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Stimulation of the PI3K/Akt/mTOR protein synthesis pathway: Upon receptor activation, IGF-1 LR3 triggers intracellular cascades including PI3K and Akt phosphorylation

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In CKD, a decrease in viable nephrons and reduction in glomerular filtration rate (GFR) change the kidneys normal physiology and sodium balance.67 68 Even though an adaptive fractional increase in sodium excretion per individual nephron unit compensates for the reduced number of working nephrons, the kidneys inability to excrete sufficient amounts of sodium results in sodium retention, extracellular fluid expansion, and blood pressure increase.68 69 Likewise, the reninangiotensinaldosterone system is activated in CKD, further exacerbating sodium retention and causing vasoconstriction which could significantly raise blood pressure.69 Sodium retention and its association with blood pressure in CKD are often referred to as sodium-sensitive hypertension.70 Therefore, reducing salt intake is recommended to manage hypertension in patients with CKD.68 The natriuretic and diuretic effect of the ketogenic diet may help alleviate sodium retention and improve systemic and glomerular blood pressure

Within the CNS, GLP-1R is found in neurons, astrocytes, and oligodendrocytes