Leptin at birth and at age 7 in relation to appetitive behaviors at age 7 and age 10

Abstract Background Given the great variability in adiposity and the exposure to obesogenic food environments, it has been suggested that individuals respond in divergent ways to the environment they live in. Our aim was to explore the genetic and environmental contribution of variations on appetitive behaviors in 10-year-old Portuguese children. Methods Participants were twins from the Generation XXI cohort (n = 86 pairs). Appetitive behaviors at 10 years was assessed through the Children Eating Behavior Questionnaire. Intra-class correlations for appetitive behaviors were calculated for monozygotic and dizygotic twins, and structural equation modelling was conducted to estimate genetic (A), shared (C) and non-shared (E) environmental variances. Results Twins were mainly dizygotic (65%), and a third was classified as having excess weight (30.2%). For all appetitive behaviors, with exception to Emotional Undereating, moderate to strong heritability were found and non-shared environmental effects contributed to appetite variability. For Emotional Undereating, environmental effects seem to be more important than genetic effects (C: 0.81; 95%CI 0.71;0.88 and E: 0.19; 95%CI 0.12;0.29). Conclusions There is a significant genetic contribution, followed by non-shared environmental effects, on appetitive behaviors in school-age years. Results indicate that Emotional Undereating was not heritable, being explained by shared and non-shared environmental factors. Key messages Appetitive behaviors among 10-year-olds seem to be genetically determined, with exception to Emotional Undereating, which showed to be explained by environmental factors. Understanding which genes are associated with child appetitive behaviors would give an insight in biological and behavioral influences on child eating and obesity risk.

Download Full-text

Intrinsic and Extrinsic Modulation of a Single Central Pattern Generating Circuit

Journal of Neurophysiology ◽

10.1152/jn.2000.84.3.1186 ◽

2000 ◽

Vol 84 (3) ◽

pp. 1186-1193 ◽

Cited By ~ 47

Author(s):

Peter T. Morgan ◽

Ray Perrins ◽

Philip E. Lloyd ◽

Klaudiusz R. Weiss

Keyword(s):

Neural Circuits ◽

Central Pattern Generators ◽

Motor Program ◽

Pattern Generator ◽

Motor Programs ◽

Appetitive Behavior ◽

Protraction Phase ◽

Pattern Generators ◽

Rhythmic Behaviors ◽

Appetitive Behaviors

Intrinsic and extrinsic neuromodulation are both thought to be responsible for the flexibility of the neural circuits (central pattern generators) that control rhythmic behaviors. Because the two forms of modulation have been studied in different circuits, it has been difficult to compare them directly. We find that the central pattern generator for biting in Aplysia is modulated both extrinsically and intrinsically. Both forms of modulation increase the frequency of motor programs and shorten the duration of the protraction phase. Extrinsic modulation is mediated by the serotonergic metacerebral cell (MCC) neurons and is mimicked by application of serotonin. Intrinsic modulation is mediated by the cerebral peptide-2 (CP-2) containing CBI-2 interneurons and is mimicked by application of CP-2. Since the effects of CBI-2 and CP-2 occlude each other, the modulatory actions of CBI-2 may be mediated by CP-2 release. Although the effects of intrinsic and extrinsic modulation are similar, the neurons that mediate them are active predominantly at different times, suggesting a specialized role for each system. Metacerebral cell (MCC) activity predominates in the preparatory (appetitive) phase and thus precedes the activation of CBI-2 and biting motor programs. Once the CBI-2s are activated and the biting motor program is initiated, MCC activity declines precipitously. Hence extrinsic modulation prefacilitates biting, whereas intrinsic modulation occurs during biting. Since biting inhibits appetitive behavior, intrinsic modulation cannot be used to prefacilitate biting in the appetitive phase. Thus the sequential use of extrinsic and intrinsic modulation may provide a means for premodulation of biting without the concomitant disruption of appetitive behaviors.

Download Full-text

Rapid appetitive transitions are sculpted by amygdala to accumbens pathways

10.1101/2021.04.11.435530 ◽

2021 ◽

Author(s):

E. Zayra Millan ◽

Jun Hua Lim ◽

John Power ◽

Gavan McNally

Keyword(s):

Functional Connectivity ◽

Discrimination Task ◽

Male Rats ◽

Switching System ◽

Core Component ◽

Appetitive Behavior ◽

State Dependent ◽

Reward Delivery ◽

Before And After ◽

Appetitive Behaviors

Foraging, pursuit, and predation rapidly transition into behavioral quiescence during reward capture and consumption. While appetitive-consummatory dissociations are embedded at both psychological and neural levels, the mechanisms controlling switches or transitions between appetitive seeking and consummatory behaviors remain poorly understood. Here we identify the BLA→AcbSh pathway as critical to these transitions by showing that this pathway inhibits the appetitive seeking response in the presence of consummatory demands. Using an appetitive cue-discrimination task in male rats, we show that reward delivery is a significant driver of seeking inhibition and that a BLA→AcbSh pathway mediates this inhibition. This role in suppressing seeking responses during periods of consumption was not due to a general suppression of behavior because responding to other cues during the same test was unaffected. Moreover, it was specific to the BLA→AcbSh pathway, because the contribution of the BLA→AcbC pathway to appetitive switching was distinct and modest. State-dependent silencing of BLA→AcbSh revealed that the modulation of seeking before and after reward delivery are co-dependent. Finally, we found that BLA terminals in AcbSh have functional connectivity to LH-projecting AcbSh neurons, thereby identifying a BLA→AcbSh→LH pathway as a putative route for the rapid regulation of appetitive behaviors. Taken together, these findings suggest that the BLA→AcbSh pathway is a core component of an appetitive switching system, recruited under conditions requiring rapid or dynamic shifts in appetitive behavior, and that this pathway enables these shifts by actively inhibiting seeking.

Download Full-text

Appetitive Regulation in Anorexia Nervosa and Bulimia Nervosa

10.1093/oxfordhb/9780190620998.013.4 ◽

2017 ◽

Author(s):

Walter Kaye ◽

Alice V. Ely

Keyword(s):

Eating Disorders ◽

Bulimia Nervosa ◽

Reward Processing ◽

Emission Tomography ◽

Complex Disorders ◽

Eating Disorder Symptoms ◽

Positron Emission ◽

Underlying Causes ◽

The Brain ◽

Appetitive Behaviors

Anorexia and bulimia nervosa are complex disorders with dysregulated appetitive behaviors. The underlying causes of disturbed patterns of eating are unknown, but a growing body of research suggests that aberrant functioning of brain or peripheral systems may be responsible. Neuroimaging technologies, such as positron emission tomography (PET) and functional MRI (fMRI), can be used to explore whether there are perturbations of the monoamine systems, the neurocircuitry of gustatory processing in eating disorders, and their relationship to metabolic homeostatic states. Together, PET and fMRI data suggest that individuals with eating disorders have disturbance of taste- and reward-processing regions of the brain, which may contribute to eating disorder symptoms.

Download Full-text