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Frontiers in Biology

ISSN 1674-7984

ISSN 1674-7992(Online)

CN 11-5892/Q

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Front. Biol.    2014, Vol. 9 Issue (3) : 169-174    https://doi.org/10.1007/s11515-014-1309-z
REVIEW
Appetite control: why we fail to stop eating even when we are full?
Kristen DAVIS,Young-Jai YOU()
Department of Biochemistry and Molecular Biology, Virginia Commonwealth University, Richmond, VA 23298, USA
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Abstract

We often eat more than our body needs. We live in an environment where high calorie food is abundant and physical activities are limited. Living in this environment, maintaining healthy bodyweight becomes challenging and obesity becomes a social burden. Why do we continue to eat even after the metabolic needs are satisfied? Feeding is an ancient behavior essential to survive. Thus the mechanisms to regulate appetite, energy expenditure, and energy storage are well conserved throughout animals. Based on this conservation, we study why we fail to control appetite using a simple genetic model system C. elegans. We have discovered certain genetic components that when misregulated have animals eat more and store more fat. In this review we discuss how these genes work in the appetite control circuit to ultimately understand overall appetite control behavior. We will also briefly discuss how social influence affects feeding regardless of the metabolic status of an animal.
Keywords satiety      appetite      obesity      cGMP      TGFβ      C. elegans     
Corresponding Author(s): Young-Jai YOU   
Issue Date: 24 June 2014
 Cite this article:   
Kristen DAVIS,Young-Jai YOU. Appetite control: why we fail to stop eating even when we are full?[J]. Front. Biol., 2014, 9(3): 169-174.
 URL:  
https://academic.hep.com.cn/fib/EN/10.1007/s11515-014-1309-z
https://academic.hep.com.cn/fib/EN/Y2014/V9/I3/169
Fig.1  Locomotive activity reflects metabolic status: A schematic diagram to show how metabolic status can be reflected by locomotive activity.
Fig.2  Neuronal circuitry to regulate appetite in C. elegans. (A) Upon activation by nutritional well-being, ASI releases DAF-7 TGFβ. Binding of TGFβ to its receptor DAF-1 in RIM and RIC neurons inhibits RIM and RIC’s role in releasing hunger signals. In the absence of hunger signals worms become satiated and quiescent. (B) When food is not available, DAF-7 is not released therefore RIM and RIC are activated to release hunger signals.
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