Translations:Insulin/47/en

The actions of insulin (indirect and direct) on cells include:

• Stimulates the uptake of glucose – Insulin decreases blood glucose concentration by inducing 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 fat synthesis – insulin forces fat cells to take in blood glucose, which is converted into triglycerides; 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 – 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 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 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 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 (CPT1), a mitochondrial enzyme necessary for the translocation of fatty acids into the intermembrane space of the mitochondria for fatty acid metabolism.