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Influence on adipocyte plasma membrane bound protein kinase by feedback regulator
Journal of Cyclic Nucleotide Research
|January 1, 1975
Summary
Feedback regulator (FR) significantly impacts adipocyte plasma membrane enzymes, notably stimulating protein kinase while inhibiting adenylate cyclase and phosphodiesterases, suggesting a key role in cAMP metabolism.
Area of Science:
- Biochemistry
- Cell Biology
- Metabolic Regulation
Background:
- Adipocyte plasma membranes contain key enzymes like protein kinase, phosphodiesterase, and adenylate cyclase that regulate cellular functions.
- The feedback regulator (FR) is a known modulator of these enzymatic activities, but its specific effects and regulatory role require detailed investigation.
Purpose of the Study:
- To quantify the basal activity ratios of adenylate cyclase, phosphodiesterase, and protein kinase in adipocyte plasma membranes.
- To investigate the effect of the feedback regulator (FR) on these three enzymes and elucidate its regulatory role in adipocyte cAMP metabolism.
Main Methods:
- Enzyme activity assays were performed on adipocyte plasma membrane preparations.
- Concentration-dependent effects of FR and epinephrine on protein kinase, phosphodiesterase, and adenylate cyclase were measured.
- Histone type 11A and NaF were used as substrates and activators for protein phosphorylation studies.
Main Results:
- The basal enzyme ratio was determined as 1:1.9:3.0 for adenylate cyclase:phosphodiesterase:protein kinase.
- FR significantly stimulated protein kinase activity (up to 3-fold) and inhibited adenylate cyclase and phosphodiesterase activities, with adenylate cyclase inhibition being most potent.
- FR's stimulatory effect on protein kinase was greater than cAMP and appeared additive, indicating a cAMP-independent mechanism.
Conclusions:
- Feedback regulator (FR) plays a crucial role in modulating adipocyte plasma membrane enzyme activity.
- FR's differential effects on protein kinase, adenylate cyclase, and phosphodiesterase suggest a regulatory role in controlling cyclic AMP (cAMP) metabolism within adipocytes.