An investigation of glucose uptake in relation to steroidogenesis in rat testis and tumour Leydig cells.

نویسندگان

  • P Amrolia
  • M H Sullivan
  • D Garside
  • S A Baldwin
  • B A Cooke
چکیده

The mechanisms of the requirement of glucose for steroidogenesis were investigated by monitoring the uptake of the glucose analogue 2-deoxy-D-glucose by rat testis and tumour Leydig cells. The characteristics of glucose transport in both of these cell types were found to resemble those of the facilitated-diffusion systems for glucose found in most other mammalian cells. The Leydig cells took up 2-deoxy-D-glucose but not L-glucose, and the uptake was inhibited by both cytochalasin B and forskolin. In the presence of luteinizing hormone, the rate of 2-deoxy-D-glucose uptake by both cell types was increased by approx. 50%. In addition to D-glucose, it was shown that the Leydig cells could also utilize 3-hydroxybutyrate or glutamine to maintain steroidogenesis.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

P-220: Co-Administration of Testosterone and Vitamin E Inhibited The Atrazine-Induced Damages on Testis; Evidence for RNA Damage and Leydig Cells Steroidogenesis

Background: Atrazine (ATR), an herbicide, is used in order to control broadleaf and grassy weed. ATR has been estimated to impact the testicular tissue both by inhibiting the endocrine system and partly by reducing the antioxidant status. Thus, current study was designed to evaluate the protective effect of vitamin E and testosterone against ATR-induced damages in testicular tissue. Materials a...

متن کامل

Expression and regulation of glucose transporter 8 in rat Leydig cells.

Basal and LH/human chorionic gonadotropin (hCG)-stimulated testosterone formation by Leydig cells is dependent on ambient glucose levels. Inhibition of glucose uptake is associated with decreased testosterone formation. Recently, glucose transporter 8 (GLUT8) has been shown to be highly expressed in the testis. In the present study, we have investigated the expression and regulation of the GLUT...

متن کامل

A Transcriptome-Wide Screen for mRNAs Enriched in Fetal Leydig Cells: CRHR1 Agonism Stimulates Rat and Mouse Fetal Testis Steroidogenesis

Fetal testis steroidogenesis plays an important role in the reproductive development of the male fetus. While regulators of certain aspects of steroidogenesis are known, the initial driver of steroidogenesis in the human and rodent fetal testis is unclear. Through comparative analysis of rodent fetal testis microarray datasets, 54 candidate fetal Leydig cell-specific genes were identified. Feta...

متن کامل

Aqueous Extract of Nigella sativa Seeds Suppresses Testicular Steroidogenesis In Mice Leydig Cells, in vitro

Nigella sativa (black seed) is an important medicinal herb with folkloric use in wide range of diseases. It is well studied for its biological activities. However, there is limited information regarding its effect on the male reproductive system. This study describes the effect of the aqueous extract of N. sativa (NSE) on testicular steroidogenesis from mice Leydig cells in vitro . Mice tes...

متن کامل

The role of calcium in luteinizing hormone-releasing hormone agonist (ICI 118630)-stimulated steroidogenesis in rat Leydig cells.

The luteinizing hormone-releasing hormone (LHRH) agonist ICI 118630 was found to increase testosterone production in purified rat testis Leydig cells in a concentration- and time-dependent manner, but no consistent changes in cyclic AMP levels were detectable. The stimulation of steroidogenesis by LHRH agonist was found to be dependent on the concentration of Ca2+ in the incubation medium; at l...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • The Biochemical journal

دوره 249 3  شماره 

صفحات  -

تاریخ انتشار 1988