The Molecular Mechanism Underlying Continuous Exercise Training-Induced Adaptive Changes of Lipolysis in White Adipose Cells.

Junetsu Ogasawara,Hitoshi Ishida,Ken Shirato,Takuya Sakurai,Hideki Ohno,Takako Kizaki,Tomonobu Sakurai,Yoshinaga Ishibashi,Tetsuya Izawa

doi:10.1155/2015/473430

Junetsu Ogasawara, Hitoshi Ishida + Show 7 more

Open Access

https://doi.org/10.1155/2015/473430

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Abstract

Physical exercise accelerates the mobilization of free fatty acids from white adipocytes to provide fuel for energy. This happens in several tissues and helps to regulate a whole-body state of metabolism. Under these conditions, the hydrolysis of triacylglycerol (TG) that is found in white adipocytes is known to be augmented via the activation of these lipolytic events, which is referred to as the “lipolytic cascade.” Indeed, evidence has shown that the lipolytic responses in white adipocytes are upregulated by continuous exercise training (ET) through the adaptive changes in molecules that constitute the lipolytic cascade. During the past few decades, many lipolysis-related molecules have been identified. Of note, the discovery of a new lipase, known as adipose triglyceride lipase, has redefined the existing concepts of the hormone-sensitive lipase-dependent hydrolysis of TG in white adipocytes. This review outlines the alterations in the lipolytic molecules of white adipocytes that result from ET, which includes the molecular regulation of TG lipases through the lipolytic cascade.

Highlights

Obesity, which results from the energy intake that is in excess of energy expenditure, is a major global health problem in developed nations but in lowand middle-income countries [1]
White adipocytes are capable of storing excess energy as triacylglycerol (TG), and they play a key role in energy metabolism by providing free fatty acids (FFA) and glycerol through the hydrolysis of TG
It is known that both Gs protein α subunit (Gsα) and Gi protein α subunit (Giα), which are dissociated from β- and γ-subunits by stimulation of α- and β3-adrenergic receptors (β-ARs), play key roles in the synergistic action of adenylyl cyclase (AC) in white adipocytes

Summary

Introduction

Obesity, which results from the energy intake that is in excess of energy expenditure, is a major global health problem in developed nations (western world) but in lowand middle-income countries (less developed countries) [1]. Clarifying the mechanisms underlying the physical exerciseinduced alteration of lipolytic molecules in white adipocytes would be useful for establishing a new method for exercise therapy as well as for understanding the biological meanings of the lipolytic events themselves This elucidation of lipolysis has demonstrated how ectopic lipid accumulation in skeletal muscle and liver is closely associated with insulin resistance syndrome and diabetes [2]. The molecular mechanisms underlying lipolysis in white adipocytes are known to be regulated mainly by hierarchical activation of the lipolytic cascade, which is modified through both an α- and β-AR-cAMP production system, thereby distally exerting a changeover to the hydrolytic action of lipases The stimulation of these two ARs induces opposite effects: α-antilipolytic and β-lipolytic (details are described ). Attention is focused on the ET-induced adaptive changes of lipolytic molecules, which were mainly obtained from our studies of white adipocytes

Basic Structure of the Lipolytic

Regulation of Lipolysis via the Coordinated Action of Lipases and Cofactors

Adaptive Alteration in G-Proteins by Habitual Physical Exercise

Manipulation of Lipolytic Molecules by Physical Exercise to Supply Energy

Conclusion