Volume 1, Issue 3, 02/02/2009
How does metformin (Glucophage®) lower fasting glucose levels different from other glucose lowering medications without causing hypoglycemia?
It is well known that patients with type 2 diabetes mellitus (T2DM) are characterized as having insulin resistance, a decrease in insulin mediated glucose uptake by peripheral tissues (despite elevated insulin levels) and excessive basal rates of hepatic gluconeogenesis.(1,2) An impairment in peripheral glucose uptake and suppression of gluconeogenesis both contribute to worsening postprandial (post-meal) hyperglycemia whereas excessive basal rates of hepatic gluconeogenesis primarily contributes to the worsening of fasting glucose levels. To date, the biguanide class of medications primarily suppresses the excessive basal rates of gluconeogenesis which includes primarily metformin (Glucophage®).(3,4) The other biguanide, phenformin (Azucaps, Insoral, Fenformin), is no longer FDA approved in the United States because of unacceptable rates of lactic acidosis but can still be used and/or purchased by clinicians/patients in other countries.(5) So why do type 2 diabetics have excessive rates in basal hepatic glucose production?......To read the full answer please LOGIN or SUBSCRIBE NOW.

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