I'll post my notes here.

Some of the salt regulating pathways, have only been considered in terms of water regulation, but these also have a impact on metabolic processes especially in fat cells

Why does sodium matter? It's essential, without enough sodium the body stops functioning. Electrolyte balance and fluid regulation. Where salt goes, water follows. We need sodium, and other electrolytes, for nerve function. Acid / Base balance - maintaining PH balance. Absorption of nutrients (they follow the sodium from the digestive tract).

Renin Angiotensin Aldosterone System - RAAS - ras. Main system for regulating salt in the body, primary signal is low blood pressure triggering RAAS. Secondary trigger when sodium levels drop. Once its turned on, kidneys release Renin. At the same time the liver produces Angiotensinogen - A hormone/protein. inogen implies it is not in its primary form yet. Renin+Angiotensinogen = Angiotensin1. ACE - Angiotension converting enzyme (produced by the lungs - which actually are a endocrine gland!) + Angiotension1 = Angiotensin 2.

Angiotensin 2 - elicits powerful vasoconstriction - restoring blood pressure by narrowing blood vessels. Also has a anti-diuretic effect. Stimulates thirst centers - drinking water will help restore blood volume and pressure. Most famously - in the Adrenal cortex and stimulates the production of aldosterone.

Aldosterone has a powerful effect in the kidneys to reabsorb any sodium that had been removed from the blood, and reintroduced into the blood. The theory being the body is setting up the stage to encourage osmosis for water to correct blood pressure.

This system has a built in negative feedback loop, once aldosterone has stimulated the kidney effect, the RAAS system should shutdown as the stimulants are removed.

Anti-hypertension medications interfere with this system. ACE inhibitors - block the ACE from the lungs in the above cycle. Also Angiotension Receptor blockers.

Insulin also has an effect on salt handling. Part of its anabolic effects - you need more electrolytes to grow. Insulin directly stimulates sodium reabsorption in the kidney tubules particularly in the distal part. This activity is mediated by insulins effect on sodium potassium pumps - driving more sodium back into the body. Insulin also has a heavy impact on the RAAS system via sympathetic nervous system increasing renin production and thus the RAAS cycle resulting in higher aldosterone (which even more aggressively collects sodium). Insulin also enhances vascular sensitivity to Angiotensin 2 - increasing the vasoconstriction effect (restoring/increasing blood pressure).

People who are deficient in salt (such as a low salt diet), chronically triggering the RAAS system - and insulin levels - in a attempt to compensate for the low sodium levels. Therefor mechanistically salt restriction increases insulin resistance (there is a study -Lastra 2010, Sharma 1999 Maybe?.

Fat cells - have receptors for both Aldosterone, Angiotensin 2

Aldosterone receptors - mineralocorticoid receptors. Corticoid means it coming from the cortex of the adrenal gland, mineralo evokes minerals i.e. salt. When aldosterone binds to fat cells, stimulates fat cell growth (hypertrophy).

Angiotensin 2 - Many receptors - stimulates the expression of multiple lipogenic (synthesis of fat) enzymes, turns on fatty acid synthes, and acetyl coa carboxylase (links carbons) - the combination will take carbons and create new fat cells. Can also promote fibrosis of fat cells, key development for fat cell going from insulin sensitive to insulin resistant state (promoting inflammation). Therefor Angiotension 2 promotes inflammation in the fat cells. ppar gamma is activated as well, and tells proto-cells to become fat cells.

When insulin binds to its receptor on a cell, a signaling cascade, but with Angiotensin 2 is involved it disrupts/antagonizes this signal chain.

No signal in the body can promote fat cell growth in the absence of insulin.

TLDR - Salt is good.