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Calcium release from membrane-bound calcium pool induced by ACTH.
International Journal of Clinical Pharmacology, Therapy, and Toxicology
|May 1, 1982
Summary
Adrenocorticotropic hormone (ACTH) decreases calcium binding to rat fat cell membranes, suggesting it releases calcium into the cell. This differs from epinephrine's effect on calcium.
Area of Science:
- Biochemistry
- Cell Biology
- Endocrinology
Background:
- Calcium ions (Ca2+) play crucial roles in cellular signaling and function.
- Adrenocorticotropic hormone (ACTH) is known to regulate various physiological processes, including lipolysis.
Purpose of the Study:
- To investigate the effect of ACTH on Ca2+ binding to the plasma membrane of rat fat cells.
- To elucidate the mechanism of ACTH-induced Ca2+ mobilization in adipocytes.
Main Methods:
- Utilized synthetic I-24 ACTH to examine its dose-dependent effects on 45Ca binding to rat fat cell membranes.
- Employed verapamil and calcium ionophore A23187 to further probe the Ca2+ binding dynamics.
- Compared the Ca2+ dependence of ACTH action with that of epinephrine.
Main Results:
- Synthetic I-24 ACTH significantly reduced 45Ca binding to fat cell membranes in a dose-dependent manner.
- Verapamil increased Ca2+ binding, while the Ca ionophore A23187 decreased it.
- ACTH-induced Ca2+ binding involved both high and low affinity sites, and this effect differed from epinephrine's non-significant influence on 45Ca binding.
Conclusions:
- ACTH promotes the release of Ca2+ from the plasma membrane-bound pool into the cytosol.
- The findings highlight distinct Ca2+ dependency mechanisms for the lipolytic actions of ACTH and epinephrine.
- This study provides insights into the role of calcium signaling in ACTH-mediated adipocyte function.