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Loss of glucose from the urine could lead to a continued high concentration of glucose in the kidneys. would it lead to excessive glycation of kidney proteins and thereby damage of kidneys
You identify one of zillions of conceivable issues with this new class of drugs; at this moment I have no idea, but it would seem likely that your question won't be answered until big studies are done that last a longer time, or perhaps until the drug has been on the market for several years.
Which, of course, is why the FDA and other regulatory authorities in other countries require large trials (called Phase III trials) that last at least a year before they will consider approving a drug for general use. And why they require continuing surveillance after they're approved.
Good question!
Dr.Q, very well put & hope all can appreciate some further supporting data that clarifies some much wanted answerd questions... enjoy the indepth read...on Apple Trees to Sodium Glucose Co-Transporter Inhibitors: A Review of SGLT2 Inhibition
http://clinical.diabetesjournals.org/content/28/1/5.full.pdf
http://clinical.diabetesjournals.org/content/28/1/5.full
I've written another SharePost about one of the SGLT-2 inhibitors: dapagliflozin. The FDA's Advisory Committee has voted against its approval because of safety concerns. See Dapagliflozin, a New Drug for T2D, Rejected by an FDA Advisory Committee.
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interesting post- i found the Mg results the most intriguing- magnesium deficiency has been implicated in the etiology of insulin resistance- and the suspected process is via urinary losses- studies have shown that higher Mg intake can increase insulin sensitivity, but from this post idea, decreasing urinary losses of Mg might also work to increase insulin sensitivity- and i've also wondered if there's any link between chronic diuretic use and insulin resistance, via the same process of increased Mguria