Paul Saladino· MD
what we know is that the signaling of insulin a molecule that often gets vilified is critical at the level of the kidney for proper maintenance of electrolytes
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The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
what we know is that the signaling of insulin a molecule that often gets vilified is critical at the level of the kidney for proper maintenance of electrolytes
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insulin can directly increase the activity of the epithelial sodium channel the sodium phosphate co-transporter the sodium hydrogen exchanger type 3 and the sodium potassium atpase
insulin has been shown to have anti nitric actions in humans and animal models natures is the loss of sodium so insulin is resulting in retention of sodium that's normal human physiology that's important in this review we present the current state of understanding with regard to the regulation of the major renal sodium transporters by insulin in the kidney
insulin can directly increase the activity of the epithelial sodium channel the sodium phosphate co-transporter the sodium hydrogen exchanger type 3 and the sodium potassium atpase
insulin has been shown to have anti nitric actions in humans and animal models natures is the loss of sodium so insulin is resulting in retention of sodium
several groups using primary cell culture have demonstrated that insulin can directly increase activity of the epithelium sodium channel the sodium phosphatase co-transporter the sodium hydrogen exchanger type 3
insulin has been shown to have anti nitric actions in humans and animal mammals nitrous natures is the loss of electrolytes in the kidney okay so the majority of renal sodium transporters are controlled by insulin in the kidney
the majority of renal sodium transporters are controlled by insulin in the kidney several groups using primary cell culture have demonstrated that insulin can directly increase activity of the epithelium sodium channel the sodium phosphatase co-transporter the sodium hydrogen exchanger type 3 and the sodium potassium atpase
we need it at the level of the kidneys to hang on to sodium and potassium and other electrolytes
insulin has been shown to have anti-natural that is the loss of electrolytes especially sodium actions in humans and animal models they say several groups using primarily cell culture have demonstrated that insulin can directly increase the activity of the epithelial sodium channel sodium phosphate co-transporter sodium hydrogen hydrogen exchanger type 3 sodium potassium atpase
in this review we present the currency state of understanding with regard to the regulation of the major renal sodium Transporters by insulin in the kidney several groups using primary cell culture have demonstrated that insulin can directly increase the activity of the epithelial sodium channel the sodium phosphate co-transporter the sodium hydrogen exchanger type 3 and the sodium potassium atpase in the kidney
but there's just at the level of the kidneys I think that insulin has value in a postprandial State not all the time we don't want to be insulin resistant and have chronically elevated insulin but I don't really understand why insulin has gotten such a bad rap when it literally Keeps Us Alive and the post-prandial after eating insulin spike is valuable for us at the level of maintenance of electrolytes in the kidney
I've since learned that insulin has a crucial role in signaling at the kidney to hold on to electrolytes, specifically sodium, but connected with sodium, insulin is going to affect the resorption, the way your body reabsorbs and holds on to all sorts of electrolytes, all sorts of minerals, sodium potassium chloride magnesium and others.