Adiponectin influences progesterone production from MA-10 Leydig cells in a dose-dependent manner

被引:20
作者
Landry, David [1 ]
Pare, Aurelie [1 ]
Jean, Stephanie [1 ]
Martin, Luc J. [1 ]
机构
[1] Univ Moncton, Dept Biol, Moncton, NB E1A 3E9, Canada
基金
加拿大自然科学与工程研究理事会;
关键词
Adiponectin; Star; Cyp11a1; Sox9; Progesterone; Leydig cells; ADIPOSE-TISSUE; GRANULOSA-CELL; INSULIN SENSITIVITY; GENE-EXPRESSION; RECEPTORS; PROTEIN; TESTOSTERONE; TRANSCRIPTION; BINDING; STEROIDOGENESIS;
D O I
10.1007/s12020-014-0456-y
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Obesity in men is associated with lower testosterone levels, related to reduced sperm concentration and the development of various diseases with aging. Hormones produced by the adipose tissue may have influences on both metabolism and reproductive function. Among them, the production and secretion of adiponectin is inversely correlated to total body fat. Adiponectin receptors (AdipoR1 and AdipoR2) have been found to be expressed in testicular Leydig cells (producing testosterone). Since StAR and Cyp11a1 are essential for testosterone synthesis and adiponectin has been shown to regulate StAR mRNA in swine granulosa cells, we hypothesized that adiponectin might also regulate these genes in Leydig cells. Our objective was to determine whether adiponectin regulates StAR and Cyp11a1 genes in Leydig cells and to better define its mechanisms of action. Methods used in the current study are qPCR for the mRNA levels, transfections for promoter activities, and enzyme-linked immunosorbent assay for the progesterone concentration. We have found that adiponectin cooperates with cAMP-dependent stimulation to activate StAR and Cyp11a1 mRNA expressions in a dose-dependent manner in MA-10 Leydig cells as demonstrated by transfection of a luciferase reporter plasmid. These results led to a significant increase in progesterone production from MA-10 cells. Thus, our data suggest that high doses of adiponectin typical of normal body weight may promote testosterone production from Leydig cells.
引用
收藏
页码:957 / 967
页数:11
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