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Ca2+ and lipolysis in adipocytes from exercise-trained rats
1Department of Health and Sports Sciences, University of Electro-Communications, Tokyo, Japan.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|December 1, 1994
Summary
Exercise training enhances fat breakdown (lipolysis) in rat adipocytes by altering calcium (Ca2+) signaling. Trained rats show increased lipolysis and altered protein kinase regulation, indicating improved metabolic adaptation.
Area of Science:
- Cellular Physiology
- Metabolic Regulation
- Exercise Science
Background:
- Adipocyte lipolysis is a key process in energy metabolism.
- Calcium ions (Ca2+) play a role in regulating cellular functions, including lipolysis.
- The impact of exercise training on Ca2+ dynamics and lipolysis in adipocytes requires further investigation.
Purpose of the Study:
- To investigate the effects of chronic exercise on Ca2+-dependent lipolysis and protein kinase activity in rat adipocytes.
- To determine how exercise training influences intracellular free Ca2+ concentration ([Ca2+]i) and its response to hormonal stimuli.
Main Methods:
- Adipocytes were isolated from exercise-trained and sedentary rats.
- Lipolysis was stimulated using norepinephrine and dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP).
- Calmodulin inhibitor N-(6-aminohexyl)-5-chloro-1-naphthalene sulfonamide (W-7) was used to assess Ca2+-calmodulin involvement.
- Intracellular free Ca2+ concentration ([Ca2+]i) was measured using fluorescent indicators.
- cAMP-dependent protein kinase activity was assessed.
Main Results:
- Chronic exercise significantly enhanced lipolytic responses to norepinephrine and dibutyryl cAMP.
- The inhibitory effect of W-7 on stimulated lipolysis and protein kinase activity was more pronounced in trained rats.
- Trained rats exhibited higher basal [Ca2+]i levels and altered [Ca2+]i responsiveness to hormonal stimulation, with lower transient but higher sustained increases.
- Exercise training did not alter basal cAMP-dependent protein kinase activity but increased its sensitivity to Ca2+-calmodulin inhibition.
Conclusions:
- Exercise training alters adipocyte intracellular Ca2+ homeostasis, affecting basal levels and hormonal responsiveness.
- In trained rats, the regulation of protein kinase activity by cAMP is more dependent on the Ca2+-calmodulin complex.
- These findings suggest that altered Ca2+ signaling contributes to the enhanced metabolic adaptations observed with exercise training.