AIMS: The present study aimed to investigate the pathophysiological role of SGK1 in the development of metabolic syndrome by investigating the expression and regulation of serum and glucocorticoid-inducible kinase 1 (SGK1) in adipose tissues in obesity and diabetes. METHODS: SGK1 expression in adipose tissue was investigated using reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry. SGK1 regulation in differentiated 3T3-L1 adipocytes by metabolic-related factors was assessed using Northern blot analysis. Humans with obesity and type 2 diabetes and KKAy and db/db mice were used to evaluate SGK1 expression in the adipose tissue of subjects with obesity and diabetes using quantitative real-time PCR and Western blot analysis. RESULTS: SGK1 was expressed in white adipose tissue as shown by mRNA and protein levels. Aldosterone and glucocorticoids stimulated SGK1 expression in a time- and dose-dependent manner, whereas PPAR-γ agonists inhibited SGK1 expression in differentiated 3T3-L1 adipocytes. Furthermore, SGK1 mRNA and protein were overexpressed in the adipose tissue of mice and humans with obesity and type 2 diabetes. CONCLUSION: Aldosterone, glucocorticoids and other factors contribute to excessive SGK1 expression in adipose tissue. This excessive SGK1 expression may be related to adipose tissue dysfunction, which may contribute to the development of obesity, diabetes and metabolic syndrome.
AIMS: The present study aimed to investigate the pathophysiological role of SGK1 in the development of metabolic syndrome by investigating the expression and regulation of serum and glucocorticoid-inducible kinase 1 (SGK1) in adipose tissues in obesity and diabetes. METHODS:SGK1 expression in adipose tissue was investigated using reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry. SGK1 regulation in differentiated 3T3-L1 adipocytes by metabolic-related factors was assessed using Northern blot analysis. Humans with obesity and type 2 diabetes and KKAy and db/db mice were used to evaluate SGK1 expression in the adipose tissue of subjects with obesity and diabetes using quantitative real-time PCR and Western blot analysis. RESULTS:SGK1 was expressed in white adipose tissue as shown by mRNA and protein levels. Aldosterone and glucocorticoids stimulated SGK1 expression in a time- and dose-dependent manner, whereas PPAR-γ agonists inhibited SGK1 expression in differentiated 3T3-L1 adipocytes. Furthermore, SGK1 mRNA and protein were overexpressed in the adipose tissue of mice and humans with obesity and type 2 diabetes. CONCLUSION:Aldosterone, glucocorticoids and other factors contribute to excessive SGK1 expression in adipose tissue. This excessive SGK1 expression may be related to adipose tissue dysfunction, which may contribute to the development of obesity, diabetes and metabolic syndrome.