Glucocorticoid effect on the prostaglandin system in fat tissue

Area of Science:

• Biochemistry
• Pharmacology
• Adipose Tissue Biology

Background:

• Lipolysis in subcutaneous adipose tissue is accompanied by prostaglandin-mediated vasodilatation.
• The roles of prostaglandin synthesis and release in this process require further elucidation.

Purpose of the Study:

• To investigate the mechanisms by which prostaglandin-synthetase inhibitors and anti-inflammatory steroids affect lipolysis-induced vasodilatation in rabbit adipose tissue.
• To determine the specific site of action for these agents in the prostaglandin pathway.

Main Methods:

• Lipolysis was induced in rabbit subcutaneous adipose tissue.
• The effects of prostaglandin-synthetase inhibitors (aspirin, indomethacin) and anti-inflammatory steroids (hydrocortisone, prednisolone) on lipolysis, prostaglandin content, and vasodilatation were measured.
• In vitro experiments assessed prostaglandin release into the incubation medium.

Main Results:

• Prostaglandin-synthetase inhibitors reduced prostaglandin levels and vasodilatation but did not inhibit lipolysis.
• Anti-inflammatory steroids inhibited vasodilatation but did not decrease prostaglandin content; they reduced prostaglandin release into the medium.
• Steroids increased intracellular prostaglandin content while decreasing its release.

Conclusions:

• Prostaglandin-synthetase inhibitors act by reducing prostaglandin synthesis.
• Anti-inflammatory steroids likely inhibit prostaglandin-mediated vasodilation by preventing the release of prostaglandins from fat cells.
• These findings differentiate the mechanisms of action for prostaglandin synthesis inhibitors and anti-inflammatory steroids in regulating adipose tissue vascular responses.