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Abdominal Fat Connection – Salt, Cortisol, and Fat – Thomas DeLauer
Cortisol & Salt
Mineralocorticoids play a critical role in regulating concentrations of minerals – particularly sodium and potassium – in extracellular fluids
For example, loss of adrenal glands leads rapidly to life-threatening abnormalities in electrolyte and fluid balance (urinary excretion of sodium is high and the concentration of sodium in extracellular fluid decreases significantly)
The major target of aldosterone is the distal tubule of the kidney, where it stimulates exchange of sodium and potassium – three primary physiologic effects of aldosterone result:
Increased resorption of sodium: sodium loss in urine is decreased under aldosterone stimulation
Increased resorption of water, with consequent expansion of extracellular fluid volume – this is an osmotic effect directly related to increased resorption of sodium
Increased renal excretion of potassium
What’s more, cortisol increases glomerular filtration rate, and renal plasma flow from the kidneys thus increasing increasing sodium and water retention and potassium excretion in high amounts acting as aldosterone
This is because in high amounts cortisol is converted to cortisone which acts on mineralocorticoid receptor mimicking the effect of aldosterone
It also increases sodium and water absorption and potassium excretion in the intestines
Low sodium status can also increase aldosterone, an adrenal hormone that seeks to preserve sodium in the body when it’s perceived to be scarce.
Simply, as cortisol elevates your body holds onto more sodium
Aldosterone is responsible for telling the kidneys to retain the salt that your body needs.
A lack of sodium can cause the brain to send signals to the adrenal gland to increase the release of hormones responsible for water balance. Cortisol is released alongside these other hormones.
Causes the release of aldosterone alongside cortisol
Study – Practical Laboratory Medicine
The relationship between serum cortisol and serum sodium levels
Data were gathered over a 23 month period (from the Laboratory Information Management System at the Leeds Teaching Hospitals NHS Trust) for instances where serum sodium and cortisol had been measured on a single sample
Data were also gathered over the same time period for all patients with severe hyponatremia, (serum sodium ≤120 mmol/L) in order to determine the frequency of cortisol requesting and the incidence of adrenal insufficiency
*Hyponatremia refers to a low level of sodium in the blood*
Analysis of the data (3268 patients) revealed a trend showing higher cortisol concentrations in patients who were severely hypo- or hypernatremia
The median cortisol concentration for patients with sodium ≤110 mmol/L was 856 nmol/L, and there was a gradual decrease in cortisol over the sodium range ≤110–150 mmol/L
Patients with sodium ≥151 mmol/L had a median cortisol of 725 nmol/L
42% of the 978 patients with serum sodium ≤120 mmol/L had serum cortisol measured within two weeks, of whom 1.7% were diagnosed with adrenal insufficiency
Additional – NST Receptors
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
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
Taste responsiveness was generally reduced in sodium-depleted rats
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