Metformin HCl

Metformin (500 μM) activates AMPK in hepatocytes, as a result, acetyl-CoA carboxylase (ACC) activity is reduced, fatty acid oxidation is induced, and expression of lipogenic enzymes is suppressed. Metformin (2 mM) activates muscle AMPK and promotes glucose uptake. Metformin (500 μM) or AICAR strongly suppresses SREBP-1 mRNA expression in rat hepatocytes. Metformin ameliorates hyperglycemia without stimulating insulin secretion, promoting weight gain, or causing hypoglycemia. Metformin has beneficial effects on circulating lipids linked to increased cardiovascular risk. Metformin decreases hepatic glucose production and increases skeletal myocyte glucose uptake. ^[1]

Metformin requires LKB1 in the liver to lower blood glucose levels. ^[2]

Metformin (2 mM) leads to a significant increase in the activity of both α1- and α2-containing complexes in muscle cells. Metformin (2 mM) also increases threonine 172 phosphorylation in muscle cells. ^[3]

Metformin (100 mg/ml, po) treatment produces significant decreases in hepatic expression of mRNAs for SREBP-1, FAS, and S14 in SD rats that are consistent with effects documented in cells. Metformin also decreases hepatic lipids in obese mice. ^[1]

Metformin (250 mg/kg, i.p.) increases AMPK phosphorylation in livers of wild-type mice. Metformin (250 mg/kg, i.p.) treatment reduces blood glucose by more than 50% in the wild-type mice on a high-fat diet. Metformin (250 mg/kg, i.p.) treatment also loweres blood glucose in the ob/ob mice by 40%. ^[2]

• Cell lines

  Rat primary hepatocytes

• Concentrations

  500 µM

• Incubation Time

  1 h

• Method

  Cells were treated with different concentrations of metformin.

• Animal Models

  Male Sprague-Dawley rats

• Dosages

  100 mg/300 mg

• Administration

  o.g.