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© Georg Thieme Verlag KG Stuttgart · New York
19 March 2009 (online)
Siervo M, Wells JCK, Cizza G. The Contribution of Psychosocial Stress to the Obesity Epidemic: An Evolutionary Approach. Horm Metab Res 2009; 41: 261–270
Fig. 1 The model proposes that thrifty and profligate genes are regulated by two independent mechanisms activated by states of energy surplus (orex-genergostat) or depletion (anorex-energostat). For example, in a state of negative energy balance (Famine) the decrease in energy availability induces an activation (solid lines) of the anorex-energostat and an inhibition (dotted lines) of the orex-genergostat. The sensor would then activate the catabolic genes (profligate) and inhibit the anabolic (thrifty) ones to exert their catabolic action. A feedback mechanism between these genes can be envisaged to modulate their actions (double arrow lines). The system in a state of positive energy balance (Feast) would operate with a similar but opposite mechanism.
Fig. 2 Classification of Energy Sensing Mechanisms based on their properties (Storage, Substrate, Physical, Redox, Chemical) and ability to signal changes (very short-term, short-term, medium-term, long-term) in energy balance. ROS=Reactive Oxygen Species; ATP=Adenosine Triphosphate; AMP=Adenosine Monophosphate.
This article is an erratum to 627 in: Journal of HMR, Issue 4, 2009 .