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Central Amino Acid Sensing in the Control of Feeding Behavior

View Article: PubMed Central - PubMed

ABSTRACT

Dietary protein quantity and quality greatly impact metabolic health via evolutionary-conserved mechanisms that ensure avoidance of amino acid imbalanced food sources, promote hyperphagia when dietary protein density is low, and conversely produce satiety when dietary protein density is high. Growing evidence supports the emerging concept of protein homeostasis in mammals, where protein intake is maintained within a tight range independently of energy intake to reach a target protein intake. The behavioral and neuroendocrine mechanisms underlying these adaptations are unclear. While peripheral factors are able to signal amino acid deficiency and abundance to the brain, the brain itself is exposed to and can detect changes in amino acid concentrations, and subsequently engages acute and chronic responses modulating feeding behavior and food preferences. In this review, we will examine the literature describing the mechanisms by which the brain senses changes in amino acids concentrations, and how these changes modulate feeding behavior.

No MeSH data available.


Related in: MedlinePlus

Central detection of amino acid availability in the regulation of feeding behavior. Discrete cell populations in the brain monitor extracellular amino acid availability through a variety of mechanisms and engage downstream feeding-regulatory circuits to prevent or limit the ingestion of diets with imbalanced essential amino acid content, produce hyperphagia if dietary protein content is low and conversely reduce food intake if dietary protein content is high.
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Figure 2: Central detection of amino acid availability in the regulation of feeding behavior. Discrete cell populations in the brain monitor extracellular amino acid availability through a variety of mechanisms and engage downstream feeding-regulatory circuits to prevent or limit the ingestion of diets with imbalanced essential amino acid content, produce hyperphagia if dietary protein content is low and conversely reduce food intake if dietary protein content is high.

Mentions: Collectively, the data reviewed here support a role for a distributed network of discrete brain regions in primary amino acid sensing in the control of multiple behavioral responses to changes in dietary amino acid intake, as summarized in Figure 2. Many gaps remain to be filled to complete our understanding of these processes, and a key poorly described step is the intracellular coupling of intracellular amino acid availability to neuronal electrical and synaptic activity, as highlighted in Figure 1B. Does this coupling rely on specific intracellular components that could perhaps represent a unique molecular signature of amino acid sensing neurons, making these cells amenable to molecular genetics? Identifying a molecular marker for amino acid sensing neurons would prove extremely useful in the characterization of neurocircuits engaged downstream from primary brain sensors to regulate feeding behavior.


Central Amino Acid Sensing in the Control of Feeding Behavior
Central detection of amino acid availability in the regulation of feeding behavior. Discrete cell populations in the brain monitor extracellular amino acid availability through a variety of mechanisms and engage downstream feeding-regulatory circuits to prevent or limit the ingestion of diets with imbalanced essential amino acid content, produce hyperphagia if dietary protein content is low and conversely reduce food intake if dietary protein content is high.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5120084&req=5

Figure 2: Central detection of amino acid availability in the regulation of feeding behavior. Discrete cell populations in the brain monitor extracellular amino acid availability through a variety of mechanisms and engage downstream feeding-regulatory circuits to prevent or limit the ingestion of diets with imbalanced essential amino acid content, produce hyperphagia if dietary protein content is low and conversely reduce food intake if dietary protein content is high.
Mentions: Collectively, the data reviewed here support a role for a distributed network of discrete brain regions in primary amino acid sensing in the control of multiple behavioral responses to changes in dietary amino acid intake, as summarized in Figure 2. Many gaps remain to be filled to complete our understanding of these processes, and a key poorly described step is the intracellular coupling of intracellular amino acid availability to neuronal electrical and synaptic activity, as highlighted in Figure 1B. Does this coupling rely on specific intracellular components that could perhaps represent a unique molecular signature of amino acid sensing neurons, making these cells amenable to molecular genetics? Identifying a molecular marker for amino acid sensing neurons would prove extremely useful in the characterization of neurocircuits engaged downstream from primary brain sensors to regulate feeding behavior.

View Article: PubMed Central - PubMed

ABSTRACT

Dietary protein quantity and quality greatly impact metabolic health via evolutionary-conserved mechanisms that ensure avoidance of amino acid imbalanced food sources, promote hyperphagia when dietary protein density is low, and conversely produce satiety when dietary protein density is high. Growing evidence supports the emerging concept of protein homeostasis in mammals, where protein intake is maintained within a tight range independently of energy intake to reach a target protein intake. The behavioral and neuroendocrine mechanisms underlying these adaptations are unclear. While peripheral factors are able to signal amino acid deficiency and abundance to the brain, the brain itself is exposed to and can detect changes in amino acid concentrations, and subsequently engages acute and chronic responses modulating feeding behavior and food preferences. In this review, we will examine the literature describing the mechanisms by which the brain senses changes in amino acids concentrations, and how these changes modulate feeding behavior.

No MeSH data available.


Related in: MedlinePlus