Because of these reasons, phlorizin was never pursued in humans.
2.
Unfortunately, in spite of these properties, phlorizin was not suitable enough for clinical development for several reasons.
3.
Phlorizin has very poor oral bioavailability, it is broken down in the gastrointestinal tract, so it had to be given parenterally.
4.
Although phlorizin was not suitable for further clinical trials, it served an important role in the development of a new class of drugs, SGLT-2 inhibitors.
5.
The encoded protein is known to bind to hepatocyte nuclear factor-1alpha ( HNF-1alpha ), and this interaction is essential for cooperative activation of the intestinal lactase-phlorizin hydrolase promoter.
6.
Phloretin, the active metabolite of phlorizin, is a potent inhibitor of facilitative glucose transporters and also, phlorizin seem to lead to serious adverse events in the gastrointestinal tract like diarrhea and dehydration.
7.
Phloretin, the active metabolite of phlorizin, is a potent inhibitor of facilitative glucose transporters and also, phlorizin seem to lead to serious adverse events in the gastrointestinal tract like diarrhea and dehydration.
8.
Phlorizin seemed to have very interesting properties and the results in animal studies were encouraging, it improved insulin sensitivity and in diabetic rat models it seemed to increase glucose levels in urine and also normal glucose concentration in plasma occurred without hypoglycemia.
9.
In the rabbit Na + : D-glucose co-transporter, SGLT1, the glucose translocation pathway probably involves TMSs 10-13, and the binding site for the inhibitor, phlorizin, involves loop 13 ( residues 604-610 ).
10.
Phlorizin is a flavonoid that is found in apple trees, particularly in the leaves, and in only small amounts if at all in other plants, even other species of the " Malus " genus or related plants such as pear trees.
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