SGLT2 inhibitors (from "Sodium dependent glucose transporter") are drugs that are currently being tested for the treatment of diabetes mellitus type 2. In the clinical trial, which involved up to 10,000 volunteers to the, was a significant therapeutic efficacy must be proven. As a first active ingredient, the European Medicines Agency (EMA) issued on 12 November 2012 for dapagliflozin drug approval. Other substances, such as Canagliflozin, Empagliflozin, Ipragliflozin and Tofogliflozin are in advanced clinical testing, respectively. are approved in both the US and in Europe.
SGLT-2 (sodium-glucose linked transporter 2) is a secondary active carrier protein absorbed in the kidney proximal tubule from the primary urine glucose and sodium (the Natriumgradient built up by the sodium-potassium pump provides the driving force for this the glucose absorption is). Is this protein due to a hereditary disorder not functional, can be found in individuals affected high sugar levels in the urine, without that this would be caused by high blood sugar levels.
This make the SGLT2 inhibitors advantage by mimicking the effect and inhibit the renal sodium-dependent glucose transporter type 2 (SGLT-2) in the renal tubules. The function is that they promote the urinary excretion of glucose concentration dependent. This leads to both a reduction in blood glucose concentration as well as to a loss of calories. However, no hypoglycemia. This mechanism of blood glucose lowering is independent of insulin action and -ausschüttung as well as insulin resistance or a lack of insulin production by the beta cells of the pancreas.
Appropriate drugs are taken orally and used as a monotherapy or in combination with other antidiabetic agents.
Moreover, in the kidney exist SGLT-1 transporter (in the distal tubule), which have a greater affinity for glucose compared with SGLT2 inhibitors. Therefore, it comes despite the use of SGLT2 inhibitors for the absorption of glucose. Since SGLT-1 transports two sodium ions in symport with glucose, the energy required for this reabsorption is significantly higher. Moreover thereby explain why the one the inhibition of SGLT-2 not to hypoglycemia (low blood sugar) leads and it does not get to the other despite the inhibition of sodium re a disturbance of the electrolyte balance.
SGLT-2 (sodium-glucose linked transporter 2) is a secondary active carrier protein absorbed in the kidney proximal tubule from the primary urine glucose and sodium (the Natriumgradient built up by the sodium-potassium pump provides the driving force for this the glucose absorption is). Is this protein due to a hereditary disorder not functional, can be found in individuals affected high sugar levels in the urine, without that this would be caused by high blood sugar levels.
This make the SGLT2 inhibitors advantage by mimicking the effect and inhibit the renal sodium-dependent glucose transporter type 2 (SGLT-2) in the renal tubules. The function is that they promote the urinary excretion of glucose concentration dependent. This leads to both a reduction in blood glucose concentration as well as to a loss of calories. However, no hypoglycemia. This mechanism of blood glucose lowering is independent of insulin action and -ausschüttung as well as insulin resistance or a lack of insulin production by the beta cells of the pancreas.
Appropriate drugs are taken orally and used as a monotherapy or in combination with other antidiabetic agents.
Moreover, in the kidney exist SGLT-1 transporter (in the distal tubule), which have a greater affinity for glucose compared with SGLT2 inhibitors. Therefore, it comes despite the use of SGLT2 inhibitors for the absorption of glucose. Since SGLT-1 transports two sodium ions in symport with glucose, the energy required for this reabsorption is significantly higher. Moreover thereby explain why the one the inhibition of SGLT-2 not to hypoglycemia (low blood sugar) leads and it does not get to the other despite the inhibition of sodium re a disturbance of the electrolyte balance.