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Peptide Hormones: Insulin

Insulin is produced in the beta cells of the pancreas from a larger peptide called preproinsulin. Endogenous insulin has a half-life of three to five minutes and the pancreas secretes about 40 to 50 units of insulin per day in normal adults. Insulin secretion is stimulated in response to feeding with glucose being the strongest stimulator. Insulin binds to a cell surface receptor resulting in increased glucose and amino acid transport through the cell membrane and glycogen and lipid synthesis and storage. This is accomplished through the increased movement of Glut4 molecules to the surface of the cell membrane. Glut4 is the main transporter of glucose across cell membranes into cells. Insulin also binds to the type 1 IGF receptor which results in growth stimulating effects in muscle cells.

Insulin is the main “storage” hormone and is very anabolic as well as anti-catabolic. In addition to increasing glycogen and lipid synthesis and storage, insulin also promotes protein synthesis in skeletal muscle and promotes glycogen storage by increasing glucose transport in skeletal muscle cells1,2,3.

Insulin and insulin syringes are available in many states without a prescription making insulin a more available anabolic hormone than AAS. That being said, the dangers of insulin are immediate and potentially deadly. Insulin can produce in a state of severe hypoglycemia that can result in coma or death with a matter of minutes. In addition, insulin resistance will occur over time in healthy individuals using insulin. While this risk is down-played by users and on boards discussing insulin, it should be considered a very real risk. Though insulin is highly anabolic in skeletal muscle, it is also very anabolic in adipose tissue. This can result in increases in body fat, especially when used in high doses on its own. Often insulin is combined with growth hormone to take advantage of growth hormone’s fat burning ability and to combat the decrease in insulin sensitivity with GH. IGF-1 is sometimes combined with insulin (and GH) but this increases the risk of hypoglycemia.

 

1. Zierath JR, Krook A, Wallberg-Henriksson H. Insulin action and insulin resistance in human skeletal muscle. Diabetologia. Jul;43(7):821-35, 2000

2. Wojtaszewski JF, Hansen BF, Kiens B, Richter EA. Insulin signaling in human skeletal muscle: time course and effect of exercise. Diabetes. Nov;46(11):1775-81, 1997

3. Biolo G, Williams BD, Fleming RY, Wolfe RR. Insulin action on muscle protein kinetics and amino acid transport during recovery after resistance exercise. Diabetes. May;48(5):949-57, 1999

 


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