当前位置： SCI文献检索 > DIABETES RESEARCH AND CLINICAL PRACTICE期刊下所有文献 > SGK1 is regulated by metabolic-related factors in 3T3-L1 adipocytes and overexpressed in the adipose tissue of subjects with obesity and diabetes.

SGK1 is regulated by metabolic-related factors in 3T3-L1 adipocytes and overexpressed in the adipose tissue of subjects with obesity and diabetes.

Abstract：

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.

journal_name

Diabetes Res Clin Pract

journal_title

Diabetes research and clinical practice

authors

Li P,Pan F,Hao Y,Feng W,Song H,Zhu D

doi

10.1016/j.diabres.2013.08.009

subject

Has Abstract

pub_date

2013-10-01 00:00:00

pages

35-42

issue

1

eissn

0168-8227

issn

1872-8227

pii

S0168-8227(13)00298-2

journal_volume

102

pub_type

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