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The actions of insulin (indirect and direct) on cells include:
* Stimulates the uptake of glucose – Insulin decreases blood glucose concentration by inducing [[cellular glucose intake|intake of glucose]] by the cells. This is possible because Insulin causes the insertion of the GLUT4 transporter in the cell membranes of muscle and fat tissues which allows glucose to enter the cell.
* Increased [[Fatty acid metabolism#Glycolytic endy products are used in the conversion of carbohydrates into fatty acids|fat synthesis]] – insulin forces fat cells to take in blood glucose, which is converted into [[triglyceride]]s; decrease of insulin causes the reverse.
* Increased [[esterification]] of fatty acids – forces adipose tissue to make neutral fats (i.e., [[triglycerides]]) from fatty acids; decrease of insulin causes the reverse.
* Decreased [[lipolysis]] in – forces reduction in conversion of fat cell lipid stores into blood fatty acids and glycerol; decrease of insulin causes the reverse.
* Induced glycogen synthesis – When glucose levels are high, insulin induces the formation of glycogen by the activation of the hexokinase enzyme, which adds a phosphate group in glucose, thus resulting in a molecule that cannot exit the cell. At the same time, insulin inhibits the enzyme glucose-6-phosphatase, which removes the phosphate group. These two enzymes are key for the formation of glycogen. Also, insulin activates the enzymes phosphofructokinase and glycogen synthase which are responsible for glycogen synthesis.
* Decreased [[gluconeogenesis]] and [[glycogenolysis]] – decreases production of glucose from noncarbohydrate substrates, primarily in the liver (the vast majority of endogenous insulin arriving at the liver never leaves the liver); decrease of insulin causes glucose production by the liver from assorted substrates.
* Decreased [[proteolysis]] – decreasing the breakdown of protein
* Decreased [[Autophagy (cellular)|autophagy]] – decreased level of degradation of damaged organelles. Postprandial levels inhibit autophagy completely.
* Increased amino acid uptake – forces cells to absorb circulating amino acids; decrease of insulin inhibits absorption.
* Arterial muscle tone – forces arterial wall muscle to relax, increasing blood flow, especially in microarteries; decrease of insulin reduces flow by allowing these muscles to contract.
* Increase in the secretion of [[hydrochloric acid]] by parietal cells in the stomach.
* Increased potassium uptake – forces cells synthesizing [[glycogen]] (a very spongy, "wet" substance, that [[Glycogen#Structure|increases the content of intracellular water, and its accompanying K+ ions]]) to absorb potassium from the extracellular fluids; lack of insulin inhibits absorption. Insulin's increase in cellular potassium uptake lowers potassium levels in blood plasma. This possibly occurs via insulin-induced translocation of the [[Na+/K+-ATPase|Na+/K+-ATPase]] to the surface of skeletal muscle cells.
* Decreased renal sodium excretion.tocytes, insulin binding acutely leads to activation of protein phosphatase 2A (PP2A), which dephosphorylates the bifunctional enzyme [[Phosphofructokinase_2#PFKB1:_Liver,_muscle,_and_fetal | fructose bisphosphatase-2 (PFKB1)]], activating the phosphofructokinase-2 (PFK-2) active site. PFK-2 increases production of fructose 2,6-bisphosphate. [[Fructose 2,6-bisphosphate]] allosterically activates [[PFK-1]], which favors glycolysis over gluconeogenesis. Increased glycolysis increases the formation of [[malonyl-CoA]], a molecule that can be shunted into lipogenesis and that allosterically inhibits of [[Carnitine palmitoyltransferase I | carnitine palmitoyltransferase I (CPT1)]], a mitochondrial enzyme necessary for the translocation of fatty acids into the intermembrane space of the mitochondria for fatty acid metabolism.

Translations:Insulin/47/en - Revision history

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