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Lack of Salt Can Make You Gain Fat and Crave Sweets

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Lack of Salt Can Make You Crave Sugar and Gain Weight

Sodium Appetite

The neurocircuitry regulating fluid balance requires coordination between hindbrain and forebrain nuclei that essentially serve the purpose of sensing changes in mineral-fluid balance and blood volume

In the hindbrain, the nucleus of the solitary tract (NST) and adjacent area postrema (AP) play a critical role in monitoring body fluid homeostasis

These areas are sensitive to circulating Ang II and aldosterone, osmotic concentration, and changes in blood pressure

The NST projects to the lateral parabrachial nucleus (LPBN), and together these structures exert tonic inhibition on sodium appetite

Although structures along the LT and hindbrain detect when the body is in a state of a sodium deficit, these sensory areas must work in tandem with neural circuitry that promotes motivated behavior to promote thirst and salt appetite

Brain areas that mediate appetitive motivated behaviors essentially energize behavior (i.e., promote a state of physiological and psychological arousal) and direct behavior towards a goal object in the environment

An important neural pathway that appears to mediate all appetitive motivated behaviors is the dopaminergic projections from the ventral tegmental area (VTA) to the nucleus accumbens (NAc), referred to as the mesolimbic dopamine system

Increased activity in the NAc is correlated with the presence of a sodium appetite

Sodium depletion alters how the nervous system, including structures within the mesolimbic dopamine system, processes the taste of salt

Sodium deficiency reduces gustatory nerve responses to salt – Neurons within the NST, which receives afferent information from the gustatory nerves, also exhibit altered firing patterns to the taste of salt during deficiency

Similar to the changes in firing observed in the gustatory nerves, the salt-responsive neurons in the NST exhibit reduced firing during deficiency

Interestingly, neurons that respond to sweet tastes such as sucrose begin to fire in response to salty tastes in the depleted animal

Areas in the forebrain that code the motivational and rewarding value of stimuli exhibit a different profile of responses to the taste of salt during sodium deficiency

Study – The Journal of Physiology

This study recorded taste activity from 94 single neurons in the nucleus tractus solitarius of sodium-replete (44) and of deprived (50) rats

12 rats were given a nominally sodium-free diet for 10-13 days – 9 rats provided control data

Taste stimuli included five concentrations of NaCl plus eight other salts, acids, sugars and alkaloids

Spontaneous activity was 33% lower while responses to sodium salts lagged by a mean of 30%, to acids by 25% and to bitter salts and quinine by 17%

Mean activity to sugars was 60% higher in the deprived group

Activity in sugar- and salt-profile neurons was most affected:

In deprived animals, responses to sodium salts were lower by 80% among salt-profile cells while among sugar-profile neurons activity to these stimuli was nearly 10 times greater than in controls

These changes in activity resulted in a dramatic shift in the participation of sodium- and sugar-profile cells in the afferent signal for NaCl

In replete animals, 60% of sodium-induced activity was transmitted through salt-profile cells while only 1% occurred in sugar-profile neurons

In deprived subjects, this situation was nearly reversed as 7% of the total NaCl response was conveyed through salt-profile cells while the contribution of neurons with sugar-profiles rose to 46%

Multidimensional stimulus spaces based on average activity in each of four identifiable neuron subgroups demonstrated a shift in the affiliation of sodium salts away from bitter and acid stimuli and towards sugars

References

1) The biopsychology of salt hunger and sodium deficiency. (n.d.). Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4433288/
2) Jacobs KM , et al. (n.d.). Taste responses in the nucleus tractus solitarius of sodium-deprived rats. – PubMed – NCBI. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/3254418/
3) Unexpected effect of the appetite-stimulating hormone ghrelin on ENaC: hunger for sodium? (n.d.). Retrieved from https://www.sciencedirect.com/science/article/pii/S0085253815559875
4) Unexpected effect of the appetite-stimulating hormone ghrelin on ENaC: hunger for sodium? (n.d.). Retrieved from https://www.semanticscholar.org/paper/Unexpected-effect-of-the-appetite-stimulating-on-Seki/5303124f720ac6369918cbb4cb9fb3a9e1b9df9d
5) Loriaux AL , et al. (n.d.). Nucleus accumbens shell, but not core, tracks motivational value of salt. – PubMed – NCBI. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/21697439/

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