darrenG10
Well-known member
Recent research has demonstrated that Metformin can decrease testosterone production and raise sex hormone binding globulin when dosed consistently for 2 weeks at 1700 mgs a day. When you dose Metformin infrequently as in twice a week, the negative effect on testosterone levels will be miniscule to non- existent. You will benefit from an increased level of AMP-activated protein kinase activity in skeletal muscle, which will increase the translocation of GLUT-4 transporters to skeletal muscle, increasing glucose uptake. AMP-activated protein kinase will also increase fatty acid oxidation by inactivating acetyl-CoA-carboxylase. By regulating acetyl- CoA-carboxylase, carnitine palmitoyltransferase (CPT-1) is not blocked and able to transport fatty acids into the mitochondria for oxidation.
Metformin has selectivity towards muscle cells opposed to fat cells when clearing nutrients from the blood. It has also been demonstrated to serve as an anti-catabolic agent when muscles have been immobilized due to bone or joint complications. A study was conducted to observe the effect Metformin had on maintaining muscle glycogen inside muscle fibers and stabilizing muscle weight during inactivity of muscles in test rats. Researchers discovered that rats not treated with Metformin lost significant muscle glycogen and muscle weight when muscles were immobilized. Inactive muscles also became insulin resistant due to down regulation of insulin receptor substrate-1 (IRS-1) in intra-cellular tissues. Decreased IRS-1 along with GLUT-4 translocation is a recipe for muscular atrophy.
Metformin has selectivity towards muscle cells opposed to fat cells when clearing nutrients from the blood. It has also been demonstrated to serve as an anti-catabolic agent when muscles have been immobilized due to bone or joint complications. A study was conducted to observe the effect Metformin had on maintaining muscle glycogen inside muscle fibers and stabilizing muscle weight during inactivity of muscles in test rats. Researchers discovered that rats not treated with Metformin lost significant muscle glycogen and muscle weight when muscles were immobilized. Inactive muscles also became insulin resistant due to down regulation of insulin receptor substrate-1 (IRS-1) in intra-cellular tissues. Decreased IRS-1 along with GLUT-4 translocation is a recipe for muscular atrophy.