in the liver and of 11β-HSD1 in the liver and VAT in morbidly obese patients and to analyze their association with clinical, anthropometric, and biochemical parameters. Hepatic and VAT samples were obtained during bariatric surgery. 5α-and 5β-reductases, 11β-HSD1, and 18S expression was measured using real-time polymerase chain reaction. Anthropometric and biochemical variables were analyzed. Forty-one patients were recruited (age, 41.8 ± 10.6 years; body mass index, 42.1 ± 6.6 kg/m 2 ; 71% women). The expression of hepatic 5α-and 5β-reductases was positively correlated (r = +0.53, P = .004), and their expression levels were correlated with hepatic 11β-HSD1 expression (r = +0.61, P < .001 for 5α-reductase and r = +0.50, P < .001 for 5βreductase). Hepatic 5α-reductase was associated with insulin (r = +0.34, P = .015). Visceral adipose tissue 11β-HSD1 expression was associated with glucose (r = +0.37, P = .025) and M E T A B O L I S M C L I N I C A L A N D E X P E R I M E N T A L 6 0 ( 2 0 1 1 ) 1 7 7 5 -1 7 8 0 A v a i l a b l e a t w w w . s c i e n c e d i r e c t . c o m Metabolism w w w . m e t a b o l i s m j o u r n a l . c o m
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Papers by Mauricio Morales